ESMO 2026 trial results & KOL discussions, by trial →Each slide group below also links to its Full trial page and All posts.
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- Heme & Myeloma 9
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- KOL infographics 54
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- Last updated October 29, 2026
Heme & Myeloma 9
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#LaurenBanks from @MSKCancerCenter presented very promising data of an investigator-initiated trial of #Lifileucel in patients with #UPS and #DDLPS. Dawn of a new era of therapeutics for sarcomas.
Definitely an active treatment approach and phase 3 multicentre trial is on-going. @IovanceBio More to follow!
@ctosociety @myESMO #ESMO26 #ESMOAmbassadors #sarcoma #celltherapy
[Slide 1]
08:30 - 10:00 Rapid oral: Sarcoma
CHAIRS: MARK DICKSON, PALMA DILEO, CESAR SERRANO
Patient characteristics and cohort level outcomes
Characteristic | N = 12¹
Age at consent
Median (Q1, Q3) 59 (49.5, 64)
Mean (SD) 56.42 (8)
Min, Max 43, 66
Sex
Female 4 (33%)
Male 8 (67%)
Diagnosis
Sarcoma (DDLS) 8 (67%)
Sarcoma (UPS) 4 (33%)
First-line treatment
Doxorubicin 7 (58%)
Gemcitabine + Docetaxel 1 (8%)
Palbociclib 2 (17%)
Retifanlimab+Palbociclib 2 (17%)
First-line treatment category
Chemotherapy 8 (67%)
Combination therapies 2 (17%)
Other Small Molecule Inhibitors 2 (17%)
N treatment lines
1 2 (17%)
2 6 (50%)
3 2 (17%)
4 1 (8%)
>5 1 (8%)
¹ n (% enrolled)
Characteristic | N | 95% CI
Primary Endpoints
Feasibility¹ 10 (83.3%) 51.6%, 97.9%
AE incidence² 10 (100%) 69.2%, 100%
Secondary Endpoints²
ORR (in spec) 4 (50.0%) 15.7%, 84.3%
ORR (overall) 4 (40.0%) 12.2%, 73.8%
DCR (overall) 8 (80%) 44.4%, 97.5%
DOR Not reached
¹ n (% enrolled); ² n (% treated); Abbreviation: CI = Confidence Interval
Feasibility (enrolled patients):
• 10 /12 patients harvested had lifileucel infused
• 6 of first 10 pts infused with in spec product
• At data cutoff, 8 with in spec product
• 2/12 were not infused
• Manufacturing failure; clinical progression
Safety (infused patients):
• 10/10 pts→ grade 4 cytopenias
• 8/10 pts → grade ≥3 non-hematologic TRAE, mostly febrile neutropenia (40%)
• 1 pt → grade 4 pulmonary infection and hemorrhage after TIL harvest
• No grade 5 events related to treatment;
• 1 pt died of disease after progression
Lauren Banks
Lifileucel in patients with undifferentiated pleomorphic sarcoma (UPS) or dedifferentiated liposarcoma (DDLS)
MALAGA AUDITORIUM - HALL 3
[Slide 2]
08:30 - 10:00 Rapid oral: Sarcoma
CHAIRS: MARK DICKSON, PALMA DILEO, CESAR SERRANO
Patient-level data: Updated data cutoff
Age (y) | Sex | Diagnosis | Prior treatment lines (n) | Prior checkpoint inhibitor (Y/N) | Lifileucel infusion (Y/N) | Target SOD (mm) | IL-2 doses (n) | Best overall response | DOR++ (weeks)
66 M UPS 7 Y Y 114.7 2 PR 46
51 M DDLS 2 N Y 115.3 2 PR 26
43 F DDLS 2 N Y 39.0 5 PR 40
49 M UPS 2 Y Y 82.8 5 PR 6
45 M UPS 3 Y Y 141.0 3 SD
62 M DDLS 1 Y Y 70.3 6 SD
66 M DDLS 2 N Y 161.6 2 PD
50 M DDLS 2 Y Y 177.6 6 PD
* Infused with out of spec product:
60 M UPS 2 N Y 96.9 6 SD
66 F DDLS 1 Y Y 78.6 6 SD
Uninfused product:
61 F DDLS 3 N N
58 F DDLS 4 N N
++As of data cutoff date of 09 September 2026, all PRs were ongoing
Abbreviations: Undifferentiated pleomorphic sarcoma (UPS), Dedifferentiated liposarcoma (DDLS), Stable disease (SD), Partial response (PR), Progressive disease (PD)
Percent change in target lesion sum of diameters from baseline (%)
Weeks from baseline
Best overall response: Partial response, Stable disease, Progressive disease
Confirmed CR/PR
Progression
Ongoing surveillance
* Infused with out of spec product
Lauren Banks
Lifileucel in patients with undifferentiated pleomorphic sarcoma (UPS) or dedifferentiated liposarcoma (DDLS)
MALAGA AUDITORIUM - HALL 3
[Slide 3]
08:30 - 10:00 Rapid oral: Sarcoma
CHAIRS: MARK DICKSON, PALMA DILEO, CESAR SERRANO
Conclusions and Highlights
• IIT led to design and opening of Phase II multicenter IOV-SAR-201 (SARATOGA study)
• Many of the IIT patients would have qualified for SARATOGA
Feasibility
• 10/12 patients underwent Lifileucel infusion
• Feasibility endpoint met
Safety
• Expected grade 4 cytopenias with conditioning chemotherapy
• Expected IL-2 toxicity
• No treatment-related deaths
Efficacy
• ORR (in spec): 4/8 (50%, 2 DDLS, 2 UPS)
• Overall: 4/10 (40%)
• All PRs on-going as far out as 15 month follow up
• DCR: 8/10 (4 DDLS, 4 UPS)
Future Directions
• Analysis for exploratory endpoints ongoing
• Analysis for additional 10 patients ongoing
• SARATOGA open at US centers – including MSK
• Pilot angiosarcoma cohort enrolling
Lauren Banks
Lifileucel in patients with undifferentiated pleomorphic sarcoma (UPS) or dedifferentiated liposarcoma (DDLS)
MALAGA AUDITORIUM - HALL 3
#Surufatinib + PlatEtop + serplulimab in epNECs
@myESMO #ESMO26 #ESMOAmbassadors https://t.co/5sodZuPhr9
[Slide 1]
Study Design
Key Eligibility Criteria
• Aged ≥18 years
• Histologically confirmed NEC (except pulmonary origin)
• ECOG PS 0-1
• Measurable lesions
• Treatment naïve
N=60
Safety Run-in (n=6)
Induction (q3w, 6 cycles):
Surufatinib: 250 mg, qd, po
+ Serplulimab: 300 mg, d1, iv, q3w
+ EP regimen
Maintenance:
Surufatinib + Serplulimab
Dose expansion (n=54)
Induction (q3w, 6 cycles):
Surufatinib: RP2D
+ Serplulimab: 300 mg, d1, iv, q3w
+ EP regimen
Maintenance:
Surufatinib + Serplulimab
PD, death, or intolerable toxicity
Endpoints
• Primary endpoint: PFS (RECIST v1.1);
• Secondary endpoints: ORR, DCR, DoR, OS, AE.
• Etoposide injection: 100mg/m2, d1-3, IV, Q3W; Cisplatin: 25mg/m2, d1-3, IV, Q3W.
• Dose-limiting toxicities (DLTs) were observed for the first cycle (dose of Surufatinib would be adjusted to 200mg, qd, po, q3w if ≥ 2 DLTs were observed in the first 6 patients).
• Tumor response assessment every 6 weeks per RECIST v1.1
ECOG PS, Eastern Cooperative Oncology Group performance status; po, by mouth; qd, once daily, q3w, every 3 weeks; iv, Intravenous infusion; ORR, Objective response rate; DCR, Disease control rate; PFS, Progression-free survival; OS, Overall survival; AE, Adverse events.
Zhenyu Lin, MD
[Slide 2]
Tumor Response
In the response-evaluable population, the ORR was 69.8% and DCR was 95.3%.
Surufatinib + EP + serplulimab N=43
CR 1 | PR 29 | SD 11 | PD 2
Waterfall Plot: Tumor Change from Baseline
Change from baseline (%)
CR / PR / SD / PD
69.8% ORR
95.3% DCR
9.1 mo DoR
* New lesion appearance; ** 1st tumor assessment: SD; 2nd: target lesion shrinkage >30% with non-target lesion progression
Zhenyu Lin, MD
[Slide 3]
Conclusions
■ The quadruplet regimen of surufatinib + EP + serplulimab demonstrated promising antitumor activity as first-line treatment for extrapulmonary NEC, with a confirmed ORR of 69.8% and DCR of 95.3%.
■ The median PFS of 9.4 months is encouraging, particularly in a high-risk population with 67.4% liver metastases and a median Ki-67 of 70%. Patients achieving objective response derived a meaningful PFS benefit (11.5 months vs. 6.6 months).
■ The safety profile was manageable and consistent with the expected toxicities of the individual components, with no new safety signals identified. Grade ≥3 AEs were predominantly hematologic and attributable to the chemotherapy backbone.
■ Enrollment is ongoing to reach the planned sample size. Further exploratory analyses and long-term survival follow-up are warranted to better characterize the benefit of this quadruplet strategy in extrapulmonary NEC.
Zhenyu Lin, MD
#ESMO26 🧬 Rapid Oral | Lifileucel
💊 Autologous TIL therapy in refractory UPS/DDLS
👥 12 enrolled | 10 infused
🎯 ORR: 40% (4/10)
✅ DCR: 80%
⏳ All 4 PRs ongoing
🔬 In-spec product: ORR 50% (4/8)
⚠️ G4 cytopenias: 10/10
💡 Promising activity! Phase III SARATOGA underway
@OncoAlert
08:30 - 10:00 Rapid oral: Sarcoma
CHAIRS: MARK DICKSON, PALMA DILEO, CESAR SERRANO
NCT05607095: Lifileucel pilot trial in DDLS/UPS
10 DDLS/UPS patients:
• Unresectable/metastatic
• ≥1 prior systemic therapy
• ≥1.5 cm lesion for TIL harvest
• target lesion
• adequate organ function and ECOG 0-1
Primary endpoints:
• Feasibility - ≥6/10 pts infused with lifileucel
• Safety - grade ≥3 TRAE
Secondary endpoints:
• ORR, DCR, DOR
Exploratory endpoints:
• TIL surgical specimen sequencing
• On treatment biopsy
• Immune monitoring in blood
Screening: Candidate Identification; Multidisciplinary discussion; Screening studies per protocol
Enrollment: Tumor harvest; +/- bridging therapy; Baseline imaging
manufacturing ~ 22 days
Treatment: NMA-LD day -5 to -1; Cyclophosphamide (60 mg/kg x 2); Fludarabine (25 mg/m2 x 5); Lifileucel day 0; IL-2 (600,000 IU/kg) up to 6 doses
Assessment: Every 6 weeks for first 6 months; Every 3 months thereafter
Follow up: Up to 3 years
Lauren Banks
Lifileucel in patients with undifferentiated pleomorphic sarcoma (UPS) or dedifferentiated liposarcoma (DDLS)
MALAGA AUDITORIUM - HALL 3
#ESMO26 🧬 Epsametostat (HH2853) | Phase II
🎯 Advanced epithelioid sarcoma
💊 Dual EZH1/2 inhibitor
👥 94 pts | 75 efficacy-evaluable
📈 ORR: 40% | DCR: 77.3%
⏳ mPFS: 13.1 mo | mDoR: 15.6 mo
🎯 mOS: Not reached
⚠️ G≥3 TRAEs: 39.4%
🚀 Primary endpoint met! https://t.co/ya44WOgSgG
[Slide 1]
GLOBAL, MULTI-CENTER, FIRST-IN-HUMAN TRIAL DESIGN OF HH2853
Phase I
Dose Escalation and Expansion Cohorts
Dose Escalation: 100, 200, 200, 400, 600, 800, 1000 → Expansion cohorts; RP2D
Endpoints: MTD, DLT, Safety, PK, PD, Exploratory Efficacy
Phase II
HH2853 oral tablet BID (400 mg), 28-day cycle
Cohort 1 (N=44) Relapsed/refractory follicular lymphoma
Cohort 2 (N=94) Epithelioid sarcoma
Cohort 3 (N=61)
• Relapsed/refractory peripheral T-cell lymphoma
• Other relapsed/refractory non-Hodgkin lymphoma harboring EZH2 mutations
• Advanced solid tumors presenting specific genetic alterations (including EZH2 mutations, INI1 deficiency, BAP1 deficiency, ARID1A mutations, and/or SMARCA4 mutations)
Cohort 2: Epithelioid sarcoma (N=94)
Cohort 2 Specifics
• Treatment Regimen: HH2853, fixed dose 400 mg (RP2D) orally BID continuous, no dose adjustment by body weight/BSA; 28-day cycle
• Treatment Duration: Until disease progression, unacceptable toxicity, death, withdrawal, or other criteria.
Eligibility Criteria
• Age ≥ 18 years, Male/Female
• Histologically or cytologically confirmed ES
• Previously treated, including failure and intolerable toxicity, unresectable locally advanced or metastatic ES
• ECOG PS ≤ 1; Life expectancy ≥ 3 months
• Adequate organ function (bone marrow, liver, kidney)
• At least 1 measurable target lesion
Exclusion Criteria:
• Symptomatic CNS metastasis
• Concomitant or prior malignancy
• Serious active infection requiring systemic therapy
• Prior EZH2 or EZH1/2 inhibitor therapy
Study endpoints (cohort 2)
PRIMARY ENDPOINT
• BIRC-assessed confirmed ORR (RECIST 1.1)
SECONDARY ENDPOINTS
• Investigator-assessed confirmed ORR
• BIRC- & Investigator-assessed confirmed DoR, DCR, TTR, PFS
• Safety profile
• Population pharmacokinetic (PopPK) parameters: typical population PK parameters for HH2853 and its potential metabolites.
EXPLORATORY ENDPOINTS
• Exposure-response (E–R) relationships
• Overall survival
Study objectives: To evaluate the preliminary efficacy, safety, pharmacokinetics, and biomarker correlates of continuous twice-daily oral HH2853 in relapsed/refractory non-Hodgkin lymphoma and advanced solid tumors (Cohorts 1 & 3), as well as BIRC-confirmed ORR in previously treated epithelioid sarcoma (Cohort 2).
[Slide 2]
Efficacy endpoints assessed by BIRC — HH2853-G101 Cohort 2
Figure 2. Duration of treatment and clinical response (EAS)
[swimmer plot; legend: Treatment Failure from Last Treatment (N = 72); Intolerance from Last Treatment (N = 3)]
Swimmer plot illustrating the duration of treatment, individual response over time, and discontinuation status.
Table 2. Antitumor activity (EAS)
| Patients (N=75)
ORR, n (%), 95% CI | 30 (40.0), (28.9, 52.0)
DCR, n (%), 95% CI | 58 (77.3), (66.2, 86.2)
DoR, month, Median (95% CI) | 15.6 (7.5, NE)
TTR, month, Median (range) | 1.86 (1.4, 9.0)
As of June 30, 2025, the median treatment duration was 35.4 weeks. The primary endpoint was met, demonstrating an ORR of 40.0% (95% CI, 28.9–52.0) by BICR according to RECIST v1.1.
Figure 3. Tumor response assessed by BICR (EAS)
[waterfall plot; PR / SD / PD; HH2853 400mg BID Intolerance from Last Treatment; HH2853 400mg BID Treatment Failure from Last Treatment]
Waterfall plot showing the best percentage change from baseline in the sum of target lesion diameters. Tumor shrinkage was observed in the majority of patients (88.0%, 66/75), with 48.0% (36/75) achieving a reduction in tumor burden of ≥30%.
[Slide 3]
Secondary endpoints — HH2853-G101 Cohort 2
Figure 4. Kaplan-Meier curve of progression-free survival (PFS).
Kaplan–Meier estimates of PFS assessed by BIRC in the efficacy analysis set (N=75). As of the data cutoff date, 41 patients (54.7%) had experienced a PFS event, including 37 (49.3%) with disease progression and 4 (5.3%) deaths. The median PFS was 13.1 months (95% CI: 7.4–16.6). Numbers at risk at specified time points are shown below the horizontal axis.
Median (95% CI): Total 13.1 (7.4, 16.6); Treatment Failure 13.1 (7.4, 16.6)
Number of subjects at risk (0, 3, 6, 9, 12, 15, 18, 21, 24, 27 months)
Total | 75 | 58 | 43 | 34 | 20 | 17 | 11 | 6 | 1 | 0
Treatment Failure | 72 | 55 | 41 | 33 | 19 | 17 | 11 | 6 | 1 | 0
Figure 5. Kaplan-Meier curve of overall survival (OS). Kaplan–Meier estimates of OS in the efficacy analysis set (N=75). At the data cutoff date, with a data maturity of 24.0% (18 deaths recorded among 75 patients), the median OS was not reached (95% CI: NE–NE). Numbers at risk at specified time points are displayed beneath the x-axis.
Median (95% CI): Total NE (NE, NE); Treatment Failure NE (21.4, NE)
Number of subjects at risk (0, 3, 6, 9, 12, 15, 18, 21, 24, 27 months)
Total | 75 | 72 | 63 | 52 | 39 | 31 | 24 | 17 | 5 | 0
Treatment Failure | 72 | 69 | 61 | 50 | 37 | 29 | 22 | 16 | 5 | 0
Survival table
Endpoint: PFS (BIRC) and OS, HH2853-G101 Cohort 2 (EAS N=75)
Arm | N | Median | Median CI
Total (PFS) | 75 | 13.1 | 7.4, 16.6
Treatment Failure (PFS) | 72 | 13.1 | 7.4, 16.6
Total (OS) | 75 | NE | NE, NE
Treatment Failure (OS) | 72 | NE | 21.4, NE
[Slide 4]
Safety — HH2853-G101 Cohort 2
Table 3. Safety profile (SAS)
n (%) | Patients (N=94)
TEAEs | 93 (98.9)
Grade ≥3 | 47 (50.0)
Serious | 23 (24.5)
Leading to dose reduction | 6 (6.4)
Leading to dose interruption | 28 (29.8)
Leading to treatment discontinuation | 3 (3.2)
Leading to death | 4 (4.3)
TRAEs | 91 (96.8)
Grade ≥3 | 37 (39.4)
Serious | 7 (7.4)
Leading to dose reduction | 6 (6.4)
Leading to dose interruption | 20 (21.3)
Leading to treatment discontinuation | 3 (3.2)
Leading to death | 0
HH2853 demonstrated a favorable and manageable safety profile, characterized by a low incidence of serious TRAEs (7.4%) and infrequent AE-related dose modifications or discontinuations.
Figure 7. Common TEAEs occurring in ≥30% of patients (SAS) (Patients, %)
Alopecia 31.9
Blood lactate dehydrogenase increased 33.0
Alanine aminotransferase increased 35.1
Hyperuricemia 38.3
Weight decreased 40.4
Lymphopenia 45.7
Diarrhea 47.9
Hypertriglyceridemia 51.1
Hyperbilirubinemia 54.3
Anemia 55.3
Figure 8. Common TRAEs occurring in ≥30% of patients (SAS) (Patients, %)
Hyperuricemia 31.9
Alopecia 31.9
Alanine aminotransferase increased 31.9
Weight decreased 34.0
Hypertriglyceridemia 36.2
Lymphopenia 40.4
Diarrhea 45.7
Hyperbilirubinemia 51.1
Anemia 52.1
Cancer Vaccines: From Immune Activation to Durable Clinical Benefit
At #ESMO26, Prof. Juliane Walz highlighted five key principles shaping the future of therapeutic cancer vaccines:
1. Antigen selection: Immunopeptidomics can help identify clinically relevant tumor targets.
2. Timing matters: The adjuvant/MRD setting may offer the greatest opportunity for vaccine-induced immunity.
3. Better combinations: Novel adjuvants, checkpoint inhibitors, and bispecific antibodies may enhance T-cell responses.
4. Encouraging early data: In CLL, a personalized peptide vaccine induced T-cell responses in 95% of patients, with MRD reduction in 90%.
5. Toward personalization: Fusion-derived antigens and individualized vaccine platforms are opening new therapeutic possibilities.
The key question is no longer just whether cancer vaccines induce immunity, but whether that immunity translates into durable clinical benefit.
#ESMO26 #CancerVaccines @myESMO #Immunotherapy #PrecisionOncology @oncodaily @OncoAlert
Conclusion
Clinical effective cancer vaccines require:
• Optimal target selection
➤ Next generation immunopeptidomics to improve neoepitope selection and expansion tumor antigen categories
• Mode of application and time points
➤ Adjuvant setting for optimal effector to target ratio
➤ Potent adjuvants for long lasting T cell immunity
• Clinical translation of cancer vaccines is realized by
➤ Patient stratification
➤ Warehouse concepts
➤ Individualized cancer vaccines
MADRID 2026 ESMO congress
Caveats: ctDNA % drives sensitivity, and deletions are hardest. PTEN loss is spatially heterogeneous, with discordance both ways, so neither tissue nor plasma is a gold standard. PTEN loss in ctDNA only → worst OS (mOS 11 mo). Matched WBC DNA is a must: 10 "hits" were CHIP. 2/2 https://t.co/Qdfx6jaien
[Slide 1]
PTEN heterogeneity complicates accurate classification
Tissue NGS | Plasma ctDNA
55 tissue only | 20 both | 13 plasma only
n = 88 altered patients · circle and overlap areas proportional to patient numbers
[oncoprint: ctDNA fraction %, biopsy, PTEN tissue, PTEN ctDNA rows]
Of 17 patients with PTEN biallelic loss in tissue
8 biallelic loss
9 partial loss
despite optimising for high ctDNA ≥20%
PTEN status: Intact; Single copy loss; Mutation + LOH
PTEN mutation only present in 2 samples
Copy number loss; Missense mutation; Truncating mutation
PTEN / TP53 / RB1 / APC (samples PB3, PB1, PB4, PB2, RP7, RP4, RP3, RP6, RP1, RP5, RP8)
Warner E, Van der Eecken E, Murtha AJ et al, Nat Cancer 2024
Edmond M. Kwan, MBBS PhD
[Slide 2]
Escape of the aggressive PTEN-defective tumour clone?
Tissue NGS | Plasma ctDNA
55 tissue only | 20 both | 13 plasma only
n = 88 altered patients · circle and overlap areas proportional to patient numbers
[oncoprint: ctDNA fraction %, biopsy, PTEN tissue, PTEN ctDNA]
Of 17 patients with PTEN biallelic loss in tissue
8 biallelic loss
9 partial loss
despite optimising for high ctDNA ≥20%
PTEN loss stratified by compartment
Neither n=136, mOS 32 mo
Tissue-only n=58, mOS 29 mo
ctDNA-only n=23, mOS 11 mo
Both n=28, mOS 17 mo
Overall survival
Months from first blood draw
No. at risk (0, 12, 24, 36, 48, 60)
Neither: 136 121 91 59 45 19
Tissue-only: 58 51 36 22 16 7
ctDNA-only: 23 9 3 1 0 0
Both: 28 21 6 4 2 1
Edmond M. Kwan, MBBS PhD
Survival table
Endpoint: Overall survival from first blood draw, by PTEN loss compartment
Neither | 136 | 32 mo
Tissue-only | 58 | 29 mo
ctDNA-only | 23 | 11 mo
Both | 28 | 17 mo
We're presenting an e-poster at @myESMO 2026!
🔷 Decision Support in Multiple Myeloma: Comparison of Artificial Intelligence (AI) Models with Expert Oncologists
▶️ Abstract ID: 263eP
If you're attending ESMO 2026, stop by our poster and connect with us.
Abstract link 👉 https://t.co/EEtPHGXxhQ
Explore #ESMO26 insights here: https://t.co/JBaV2QEuxu
#LARVOL #ESMO2026 #CancerResearch #CancerData #Oncology #OncologyInsights #MedicalOncology #ClinicalTrials #MultipleMyeloma #MMSM | @Jud_Prz | @brunolarvol | @Debarat07333230 | @Dr_R_Kurzrock
LARVOL ONCO DATA AI
Decision Support in Multiple Myeloma: Comparison of Artificial Intelligence (AI) Models with Expert Oncologists
Judith Pérez-Granado¹*, Mina Nikanjam²*, Carolina Schinke³, Meera Mohan⁴, Sabarinath V. Radhakrishnan⁵, Donald A. Barkauskas⁶, Bruno Larvol¹, Anita D'Souza⁵, Razelle Kurzrock⁵,⁷
¹The LARVOL Group LLC, San Francisco, CA; ²University of California San Diego, La Jolla, CA; ³University of Arkansas, Fayetteville, AR; ⁴MD Anderson Cancer Center, Houston, TX; ⁵Medical College of Wisconsin, Milwaukee, WI; ⁶University of Southern California, Los Angeles, CA; ⁷WIN Consortium, Chevilly-Larue, France. *Equal contribution. Corresponding: judith.perez@larvol.com
MADRID SPAIN 23-27 OCTOBER 2026
INTRODUCTION
The therapeutic landscape of multiple myeloma (MM) has rapidly expanded, with new drug classes and combinations increasing the complexity of treatment selection.
We evaluated how treatment decision-making by large language models (LLMs) compares with that of expert myeloma oncologists (MD) in clinically plausible MM cases.
METHODS
9 virtual myeloma cases: 1 smoldering case, 8 MM cases (4 previously treated)
4 LLMs: ChatGPT, Gemini, Claude and Grok — Generate treatment options independently
4 expert oncologists: From 3 academic institutions
Shared treatment-option list: Consolidation and independent oncologist review
Assign treatment weights summing to 100% | Score preferred options 75/25, 50/50 or 100%
Pairwise JS divergence analysis: Expert–expert (Pairwise agreement between individual oncologists); LLM–LLM (Pairwise agreement between individual models); Expert–LLM comparisons (Each physician vs each model)
Average pairwise scores by case and across all 9 cases
JS divergence: distribution difference
RESULTS
Pairwise JS divergence across all cases
Comparison | Physician 1 | Physician 2 | Physician 3 | Physician 4 | ChatGPT | Claude | Gemini | Grok
Physician 1 | – | 0.4727 | 0.3479 | 0.2495 | 0.3662 | 0.3998 | 0.6013 | 0.4054
Physician 2 | 0.4727 | – | 0.3288 | 0.3847 | 0.3608 | 0.3260 | 0.3607 | 0.2362
Physician 3 | 0.3479 | 0.3288 | – | 0.2324 | 0.3130 | 0.3870 | 0.4871 | 0.2923
Physician 4 | 0.2495 | 0.3847 | 0.2324 | – | 0.2362 | 0.2966 | 0.4379 | 0.2792
ChatGPT | 0.3662 | 0.3608 | 0.3130 | 0.2362 | – | 0.0620 | 0.2074 | 0.1369
Claude | 0.3998 | 0.3260 | 0.3870 | 0.2966 | 0.0620 | – | 0.1771 | 0.1318
Gemini | 0.6013 | 0.3607 | 0.4871 | 0.4379 | 0.2074 | 0.1771 | – | 0.1802
Grok | 0.4054 | 0.2362 | 0.2923 | 0.2792 | 0.1369 | 0.1318 | 0.1802 | –
Average pairwise JS divergence by case
Comparison | Overall | Case 1 | Case 2 | Case 3 | Case 4 | Case 5 | Case 6 | Case 7 | Case 8 | Case 9
MD vs. MD | 0.3360 | 0.1523 | 0.5833 | 0.4270 | 0.3356 | 0.3284 | 0.2453 | 0.2540 | 0.1523 | 0.5460
MD vs. LLM | 0.3616 | 0.3059 | 0.3571 | 0.3109 | 0.4340 | 0.3297 | 0.2846 | 0.2140 | 0.5055 | 0.5128
LLM vs. LLM | 0.1492 | 0.2074 | 0.1835 | 0.0625 | 0.2075 | 0.1964 | 0.0640 | 0.0193 | 0.2362 | 0.1665
Lower Jensen–Shannon (JS) divergence indicates greater similarity. MD = expert oncologist.
Mean pairwise JS divergence Score for all physicians by LLM
Model | JS divergence
Grok | 0.3033
ChatGPT | 0.3191
Claude | 0.3524
Gemini | 0.4718
• Case 2 had the greatest physician disagreement (JS 0.5833), with several viable treatment options.
• MD–LLM divergence was greatest in cases 8 and 9 (0.5055 and 0.5128), involving interstitial lung disease and liver transplantation.
• Case 7 had the closest MD–LLM agreement (0.2140), which involved an older patient with lower performance status and fewer viable treatment options.
CONCLUSIONS
Agreement with expert oncologists varied: mean pairwise JS divergence was lowest for Grok and highest for Gemini.
Experts differed substantially. Overall LLM–physician divergence resembled physician–physician divergence, while LLMs agreed more closely with each other.
Major comorbidities challenged LLM recommendations.
These pilot findings support further investigation of AI decision support. Validation is required before clinical implementation.
More #VHIO research at #ESMO2026!
Eva Muñoz and Irene Braña are among the VHIO researchers presenting posters at this year's congress, sharing their latest findings with the international oncology community. https://t.co/AvdHJ6SK5J
[Slide 1]
Efficacy and Safety of Cosibelimab in Advanced Cutaneous Squamous Cell Carcinoma (CSCC): Update from a Pivotal Open-label Study with a Median Follow-up of ≥2.5 Years
BACKGROUND
RESULTS
METHODS
CONCLUSIONS
Presented at the European Society for Medical Oncology (ESMO) Congress, 23-27 Oct 2026, Madrid, Spain
[Slide 2]
4872P - SAFETY AND PHARMACOKINETICS OF A NOVEL, FIRST-IN-CLASS HTR1B ANTAGONIST LB-208/AOP208 IN PATIENTS WITH RELAPSED OR REFRACTORY SOLID TUMORS OR LYMPHOMA: INTERIM RESULTS FROM THE FIRST-IN-HUMAN, PHASE 1 SERONCO-1 TRIAL
I. Braña, K. Rojas Laimito, P. Nuciforo, A. Ferreira, K. Krejcy, M. Unger, C. Klade, R. M. Risueño
BACKGROUND
Patients with relapsed/refractory solid tumors have a poor prognosis and need new therapies, particularly well-tolerated, orally administered agents. LB-208/AOP208 is an oral selective HTR1B antagonist with antitumor activity in preclinical models (Figure 1). SERONCO-1 is evaluating the safety, tolerability and the maximum tolerated dose (MTD) of LB-208/AOP208.
ductal carcinoma (7.7%), and rectal adenocarcinoma (7.7%) (Table 1). Median exposure was 56 days (range 17-726). Dose cohorts from 20 to 800 mg/day, administered as 400 mg BID at the 800 mg dose level, were completed. Two patients had intra-patient dose escalation.
No DLTs have occurred among 24 DLT-evaluable participants. Grade ≥3 AEs were reported in 26.9% of patients, without any grade ≥4. TRAEs occurred in 50.0% of patients and were all grade ≤2. No serious TRAEs were observed (Table 2). Common TRAEs were asthenia and insomnia (15.4% each), increased AST (11.5%), and abdominal pain, increased ALT, anxiety and irritability (7.7% each). Six patients required a dose interruption, one due to TRAEs; one patient required a treatment-related dose reduction. No AEs led to discontinuation (Figure 3). Plasma exposure accumulated with repeated dosing and increased overall across cohorts with inter-individual variability observed.
CONCLUSIONS
At this interim analysis, LB-208/AOP208 showed a good safety profile with no DLTs and no MTD reached. PK exposure increased overall across cohorts without plateau, supporting continued dose escalation and further evaluation of split dosing, food effects and extended PK sampling.
FUNDING
The study is partially funded by the Spanish Ministerio de Ciencia e Innovación CPP2021-008715.
CORRESPONDING AUTHOR
Irene Braña
Great discussion with Prof. Silvia Stacchiotti at #ESMO26 in Madrid! Two challenging sarcoma topics, expertly presented and discussed. Really enjoyed the insightful exchange and the opportunity to learn from such an outstanding expert in the field. 👏
#Sarcoma #ESMO2026 https://t.co/OUp4u1Vajd
[Slide 2]
Background
Extensive and clinically relevant alternative splicing in sarcoma
Genome-wide analysis using TCGASpliceSeq in TCGA-SARC (n = 261)
1. Cohort and data source: TCGA-SARC (n = 261) • 261 sarcoma cases with overall survival • RNA-seq data from TCGA
2. Alternative splicing quantification: TCGASpliceSeq Genome-wide quantification of alternative splicing events (Percent Spliced In, PSI) | Exon skipping (ES) | Alternative promoter (AP) | Alternative terminator (AT) | Alt. acceptor (AA) | Alt. donor (AD) | Retained intron (RI) | Mutually exclusive exons (ME)
3. Survival association: Low PSI / High PSI; Cox regression (P < 0.05)
4. Prognostic impact: Survival-associated AS events; High-risk AS signature / Low-risk AS signature
A highly complex splicing landscape in sarcoma: 40,184 alternative splicing events in 9,673 genes; ~4.1 AS events per gene
3,610 survival-associated AS events in 2,291 genes: 3,610 (9.0%) associated with overall survival; Total 40,184 AS events; Univariate Cox analysis (P < 0.05)
Distribution of survival-associated events by splicing type:
Exon skipping (ES) | 1,359 (37.6%)
Alternate terminator (AT) | 776 (21.5%)
Alternate promoter (AP) | 758 (21.0%)
Alternate acceptor (AA) | 252 (7.0%)
Alternate donor (AD) | 252 (7.0%)
Retained intron (RI) | 203 (5.6%)
Mutually exclusive exons (ME) | 10 (0.3%)
~80% were ES, AT or AP events
Integrated AS signature shows strong prognostic performance: Time-dependent ROC (overall survival)
Integrated model (6 AS types) | AUC = 0.85
Alternate promoter (AP) | AUC = 0.82
Exon skipping (ES) | AUC = 0.80
Risk groups based on AS signature: Low AS risk / High AS risk, P < 0.0001
Alternative splicing represents a widespread and clinically relevant program in sarcoma: ~1 in 11 detectable splicing events is associated with patient survival.
Hong W et al. Ann Transl Med. 2019;7:557.
Dr. J Martin-Broto
[Slide 3]
HH2853 / epsametostat in epithelioid sarcoma (ES):
Clear biological rationale
Antitumor activity confirmed starting from 1st line
(40% ORR; responses in proximal and distal ES; mPFS 13 months)
Safety: long term hematologic follow-up needed
Any global development plan in ES, and, possibly, in other SMARCB1-deleted sarcoma, such as poorly differentiated chordoma?
Cirtuvivint in translocated sarcomas:
Overall marginal antitumor activity
Potentially preliminary encouraging signal in SFT
No safety concerns so far
Biological rationale and identification of translocated sarcoma of potential interest to be further clarified
Validation in larger cohorts essential
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MOIO
Reduced-frequency vs standard immune checkpoint inhibitor dosing in responding patients · Non-inferiority (Phase 3, NCT05078047, UNICANCER; ESMO26 LBA10)Full trial page →All posts →
ESMO 2026 | A cautionary tale for immunotherapy de-escalation!
MOIO Trial (LBA10) – Phase III non-inferiority trial testing 3-monthly immunotherapy vs standard dosing in responding patients with advanced/metastatic cancer.
📊 Key results (N=308):
• Median PFS: 21.9 vs 25 months (reduced vs standard; HR 1.35)
• Risk of death: HR 2.0 (95% CI 1.1–3.9; p=0.0143) ⚠️
• PFS HR in urothelial cancer: 2.9
• Grade 3–4 immune-related AEs: 9.5% vs 10.5%
❌ Non-inferiority NOT demonstrated.
❌ No meaningful safety advantage.
⚠️ Signal of inferior survival with reduced-frequency IO.
💡 Take-home: Less frequent immunotherapy is not necessarily equally effective!
Important: These are interim results with relatively small numbers and heterogeneous tumour types.
#ESMO26 #MOIO #Immunotherapy #Oncology @OncoAlert @myESMO
[Slide 1]
Proffered Paper session
LBA10 - MOIO: Interim analyses of a phase III randomized non inferiority trial assessing reduced frequency immune checkpoint inhibitors in responding patients with advanced/metastatic cancer
Speakers Gwenaëlle Gravis (Marseille, France)
Lecture Time 16:54 - 17:06
Abstract
Background
Immunotherapy (IO) has transformed metastatic cancer management, with durable responses and sustained target engagement beyond standard dosing intervals. MOIO assesses whether reduced IO dose-intensity preserves efficacy in responding advanced/metastatic patients (pts).
[Slide 2]
Conclusions
Reduced IO dose intensity did not achieve PFS non-inferiority, showed no meaningful safety advantage, and was associated with a signal of inferior survival. Differential treatment effects according to tumour type and treatment line argue against a uniform de-escalation strategy. Biomarker-driven strategies warrant further study.
[Slide 3]
Methods
MOIO is an academic, multicentre, phase III non-inferiority trial conducted across 36 French centres. Pts with locally advanced/metastatic solid tumors in partial or complete response (CR) after 6 months of standard-dose IO were eligible (melanoma in CR excluded). Up to 646 pts were planned to be randomized to standard or reduced dose-intensity IO every 3 months (mo) at the same dose. The primary endpoint was PFS, with non-inferiority defined by a hazard ratio (HR) margin of 1.3. Two interim futility analyses were planned at 25% (125) and 50% (249) of 498 planned events, with stopping if the one-sided P-value for HR=1 was <0.0192. Secondary endpoints were overall survival (OS), response duration and safety.
[Slide 4]
Results
Between 03/2022 and 11/2025, 340 pts were randomized. At the data cut-off (median follow-up 18.6 mo), modified intent-to-treat analysis set (N=308) the median PFS was 25 mo (95% CI 19.4-NE) in standard vs 21.9 mo (95% CI 12.1-31.6) in reduced IO (HR 1.35 95% CI 0.9-2.0 p=0.0635) exceeding the prespecified futility boundary. Reduced IO was associated with a higher risk of death (HR 2.0 95%CI 1.1-3.9; p=0.0143). Treatment effect differed across stratification factors: tumour type and treatment line. The HR (95%CI) for PFS was 2.9 (1·3–6·7) in urothelial, 1.6 (0·8–3·1) in lung, 0.7 (0·3–1·5) in renal cell and 0.6 (0·1–2·4) in head and neck cancer. Beyond first line HR was 2.9 (0·9-4·9). Grade 3-4 immune related AE occurred in 10·5% versus 9·5% and SAE in 26·3% vs 25·0% in standard versus reduced IO, respectively.
Conclusions
Reduced IO dose intensity did not achieve PFS non-inferiority, showed no meaningful safety advantage, and was associated with a signal of inferior survival. Differential treatment effects according to tumour type and treatment line argue against a uniform de-escalation strategy. Biomarker-driven strategies warrant further study.
#ESMO26 Dr. Jarushka Naidoo @DrJNaidoo with a fantastic discussion on de-escalation trials in oncology. A call out on why de-escalation studies are important and their limitations. And for MOIO in particular - lessons on trial design, non-inferiority, and pragmatism. A must-listen to all involved in trial design. #ESMOAmbassadors
Same slide also posted by @TommyJohn00, @OncBrothers
[Slide 2]
Diversity of ICI options, but a uniformity of schedules?
"Universal Schedule"
ICI-Combination x 4-6 Cycles → Maintenance ICI x 2 years / Lifelong
ICI Monotherapy → Lifelong
Q2W, Q4W, Q6W, IV or SC
Complex Pharmacology
PD-1–Receptor Occupancy (%)
0.1 mg/kg (N=11) 0.3 mg/kg (N=12) 1.0 mg/kg (N=20) 3.0 mg/kg (N=12) 10.0 mg/kg (N=10)
Dose of Anti–PD-1 Antibody
PD-1 Receptor Occupancy: 65% 0.1mg/kg
PD-1 Occupancy (%)
Pt. 4025
Time (days)
Long-term Receptor Occupancy (10mg/kg)
Nivolumab | Melanoma | NSCLC | RCC
1mg/kg | 31 | 3 | 28
3mg/kg | 41 | 24 | -
10mg/kg | 20 | 20 | 31
No clear dose/response relationship
Differences in half life/exposure by combo
Modification of Treatment Schedules:
Needs to balance clinical rationales, biologic factors, and pharmacologic features
- Agrawal et al, JITC 2016; Patnaik et al, Clin Cancer Res 2015; Topalian et al, NEJM 2012; Brahmer et al, J Clin Oncol 2010-
[Slide 4]
Phase III MOIO Trial: 3-monthly interval ICI
Study Eligibility, Design and Methods
Patients
• Adults aged ≥18 years
• Advanced /metastatic solid tumour
• CR or PR after 6 months of ICIs1+2
• Controlled brain metastases
• Melanoma in CR were not eligible
R (1:1) N=646
Standard ICI (n=323) Standard schedule
Reduced ICI (n= 323) 12-week schedule
1Approved ICI-based regimen: +/- another ICI, chemotherapy, bevacizumab, TKI
2RECIST v1.1, PERCIST v1.0, by investigators
3mITT: modified intention-to-treat population
4Randomized: received at least 1 ICI dose
Primary Endpoints:
• PFS (mITT)3 (randomized/treated)4
Secondary Endpoints:
• OS
• Safety
BROAD eligibility: are we ok with a non-inf HR 1.3, for all ICI-eligible tumours?
Is this homogenous enough a population? Does it 'pick the winners' we feel comfortable to de-escalate
Two study populations: ?no CR/PR, non-standard IOs: should these be included?
3-monthly? Were the authors unlucky? biologic justification?
The MOIO randomised phase 3 non-inferiority trial (n=340) explored early discontinuation of ICI therapy be SOC in advanced patients responding to therapy. It had many flaws (mixed tumors and treatments, small size, early discontinuation etc). Also, due to the statistics, it’s not possible to say whether non-inferiority was achieved (OS HR 1.89 [95%Cl: 1.03,3.48]). Despite these problems it highlights a concern around early discontinuation, which should be taken seriously. Tumour specific trials are needed, but I’m not sure it will be easy to randomize patients . #ESMO26 @OncoAlert @myESMO @Annals_Oncology
[Slide 1]
MADRID 2026 ESMO congress
MOIO : Study Design
Patients
Adults aged ≥18 years
Advanced /metastatic solid tumour
Complete or partial response after 6 months of immune checkpoint inhibitors 1+2
Controlled brain metastases
Melanoma in CR were not eligible
R (1:1) N=64
Standard ICI (n=323) Standard administration of immune checkpoint inhibitors
Reduced ICI (n= 323) 12-week administration of immune checkpoint inhibitors
Primary endpoints3
PFS mITT population4
PFS randomized and treated5
Secondary endpoints
OS6
Safety
Stratification
Response: CR vs PR
PD-1 vs PD-L1
Tumour type
1st Line vs > 1st Line
PFS events were defined as time from randomization to the first:
Progression
Death due to any cause
Completion study projected: 03/2027
1Approved standard ICI based regimen (monotherapy or in combination) another ICI agent, chemotherapy, bevacizumab, TKI,
2Evaluated by investigators by RECIST v1.1, PERCIST v1.0
3For this first interim analysis only the analyses highlighted in bold will be presented
4mITT: modified intention-to-treat (mITT) population
5Randomized patients [illegible] ICI dose after randomization
6Patients alive at the end of the study were censored at the last known alive date or the data cut-off date (December 1st, 2025), whichever occurred first.,
ClinicalTrials.gov: NCT05078047. EUCT number: 2024-513707-14-00.
[Slide 2]
MADRID 2026 ESMO congress
MOIO : PFS mITT at first interim analysis
The prespecified futility threshold (p < 0.0192 ) was not crossed
Progression-free survival (%)
Follow-up (in months)
HR 1.35 (96.16% CI 0.90-2.04); p=0.0635
Number at risk
Reduced
Standard
Standard ICI N=152 | Reduced ICI N=156
Events, n (%) 54 (35·5%) | 66 (42·3%)
Median PFS, months (95% CI) 25·0 (19·4- NE) | 21·9 (12·1-31·6)
HR (96.16% CI) HR=1.35 [96.16%CI:0·90-2·04]
P value (one-sided) 0·0635
Randomized and treated population
Standard ICI N=171 | Reduced ICI N=168
Events, n (%) 60 (35.09%) | 70 (41.67%)
Median PFS, months (95% CI) 25.00 [19.35-NE] | 23.49 [12.12,32.69]
HR (96.16% CI) HR=1.28 [96.16%CI: 0.86-1.90]
P value (one-sided) 0.0976
Median follow-up: 18·6 months standard ICI 18·7 months reduced ICI
Data cut-off December 1st, 2025
1two-sided 96·16% CI for the HR exceeding 1 is equivalent to one-sided p-value <0·0192
Survival table
Endpoint: Progression-free survival, mITT population (first interim analysis)
Arm | N | Median | Median CI
Standard ICI | 152 | 25.0 mo | 19.4–NE
Reduced ICI | 156 | 21.9 mo | 12.1–31.6
HR: 1.35
HR CI: 96.16% CI 0.90–2.04
P: 0.0635 (one-sided)
[Slide 3]
MADRID 2026 ESMO congress
MOIO : OS mITT at first interim analysis
Overall survival (%)
Follow-up (in months)
HR 2.04 (95% CI 1.08-3.85); 2-sided p-value=0.0286
Number at risk
Reduced
Standard
Standard ICI N=152 | Reduced ICI N=156
Events, n (%) 16 (10.5%) | 31 (19.9%)
Median OS, months (95% CI) NR | NR
HR (95% CI) 2.04 [95% CI: 1.08-3.85]
P value 0.0286
Randomized and treated population
Standard ICI N=171 | Reduced ICI N=168
Events, n (%) 18 (10.53%) | 32 (19.05%)
Median OS months (95% CI) NR | NR
HR (95% CI) 1.89 [95%CI : 1.03,3.48]
P value 0.0400
Survival table
Endpoint: Overall survival, mITT population (first interim analysis)
Standard ICI | 152 | NR
Reduced ICI | 156 | NR
HR: 2.04
HR CI: 1.08–3.85
P: 0.0286 (2-sided)
[Slide 4]
MADRID 2026 ESMO congress
Key Take Home Lessons, Conclusions, Next Steps
Ph III MOIO 3-monthly Interval ICI Clinical Trial
Reduced Frequency ICI:
Ph III Trial stopped early: 3-monthly ICI maintenance statistically inconclusive, but not likely successful.
Non-inferiority:
Pan-tumour non-inferiority may not have been the ideal trial, given heterogeneity of ICI responses & pharmacology.
Pragmatic Trials:
ICI de-intensification unlikely 'one-size-fits-all' - focus on specific tumours and settings with homogenous outcomes.
ICI de-intensification:
The field is open: exploring dose, duration, interval & omission, based on biology, pharmacology & clinical principles.
🚨 3rd Presidential Session at #ESMO26!
💉 Can we safely reduce the frequency of immunotherapy in advanced solid cancers?
The phase III MOIO trial tested 12-weekly versus standard immune checkpoint inhibitor administration in responding patients.
⚠️ Unexpected and concerning results!
📉 PFS: HR 1.35 (96.16% CI 0.90–2.04)
🚨 OS: HR 2.04 (95% CI 1.08–3.85), favouring standard treatment!
The trial stopped enrolment early following an unexpected OS imbalance.
A superb and thought-provoking discussion by @DrJNaidoo
Her key messages:
-Statistically inconclusive , but clinically reassuring? Certainly not!
-Non-inferiority margins matter! Would we really be comfortable accepting a potential 30% increase in the hazard of progression simply to reduce treatment frequency?
-One size does not fit all! Different tumour types, different immunotherapy regimens, different biology. Can a pan-tumour de-escalation strategy really work?
-Pragmatic does not mean compromising scientific rigour.
The take-home message: De-escalation remains an important goal, but it must be biologically justified, clinically meaningful and supported by robust evidence.
Doing less is only progress if we can demonstrate that patients are not paying the price in efficacy or survival.
👏 Congratulations to @DrJNaidoo for an outstanding discussion!
#ESMO26 #ESMOAmbassadors #Immunotherapy #MOIO #DeEscalation #Oncology
[Slide 2]
Ph III Non-inferiority Pragmatic MOIO Trial: 3-monthly interval ICI
Study Population
Standard ICI (N=152) | Reduced ICI (N=156)
Gender, n (%)
Men 100 (65·8) 109 (69·9)
Age
[63–76]
Triple-negative breast cancer 1 (0·7) 1 (0·6)
Cutaneous SCC³ 0 2 (1·3)
Oesophageal SCC³ 2 (1·3) 1 (0·6)
Heterogenous Population:
• 14 different tumour types
• Multiple ICI-combinations
• Range of responses at 6 months (patients with CR, PR, SD, unknown)
Key Questions:
1. Non-inferiority
2. Pragmatism
3. Interval dosing
Inform next steps in de-escalation field of ICIs
[Slide 3]
Key Question 1:
Who and what defines 'non-inferiority' in oncology trials?
Clinical:
• Loss of efficacy clinicians are 'willing to accept'
• Factors: choice of outcome, effect size, risk-benefit
• NI Margins poorly defined*:
Metric | Reporting range
OS | 1.08-1.33 (≥1.20)
Time-to-event | 1.22 (1.08–1.52)
Margin justified | 33.3% NI trials
Margin missing | 54.3% NI trials
Patients:
• Loss of efficacy patients are 'willing to accept'
• Uncommonly done: involving patients & advocates,
Patient perspectives on chemotherapy de-escalation in breast cancer
Statistically:
• 95% CI excludes non-inferiority margin
• *Constancy assumption Benefit same across treatment duration ?ICI
Regulators:
• Loss of efficacy society accepts changes policy
• FDA: lower limit 95% CI pooled point estimate (fixed margin method)
How is the non-inferiority margin chosen?
FDA EMA
- *Adapted/Thanks to S Peters; Gyawali, JAMA Netw Open 2018; Kleber, JNCI 2025; Haslam, JNCCN 2020; Rocque, Cancer Med 2021; Althunian, Trials 2017; Wangge, PLoS One 2013-
[Slide 4]
Key Question 2:
What makes a clinical trial 'pragmatic'?
• A Pragmatic Randomized Trial:
- undertaken in the "real world," with usual care
- informs decision-making on established interventions
• An Explanatory Randomized Trial:
- undertaken in an idealised setting
- intervention given best chance of beneficial effect
• PRECIS-2 Criteria:
- Nine domains of trial 'pragmatism'
- Developed by >25 trialists, statisticians, regulators
- Initial applications in primary care
Applicability to Oncology?
Eligibility Who is selected to participate in the trial?
Recruitment How are participants recruited into the trial?
Setting Where is the trial being done?
Organisation What expertise and resources are needed to deliver the intervention?
Flexibility: delivery How should the intervention be delivered?
Flexibility: adherence What measures are in place to make sure participants adhere to the intervention?
Follow-up How closely are participants followed-up?
Primary outcome How relevant is it to participants?
Primary analysis To what extent are all data included?
- Loudon et al, BMJ 2015; Sankar et al Am Soc Clin Oncol Educ Book 2024-
Deintensification trials in ICI should be in homogeneous population and based upon good biological and pharmacological rational. Excellent discussion by @DrJNaidoo @dr_yakupergun @myESMO #esmo26 https://t.co/LuPxF9AT2u
16:30 - 18:15 Presidential Symposium III
CHAIRS: ANDRES CERVANTES, ELIZABETH SMYTH
De-intensification Trials with ICIs: reported and ongoing
H+N Nivo - Dose Reduce
CM513 - Shorten Duration
NVALT30 - Interval
DIAL, ADOPT - Omit treatment
DELLI - Dose Reduce
DICIPLE - Shorten Duration
PULSE - Interval
INSIGHT - Omit treatment
Patil, J Clin Oncol 20[illegible]; Noronha, J Cli Oncol 2026; Waterhouse, J Clin Oncol 2020; Zalcman, ASCO 2023; Van Heuvel, ESMO 2024; Besse, ESMO 2025; Schmid, ELCC 2025; [illegible], ASCO 2026
Jarushka Naidoo
Invited Discussant LBA10
🆙#ESMO26 Presidential Symposium III
🔥MOIO: Phase III Randomized Non Inferiority Trial Assessing Reduced Frequency Immune Checkpoint Inhibitors in Responding Patients With Advanced/Metastatic Cancer
🎙️Dr. Gwenaëlle Gravis
🔢LBA10
🎯IDMC recommended stopping enrolment
🎯Reduced-Frequency ICI (q12wk) Failed PFS Non-Inferiority (; n=308)
🎯mPFS 25 vs 21.9mo, HR 1.35
🎯Showed Higher Death Risk (HR 2.0, p=0.0143)
🎯Effect Varied by Tumor Type (Urothelial HR 2.9, Lung 1.6)
☑️NCT05078047
🔗 https://t.co/EkpjbZHI9j
#LCSM @OncoAlert @Larvol @myESMO @IASLC
MADRID 2026 ESMO congress
MOIO : Most frequent TRAEs1-similar (all grades and grade ≥ 3) bySOC2
Safety population
Adverse Event (SOC)
Metabolism and nutrition disorders
Respiratory, thoracic and mediastinal disorders
Infections and infestations
Hepatobiliary disorders
Eye disorders
Nervous system disorders
Blood and lymphatic system disorders
Investigations
Injury, poisoning and procedural complications
Renal and urinary disorders
Skin and subcutaneous tissue disorders
Gastrointestinal disorders
Musculoskeletal and connective tissue disorders
Endocrine disorders
General disorders and administration site conditions
Proportion of patients (%)
Adverse events: Reduced IO (Any grade) Reduced IO (Grade >=3 ) Standard IO (Any grade) Standard IO (Grade >=3 )
1TRAE= treatment-related adverse event; related to immunotherapy 2SOC=system organ class, IO: immunotherapy
#ESMO26: An exquisite discussion by the 1@only @DrJNaidoo , elegantly and critically discussing:
➡️ De-escalation of IO desirable but with knowledge of the tumor-specific context and level of readiness
➡️ Objectify the arbitrary administration intervals
➡️Future trials to integrate robust statistics, tumor biology and IO combination impact with TKIs , chemo or ADCs
#ESMOAmbassadors
De-intensification Trials with ICIs: reported and ongoing
H+N Nivo — Dose Reduce
CM513 — Shorten Duration
NVALT30 — Interval
DIAL, ADOPT — Omit treatment
DELLI — Dose Reduce
DICIPLE — Shorten Duration
PULSE — Interval
INSIGHT — Omit treatment
- Patil, J Clin Oncol 2013; Noronha, J Cli Oncol 2026; Waterhouse, J Clin Oncol 2020; Zalcman, ASCO 2023; Van Heuvel, ESMO 2024; Besse, ESMO 2025; Schmid, ELCC 2025; Cetner, ASCO 2026-
‼️ While understanding of PK/PD for immune-checkpoint is not fully explained, and personalization in an individualized basis can be justified, reduced frequency administration of ICI may led to worse clinical outcomes.
⚠️ Prospective MOIO non-inferiority trial suggests and stopped earlier due to futility, potential harm ❌
🫥 When data does not meet wishes. #ESMO26 #LCSM
MOIO: Patient Characteristics – mITT (2)
Baseline demographic and disease characteristics were well balanced between the study arms
Standard ICI (N=152) | Reduced ICI (N=156)
Primary tumour type at randomization, n (%)
Lung cancer: 46 (30·3) | 47 (30·1)
Urothelial carcinoma: 40 (26·3) | 38 (24·4)
Renal cell carcinoma: 29 (19·1) | 29 (18·6)
Head and neck cancer: 11 (7·2) | 10 (6·4)
Endometrial carcinoma: 6 (3·9) | 5 (3·2)
Cervical cancer: 3 (2·0) | 4 (2·6)
Colorectal MSI¹ carcinoma: 4 (2·6) | 5 (3·2)
Melanoma: 2 (1·3) | 6 (3·8)
Gastric/GEJ² adenocarcinoma: 4 (2·6) | 3 (1·9)
Hepatocellular carcinoma: 1 (0·7) | 3 (1·9)
Merkel cell carcinoma: 3 (2·0) | 2 (1·3)
Cutaneous SCC³: 0 | 2 (1·3)
Triple-negative breast cancer: 1 (0·7) | 1 (0·6)
Oesophageal SCC³: 2 (1·3) | 1 (0·6)
¹MSI=microsatellite instability; ²GEJ=gastroesophageal junction; ³SCC=squamous cell carcinoma
Gravis: MOIO study looking to show that reduced frequency IO is non-inferior to SoC. Non-inferiority not met. Study stopped early because reduced IO did not reduce toxicity or appear to improve survival. Pragmatic but messy design and small numbers. #LCSM #ESMO26 https://t.co/0qh2ZCBLvK
MOIO: Statistical Analysis Plan ID Metrics
Primary objective
Demonstrate that Reduced ICI is non-inferior to Standard ICI in terms of efficacy
Primary endpoint
Progression-free survival (PFS) = time from randomization to first documented progression or death1
Co-primary analysis sets
mITT2 and Randomized and treated population3
Primary Analysis
Non-inferiority concluded at the final analysis if:
Upper bound of the 90% CI for HR ≤ 1.30 (NI margin).
Criterion must be met in both co-primary populations.
Interim Futility Analyses (allow study going)
Planned after approximately 25% (n≈125) and 50% of PFS events (n≈249)
Early stopping for futility/harm if4 :
One-sided p-value (H0: HR=1 vs HR>1) < 0.01925
1 Progression was determined locally by the investigator through the use of RECIST v1.1 and PERCIST v1.0.
2 All randomized patients without major eligibility violations who received at least one IO dose after randomization.
3 All randomized patients who received at least one IO dose after randomization.
4 Korn EL, Freidlin B. Interim monitoring for non-inferiority trials: minimizing patient exposure to inferior therapies. Ann Oncol. 2018:1;29(3):573-577.
5 P-value derived from stratified Cox regression with randomization factors as strata.
MOIO reduced Hz IO; n340; after 6/12 randomised to standard vs 12w IO; non inferiority design; IDMC stopped and recommended reversion to standard arm; mOS HR 2.04; inferiority esp lung urothelial, not renal;#ESMO26 https://t.co/uhbMkXi6hE
MOIO: Patient Characteristics – mITT (1)
Baseline demographic and disease characteristics were well balanced between the study arms
Standard ICI (N=152) | Reduced ICI (N=156)
Gender, n (%)
Men | 100 (65·8) | 109 (69·9)
Age
Age, median [IQR] | 69·0 [60–75] | 71·0 [63–76]
ECOG status, n (%)
ECOG 0 | 76 (50·0) | 75 (48·1)
ECOG 1 | 76 (50·0) | 81 (51·9)
Disease status at inclusion, n (%)
Locally advanced disease | 18 (11·8) | 22 (14·1)
Metastatic disease | 134 (88·2) | 134 (85·9)
Response status at randomization, n (%)
Complete response (CR) | 50 (32·9) | 46 (29·5)
Partial response (PR) | 102 (67·1) | 110 (70·5)
Treatment line at randomization, n (%)
1 | 113 (74·3) | 117 (75·0)
2 or more | 39 (25·7) | 39 (25·0)
IO drug type at randomization, n (%)
PD-11 inhibitors | 123 (80·9) | 125 (80·1)
PD-L12 inhibitors | 29 (19·1) | 31 (19·9)
1PD-1 = Programmed cell death protein 1 (Cemiplimab, Dostarlimab, Nivolumab, or Pembrolizumab); 2PD-L1= Programmed death-ligand 1(Atezolizumab, Avelumab, or Durvalumab)
MOIO: Interim analyses of a ph III rand. non inferiority trial assessing reduced frequency immune checkpoint inhibitors in responding patients with advanced/metastatic cancer by
Gwenaëlle Gravis (Marseille, France)
#ESMO2026 https://t.co/CyfjWPCp9i
MOIO (Maintenance Optimisation of Immuno-Oncology)
MOIO is a pragmatic and academic trial evaluating IF ICI dose-intensity reduction COULD preserve efficacy while limiting toxicity, in responding patients across multiple tumor types
Background
• Immune checkpoint inhibitors (ICIs) are associated with significant survival improvements and durable clinical responses across multiple advanced/metastatic malignancies1.
• ICIs alone or in combination are administered until disease progression, unacceptable toxicity, or up to two years.
• Some patients who discontinue ICIs, particularly those with response, maintain durable disease control2.
• Uncertainties persist regarding optimal duration and intensity of treatment3.
• PK/PD data suggest standard anti-PD-1 doses exceed therapeutic needs, supporting less frequent dosing 4.
• The burden of treatment is high for patients and healthcare systems.
1Robert C. Nat Commun 2020; 2Amiot ML et al. EClinicalMedicine 2024; 3Sun L et al. JAMA Oncol 2023;.4Peer CJ, L et al. J Clin Pharmacol 2022.
https://t.co/gLqCHaCB8m
MOIO: Conclusions of the first interim analyses
• The study was stopped early by sponsor decision (based on IDMC and steering committee recommendations) due to concerns regarding the overall benefit-risk balance in patients receiving reduced frequency ICI.
• This occurred despite the prespecified PFS futility threshold not being crossed.
• After 120/498 planned PFS events in the mITT population and 130/498 events in the randomized and treated population (median follow-up 18.6 months )
• Key findings underlying the overall benefit-risk assessment
• mITT (N=308): PFS: HR 1·35 (1-sided p=0·0635) and OS: HR 2·04 (2-sided p=0·0286).
• Randomized and treated (N=339): PFS: HR 1·28 (1-sided p=0·0976) and OS: HR 1.89 (2-sided p=0·0400).
• No substantial difference in adverse events was observed between the two arms.
MOIO at #ESMO26: 12-week vs standard ICI in patients responding at 6 months. Stopped early, futility bar not crossed.
📉 mITT PFS HR 1.35, median 21.9 vs 25.0 months
⚠️ OS HR 2.04 (1.08 to 3.85), 31 vs 16 deaths (stopped by DSMC)
🧪 UC PFS HR 2.91 (1.27 to 6.67), RCC 0.68 (0.32 to 1.44).
Hypothesis-generating. No safety advantage. Results can't support 12-week dosing in responders. Congrats on this huge effort, inferiority trials hard to run, pragmatic trial to better understand schedule of IO therapy.
#ESMO26 #GUonc #Immunotherapy
MOIO: Conclusions of the first interim analyses
• Several limitations must be acknowledged including: heterogeneity of the patient population, ICI regimens and short follow-up.
• Therefore, neither non-inferiority nor definitive inferiority can be formally concluded of the 12-week ICI strategy.
Results cannot support implementation of the 12-week ICI in patients responding after initial ICI-based therapy.
Further studies are needed to better define effective ICI de-intensification strategies.
Brilliant discussion with @DrJNaidoo about the MOIO trial
MOIO or Less?
Less Is MOIO: Do We Really Need So Much Immunotherapy?
Questions persists unsolved
@BalazsHalmosMD @StephenVLiu
@myESMO #ESMOAmbassadors #ESMO2026 https://t.co/v5iZ0drhgn
Ph III Non-inferiority Pragmatic MOIO Trial: 3-monthly interval ICI
Study Population
Standard ICI (N=152) | Reduced ICI (N=156)
Gender, n (%)
Men 100 (65·8) | 109 (69·9)
Age
Age, me[obscured] ... [63–76]
Primary t[obscured]
Lung ca[obscured] ... (30·1)
Urotheli[obscured] ... (24·4)
Renal c[obscured] ... (18·6)
Head an[obscured] ... (6·4)
Endome[obscured] ... (3·2)
Cervical ... (2·6)
Colorect[obscured] ... (3·2)
Melanor[obscured] ... (3·8)
Gastric/[obscured] ... (1·9)
Hepatoc[obscured] ... (1·9)
Merkel c[obscured] ... (1·3)
Cutaneous SCC3 0 | 2 (1·3)
Triple-negative breast cancer 1 (0·7) | 1 (0·6)
Oesophageal SCC3 2 (1·3) | 1 (0·6)
Heterogenous Population:
• 14 different tumour types
• Multiple ICI-combinations
• Range of responses at 6 months (patients with CR, PR, SD, unknown)
Key Questions:
1. Non-inferiority
2. Pragmatism
3. Interval dosing
Inform next steps in de-escalation field of ICIs
ARTEMIS-011
Risvutatug rezetecan (Ris-Rez, B7-H3 ADC) vs gemcitabine + docetaxel · Relapsed/refractory osteosarcoma after >=2 prior lines (Phase 3, China; ESMO26 LBA9, Presidential Symposium III; investigational)Full trial page →All posts →
ESMO 2026 | A major breakthrough in relapsed/refractory osteosarcoma!
ARTEMIS-011 (LBA9) – Phase III trial of Risvutatug rezetecan (Ris-Rez), a B7-H3-directed ADC, vs gemcitabine + docetaxel.
🇨🇳 N=122 | ≥2 prior lines
📊 Key results:
✅ Median PFS: 5.5 vs 1.4 months (HR 0.33; p<0.0001)
✅ 67% reduction in risk of progression or death!
✅ OS: Favorable trend (HR 0.51), but immature.
⚠️ Grade ≥3 AEs: 92.5% vs 83.3%
⚠️ Treatment-related serious AEs: 63.8% vs 28.6%
💡 Take-home: After years of limited progress in osteosarcoma, a B7-H3 ADC delivers a striking PFS benefit!
Promising results, but short follow-up, immature OS and substantial hematologic toxicity warrant caution.
Could ADCs finally change the treatment landscape in osteosarcoma?
#ESMO26 #ARTEMIS011 #Osteosarcoma @OncoAlert @myESMO
[Slide 1]
Proffered Paper session
LBA9 - Risvutatug rezetecan (Ris-Rez) versus gemcitabine and docetaxel (GD) in heavily pretreated patients (pts) with relapsed or refractory (R/R) osteosarcoma: Primary results from the phase 3 ARTEMIS-011 study
Speakers Lu Xie (Beijing, China)
Lecture Time 16:30 - 16:42
Abstract
Background
Ris-Rez (HS-20093/GSK5764227), a B7-H3-directed antibody-drug conjugate (ADC), previously showed promising antitumor activity with manageable toxicity in heavily pretreated pts with R/R sarcomas. Here, we report the primary results from a phase 3 ARTEMIS-011 study (NCT06935409) comparing Ris-Rez with GD in Chinese pts with R/R osteosarcoma.
[Slide 2]
Results
As of data cutoff (June 17, 2026), a total of 122 pts were randomized to receive Ris-Rez (n=80) or GD (n=42), the median (m) follow-up time was 7.1 months (mo). The median age was 21.0 years, 31 pts (25.4%) were adolescents (12-18 years). Ris-Rez demonstrated a statistically significant and clinically meaningful improvement in BICR-assessed PFS compared with GD (mPFS, 5.5 vs. 1.4 mo; HR, 0.33; p<0.0001), consistent with Investigator-assessed mPFS (5.6 vs. 1.0 mo). OS data were immature, but a favorable trend was observed toward Ris-Rez (HR, 0.51). Ris-Rez showed a manageable safety profile. Grade ≥3 TEAEs were reported in 92.5% with Ris-Rez vs. 83.3% with GD. Incidence of treatment-related SAE was numerically higher with Ris-Rez than with GD (63.8% vs. 28.6%), mainly driven by hematologic toxicities. Treatment discontinuation due to TRAE was similar between the groups (3.8% vs. 2.4%). One treatment-related interstitial lung disease was reported (CTCAE grade 2, resolved) in Ris-Rez group. No treatment-related deaths or new safety signals were observed.
[Slide 3]
Methods
ARTEMIS-011 was a multi-center, open-label, randomized phase 3 trial. Eligible pts should have progressed or relapsed after ≥2 prior lines of systemic therapy. Pts (≥12 years) were randomized (2:1) to receive either Ris-Rez 12.0 mg/kg every 3 weeks (Q3W) or GD Q3W. The primary endpoint was progression-free survival (PFS) assessed by Blinded Independent Central Review (BICR).
[Slide 4]
Conclusions
In the ARTEMIS-011 study, Ris-Rez demonstrated a statistically significant and clinically meaningful improvement in BICR-assessed PFS, accompanied by a favorable trend in OS and a manageable safety profile, highlighting its potential as a new treatment standard for patients with R/R osteosarcoma.
#ESMO26 🧬 Presidential | 🇨🇳 ARTEMIS-011
👥 122 pts | R/R osteosarcoma
💊 Ris-Rez (B7-H3 ADC) vs gemcitabine/docetaxel
📈 mPFS: 5.5 vs 1.4 mo (HR 0.33)
🎯 ORR: 15% vs 2%
✅ DCR: 76% vs 33%
⏳ OS immature (HR 0.51)
⚠️ G≥3 TRAEs: 93% vs 83%
💡 Promising new strategy!
@OncoAlert
[Slide 2]
16:30 - 18:15 Presidential Symposium III
CHAIRS: ANDRES CERVANTES, ELIZABETH SMYTH
Tumour Response Assessed by BICR
• BICR-assessed ORR and DCR were markedly higher with Ris-Rez vs Gemcitabine + Docetaxel
• Median DOR by BICR was 7.6 months with Ris-Rez and was not reached in the Gemcitabine + Docetaxel arm (only one patient achieved PR)
BICR-assessed ORR
Odds Ratio (95% CI): 7.1 (0.9–56.1)
ORR 15%
PR
ORR 2%
PR
Ris-Rez (n = 80)
Gemcitabine + Docetaxel (n = 42)
BICR-assessed DCR
Odds Ratio (95% CI): 6.2 (2.8–14.0)
DCR 76%
PR
SD
DCR 33%
PR
SD
Ris-Rez (n = 80)
Gemcitabine + Docetaxel (n = 42)
DCO: 17 June 2026. No patient had a CR
Presented by: Lu Xie, MD, PKUPH
Lu Xie
Risvutatug rezetecan (Ris-Rez) versus gemcitabine and docetaxel (GD) in heavily pretreated patients (pts) with relapsed or refractory (R/R) osteosarcoma: Primary results from the phase 3 ARTEMIS-011 study
ALICANTE AUDITORIUM - HALL 6
[Slide 3]
16:30 - 18:15 Presidential Symposium III
CHAIRS: ANDRES CERVANTES, ELIZABETH SMYTH
OS in R/R Osteosarcoma with Ris-Rez vs Gemcitabine + Docetaxel
• OS data were immature but suggested a numerical trend toward benefit with Ris-Rez
• 10 events had occurred in each arm: 13% with Ris-Rez and 24% with Gemcitabine + Docetaxel
• 17 patients* in the Gemcitabine + Docetaxel arm crossed over to Ris-Rez following PD
Ris-Rez
Gemcitabine + Docetaxel
OS (%)
Ris-Rez (n = 80) | Gemcitabine + Docetaxel (n = 42)
Median, mo Not reached Not reached
HR (95% CI) 0.51 (0.21–1.23)
Time since randomisation (mo)
Number at risk
Ris-Rez 80 78 72 45 16 1 0
Gemcitabine + Docetaxel 42 37 32 26 10 2 0
DCO: 17 June 2026. Symbols show censoring. *Crossover criteria were met.
BICR, blinded independent central review; CI, confidence interval; DCO, data cutoff; HR, hazard ratio; mo, month; OS, overall survival; PD, progressive disease; Ris-Rez, risvutatug rezetecan; R/R, relapsed/refractory
Presented by: Lu Xie, MD, PKUPH
Lu Xie
Risvutatug rezetecan (Ris-Rez) versus gemcitabine and docetaxel (GD) in heavily pretreated patients (pts) with relapsed or refractory (R/R) osteosarcoma: Primary results from the phase 3 ARTEMIS-011 study
ALICANTE AUDITORIUM - HALL 6
Survival table
Endpoint: Overall survival (immature)
Ris-Rez | 80 | Not reached
Gemcitabine + Docetaxel | 42 | Not reached
HR: 0.51
HR CI: 0.21–1.23
[Slide 4]
16:30 - 18:15 Presidential Symposium III
CHAIRS: ANDRES CERVANTES, ELIZABETH SMYTH
Safety Profile
TRAEs reported in ≥20% of patients (in either treatment arm)
Incidence, %
Ris-Rez (n = 80): Grades 1–2 / Grade ≥3 | Gemcitabine + Docetaxel (n = 42): Grade ≥3 / Grades 1–2
WBC count decreased 14 80 | 40 43
Anaemia 30 63 | 29 52
Platelet count decreased 20 71 | 60 29
Neutrophil count decreased 9 79 | 43 31
Lymphocyte count decreased 14 59 | 33 33
Pyrexia 40 1 | 10
Vomiting 34 4 | 7
Nausea 36 1 | 24
Hypoalbuminaemia 34 | 19
ALT increased 31 1 | 2 33
Decreased appetite 25 4 | 17
Asthenia 24 3 | 12
Infusion-related reaction 25 | 2
AST increased 24 | 31
Hypokalaemia 15 6 | 7
Weight decreased 21 | 10
Epistaxis 21 | 5
GGT increased 19 1 | 19
Constipation 20 | 7
Blood LDH increased 11 | 24
Rash 6 | 21
Percentage of patients
ALT, alanine aminotransferase; AST, aspartate aminotransferase; GGT, gamma glutamyltransferase; LDH, lactate dehydrogenase; Ris-Rez, risvutatug rezetecan; R/R, relapsed/refractory; TRAE, treatment-related adverse event; WBC, white blood cell
Presented by: Lu Xie, MD, PKUPH
Lu Xie
Risvutatug rezetecan (Ris-Rez) versus gemcitabine and docetaxel (GD) in heavily pretreated patients (pts) with relapsed or refractory (R/R) osteosarcoma: Primary results from the phase 3 ARTEMIS-011 study
ALICANTE AUDITORIUM - HALL 6
Congrats Prof #LuXie for an excellent presentation of the very promising data of #ARTEMIS_011 of Ris-Rez B7H3 ADC in relapsed #osteosarcoma. A potential game changer with HR 0.33 over #gemcitabine_docetaxel.
Thanks for helping put #sarcomas on the map at the #esmo26 presidential symposium and for working on advancing treatment options for our patients.
@ctosociety #ESMOAmbassadors
[Slide 2]
Ris-Rez is a B7-H3–directed ADC^6
Human Anti–B7-H3 IgG1 monoclonal Ab
TOP1 inhibitor payload (rezetecan)
Cysteine conjugation site
Cleavable linker
DAR ≈ 4
[the] Phase 3 ARTEMIS-011 study (NCT06935409) [i]n R/R osteosarcoma after failure of ≥2L therapy
Background
Patients with R/R osteosarcoma have limited treatment options, especially after failure of 2L therapy^1,2
• Current treatments can impact cognition, quality-of-life, and possibility of secondary malignancies^2
B7-H3 is an immunosuppressive checkpoint protein that is highly expressed in many tumours, including sarcoma, whereas its expression in normal tissue is limited^3–5
Risvutatug rezetecan (Ris-Rez, previously known as HS-20093 or GSK5764227), is a B7-H3–directed ADC with a TOP1 inhibitor payload^6
• Ris-Rez showed promising antitumour activity in patients with heavily pretreated R/R sarcomas (ARTEMIS-002)^7
Here we report the primary results of the Phase 3 ARTE[MIS-011 study] of Ris-Rez vs Gemcitabine + Docetaxel in R/R osteosarco[ma]
Presented by: Lu Xie, MD, PKUPH
MADRID 2026 ESMO congress
[Slide 4]
Tumour Response Assessed by BICR
• BICR-assessed ORR and DCR were markedly higher with Ris-Rez vs Gemcitabine + Docetaxel
• Median DOR by BICR was 7.6 months with Ris-Rez and was not reached in the Gemcitabine + Docetaxel arm (only one patient achieved PR)
BICR-assessed ORR
Odds Ratio (95% CI): 7.1 (0.9–56.1)
ORR 15%
PR
ORR 2%
PR
Ris-Rez (n = 80)
Gemcitabine + Docetaxel (n = 42)
Patients (%)
BICR-assessed DCR
Odds Ratio (95% CI): 6.2 (2.8–14.0)
DCR 76%
PR
SD
DCR 33%
PR
SD
Ris-Rez (n = 80)
Gemcitabine + Docetaxel (n = 42)
DCO: 17 June 2026. No patient had a CR
BICR, blinded independent central review; CI, confidence interval; CR, complete response; DCO, data cutoff; DCR, disease control rate; DOR, duration of response; ORR, objective response rate; PR, partial response; Ris-Rez, risvutatug rezetecan; SD, stable disease.
Presented by: Lu Xie, MD, PKUPH
Artemis 011 https://t.co/M7Q1l1bBZQ
LBA9 - Risvutatug rezetecan (Ris-Rez) versus gemcitabine and docetaxel (GD) in heavily pretreated patients (pts) with relapsed or refractory (R/R) osteosarcoma: Primary results from the phase 3 ARTEMIS-011 study
Speakers Lu Xie (Beijing, China)
Lecture Time 16:30 - 16:42
Abstract
Background
Ris-Rez (HS-20093/GSK5764227), a B7-H3-directed antibody-drug conjugate (ADC), previously showed promising antitumor activity with manageable toxicity in heavily pretreated pts with R/R sarcomas. Here, we report the primary results from a phase 3 ARTEMIS-011 study (NCT06935409) comparing Ris-Rez with GD in Chinese pts with R/R osteosarcoma.
Methods
ARTEMIS-011 was a multi-center, open-label, randomized phase 3 trial. Eligible pts should have progressed or relapsed after ≥2 prior lines of systemic therapy. Pts (≥12 years) were randomized (2:1) to receive either Ris-Rez 12.0 mg/kg every 3 weeks (Q3W) or GD Q3W. The primary endpoint was progression-free survival (PFS) assessed by Blinded Independent Central Review (BICR).
#ESMO26 Presidential Session and concomitant publication in @Annals_Oncology
ARTEMIS-011 Ris-Rez vs gem/doce in prev treated osteosarcoma shows PFS benefit but modest ORR and OS immature
A landmark phase III result opening the door to ADCs in osteosarcoma
@OncoAlert https://t.co/fl13gZtgwz
ADCs: what is the optimal construct?
ADC | NCT number | Age at inclusion | Target | Payload | DAR = Drug-to-antibody ratio | Phase | ORR (%) | DCR (%) | Median PFS | Reference
HS-20093 (ARTEMIS-002) | NCT05830123 | ≥18 y | B7-H3 | topoisomerase I inhibitor | 4 | II | ~20 | ~87 | 8.4 | ESMO 2025
HS-20093 (ARTEMIS-011) | NCT06935409 | ≥12 y | B7-H3 | Rezetecan topoisomerase I inhibitor | 4 | III | 15 | 76 | 5.5 | ESMO 2026
Ifinatamab deruxtecan (DS-7300a) | NCT04145622 | ≥12 y | B7-H3 | DXd topoisomerase I inhibitor | 4 | I/II | NR | NR | NR | ASCO 2023 / ESMO 2023
Trastuzumab deruxtecan (T-DXd) PEPN1924 | NCT04616560 | 12-39 y | HER2 | DXd topoisomerase I inhibitor | 8 | II | 0 | NR | NR | Reed et al. JCO OA 2025
Glembatumumab Vedotin | NCT02487979 | 12-50 y | GPNMB | MMAE Microtubule inhibitor | 4-4.5 | II | 1/19 | 3/19 | NR | Kopp et al. EJC2019
Samrotamab vedotin (ABBV-085) | NCT02565758 | ≥18 y | LRRC15 | MMAE Microtubule inhibitor | 2 | I | 20 | NR | 3.1 mo | Demetri et al. 2021
SOT106 | NCT07801222 Not yet recruiting | ≥12-18 y | LRRC15 | MMAE Microtubule inhibitor | 4 | I/II | NR | NR | NR | Preclinical data ESMO 2025
SIM0613 | NCT07618260 Just recruting | ≥18 y | LRRC15 | topoisomerase I inhibitor | 4 | I | NA | NA | NA |
Not exhaustive
ADCs: Ready for prime time?
Breelyn Wilky (Aurora, United States of America)
Friday, 23 October 2026; 16:55 - 17:15
Importance of each component for ADC efficacy
Targeting antibody → Determines where the ADC goes (selectivity)
Linker → Determines when and how the payload is released
Cytotoxic payload → Determines what happens once inside the cell (potency)
Take-home message
All three components are essential and must be optimized together for maximal ADC efficacy.
Dr Nathalie GASPAR, MD, PhD
Xie Lu presenting thr PRESIDENTIAL SYMPOSIUM of the Ris-Rez RP3 study for advanced osteosarcoma! @myESMO #ESMO26 https://t.co/ySKM9bOXhB
Same slide also posted by @MichalisLiontos
ARTEMIS-011: A Multi-Centre, Open-Label, Randomised, Controlled Phase 3 Study
Key Eligibility Criteria
• Age ≥12 years
• Pathologically confirmed diagnosis of osteosarcoma
• Progression or intolerance to at least two previous lines of therapy
• ≥1 measurable target lesion per RECIST v1.1
• ECOG PS 0–1
Study Treatment
Treatment until PD, toxicity, or withdrawal of consent
R 2:1
Ris-Rez 12.0 mg/kg IV on Day 1, Q3W (n = 80)
Crossover allowed*
Gemcitabine 1000 mg/m2 IV on Day 1 and 8 + Docetaxel 75 mg/m2 IV on Day 8, Q3W (n = 42)
Primary Endpoint
• PFS by BICR per RECIST v1.1
Secondary Endpoints
• OS
• PFS by investigator per RECIST v1.1
• ORR, DCR, DOR by BICR/investigator per RECIST v1.1
• Safety
Stratification:
• Age (12 to <18 years or ≥ 18 years)
• Lung metastases (Yes or No)
* Crossover to Ris-Rez following objective PD in patients meeting the crossover criteria
BICR, blinded independent central review; DCR, disease control rate; DOR, duration of response ECOG PS, Eastern Cooperative Oncology Group performance status; IV, intravenous; ORR, objective response rate; [illegible] overall survival; PD, progressive disease; PFS, progression-free survival; Q3W, every 3 weeks; R, randomisation; RECIST v1.1, Response Evaluation Criteria in Solid Tumors version 1.1; Ris-Rez, risvutatug rezetecan
Presented by: Lu Xie, MD, PKUPH
Risvutatug rezetecan (Ris-Rez) versus gemcitabine and docetaxel (GD) in heavily pretreated patients (pts) with relapsed or refractory (R/R) osteosarcoma: Primary results from the phase 3 ARTEMIS-011 study
by Lu Xie (Beijing, China) #ESMO2026 https://t.co/X6uoFqBhpo
Conclusions
Ris-Rez demonstrated a statistically significant and clinically meaningful improvement in BICR-assessed PFS, with a 67% reduction in the risk of disease progression or death in patients with R/R osteosarcoma
Immature OS data showed a numerical trend toward benefit with Ris-Rez
Despite higher AE rates, Ris-Rez was associated with longer treatment duration (4.5 vs 1.5 months) and a manageable safety profile
The most common AEs of any Grade and of Grade ≥3 in both arms were haematological; No Grade 5 event occurred
ARTEMIS-011 findings suggest that Ris-Rez represents a promising treatment option for patients with previously-treated R/R osteosarcoma
AE, adverse event; BICR, blinded independent central review; OS, overall survival; PFS, progression-free survival; Ris-Rez, risvutatug rezetecan; R/R, relapsed/refractory
Presented by: Lu Xie, MD, PKUPH
1. ARTEMIS-011: PhIII Ris-Rez (B7-H3 ADC) vs gem/docetaxel in heavily pretreated R/R osteosarcoma (n=122, 🇨🇳 only)
- mPFS 5.5 vs 1.4 mos (HR 0.33)
- OS trend HR 0.51 (immature)
- TEAEs 92.5% vs 83.3%
- Need global studies and better management for AEs
2/5 https://t.co/vZMfyZjRHv https://t.co/UUdIgt4FBe
[Slide 1]
Phase 3 ARTEMIS-011 Study Design
Key Eligibility Criteria
• Age ≥12 years
• Pathologically confirmed diagnosis of osteosarcoma
• Progression or intolerance to at least two previous lines of therapy
• ≥1 measurable target lesion per RECIST v1.1
• ECOG PS 0–1
R 2:1
Ris-Rez 12.0 mg/kg IV D1, Q3W (n = 80)
Crossover allowed*
Gemcitabine + Docetaxel (n = 42)
Each Q3W cycle
Gemcitabine 1000 mg/m2 IV, Days 1 and 8
Docetaxel 75 mg/m2 IV, Day 8
Treatment until PD, toxicity, or withdrawal of consent
* Crossover allowed after objective disease progression if crossover criteria were met
[Slide 2]
Primary endpoint: BICR-assessed PFS
4-mo rate
Ris-Rez 65%
Gemcitabine + Docetaxel 33%
Ris-Rez (n = 80) | Gemcitabine + Docetaxel (n = 42)
mPFS (95% CI): 5.5 mo (4.1–7.4) | 1.4 mo (0.8–2.7)
HR (95% CI) P value: 0.33 (0.20–0.55) < 0.0001
PFS (%)
Time since randomization (mo)
Patients at risk (censored), n
Survival table
Endpoint: PFS (BICR)
Arm | N | Median | Median CI
Ris-Rez | 80 | 5.5 mo | 4.1–7.4
Gemcitabine + Docetaxel | 42 | 1.4 mo | 0.8–2.7
HR: 0.33
HR CI: 0.20–0.55
P: < 0.0001
4-mo PFS rate: Ris-Rez 65% vs Gemcitabine + Docetaxel 33%
[Slide 3]
Safety
Median treatment duration: Ris-Rez: 4.5 mo | Gemcitabine: 1.5 mo; Docetaxel: 1.4 mo
TEAEs in ≥20% of patients
Ris-Rez (n = 80): Grade 1–2 / Grade ≥3 | Gemcitabine + Docetaxel (n = 42): Grade ≥3 / Grade 1–2
WBC count ↓: 14 / 80 | 40 / 43
Anemia: 30 / 63 | 31 / 52
Platelet count ↓: 20 / 71 | 60 / 28
Neutrophil count ↓: 9 / 79 | 43 / 31
Lymphocyte count ↓: 15 / 60 | 33 / 34
Pyrexia: 45 / 1 | 12
Vomiting: 36 / 4 | 7
Nausea: 37 / 1 | 24
Hypoalbuminemia: 36 | 24
ALT ↑: 33 / 1 | [illegible] / 34
Appetite ↓: 26 / 4 | 17
Asthenia: 23 / 3 | 12
Infusion-related reaction: 25 | 2
AST ↑: 24 | 31
Constipation: 24 | 12
Epistaxis: 23 | 5
Hypokalemia: 13 / 8 | [illegible] / 8
Weight ↓: 21 | 10
Blood LDH ↑: 20 | 29
GGT ↑: 19 / 1 | 19
Rash: 9 | 24
Percentage of patients
Presidential Symposium III 再発骨肉腫に対するRis-Rez vs GD の中国からのRPIII試験。PFSのHR 0.33と素晴らしい結果‼️しかしながら、mPFS 5.5か月と依然として厳しい現実… #ESMO26 https://t.co/bqGGVR65d6
OS in R/R Osteosarcoma with Ris-Rez vs Gemcitabine + Docetaxel
• OS data were immature but suggested a numerical trend toward benefit with Ris-Rez
• 10 events had occurred in each arm: 13% with Ris-Rez and 24% with Gemcitabine + Docetaxel
• 17 patients* in the Gemcitabine + Docetaxel arm crossed over to Ris-Rez following PD
OS (%)
Ris-Rez (n = 80) | Gemcitabine + Docetaxel (n = 42)
Median, mo: Not reached | Not reached
HR (95% CI): 0.51 (0.21–1.23)
Time since randomisation (mo)
Number at risk
Ris-Rez: 80 78 72 45 16 1 0
Gemcitabine + Docetaxel: 42 37 32 26 10 2 0
DCO: 17 June 2026. Symbols show censoring. *Crossover criteria were met.
Presented by: Lu Xie, MD, PKUPH
Survival table
Endpoint: OS
Ris-Rez | 80 | Not reached
Gemcitabine + Docetaxel | 42 | Not reached
HR: 0.51
HR CI: 0.21–1.23
Interested in stunning riz-Rez data in osteosarcoma (ARTEMIS 011); safety profile show lots of dose reduction/interruption; ILD in only 1 patient (n80), heam tox issue #ESMO26 https://t.co/KKTqaltOEs
[Slide 2]
Safety Summary
• Treatment-related ILD* was observed in 1 patient only in the Ris-Rez arm (CTCAE Grade 2)
Ris-Rez (n = 80) | Gemcitabine + Docetaxel (n = 42)
Treatment duration, median, mo | 4.5 | 1.5 (Gemcitabine) 1.4 (Docetaxel)
Any TRAE, n (%) | 80 (100) | 42 (100)
Grade ≥3, n (%) | 74 (93) | 35 (83)
Serious, n (%) | 51 (64) | 12 (29)
Fatal, n (%) | 0 | 0
Leading to:
Dose reduction, n (%) | 57 (71) | 11 (26)
Dose delay or interruption, n (%) | 38 (48) | 17 (40)
Permanent treatment discontinuation#, n (%) | 3 (4) | 1 (2)
[illegible]as identified using the narrow ILD SMQ. #TRAEs leading to permanent treatment discontinuation in the Ris-Rez arm: anaemia (n = 1); pneumonia (n = 1); anaemia and platelet count decreased (n = 1). The TRAE leading to permanent [illegible]nuation in the Gemcitabine + Docetaxel arm: bone pain (n = 1)
[illegible] Common Terminology Criteria for Adverse Events; ILD, Interstitial lung disease; mo, months; Ris-Rez, risvutatug rezetecan; SMQ, standardized MedDRA query; TRAE, treatment-related adverse event
[illegible]ed by: Lu Xie, MD, PKUPH
[Slide 3]
Safety Profile
TRAEs reported in ≥20% of patients (in either treatment arm)
Incidence, %
WBC count decreased
Anaemia
Platelet count decreased
Neutrophil count decreased
Lymphocyte count decreased
Pyrexia
Vomiting
Nausea
Hypoalbuminaemia
ALT increased
Decreased appetite
Asthenia
Infusion-related reaction
AST increased
Hypokalaemia
Weight decreased
Epistaxis
GGT increased
Constipation
Blood LDH increased
Rash
Ris-Rez (n = 80)
Grades 1–2
Grade ≥3
Gemcitabine + Docetaxel (n = 42)
Grades 1–2
Grade ≥3
Percentage of patients
[bar-value labels legible but not reliably attributable to rows from this angled photo; not transcribed]
ALT, alanine aminotransferase; AST; aspartate aminotransferase; GGT, gamma glutamyltransferase; LDH, lactate dehydrogenase; Ris-Rez, risvutatug rezetecan; R/R, relapsed/refractory; TRAE, treatment-related adverse event; WBC, white blood cell
Presented by: Lu Xie, MD, PKUPH
Amazing data of the risvetatug rezutecan in heavily pretreated osteosarcoma in the presidential session in #ESMO2026 Ris-Rez is superior to gem-docetaxel in a joint adolescent and adult population with a HR 0.3!!! 5.5 m vs 1.5 m mods. This is practice changing!! https://t.co/4EIoVb2rWp
Efficacy Assessed by Investigator
• Investigator-assessed PFS, ORR, and DCR were consistent with BICR-assessed results
Investigator-assessed PFS
Ris-Rez (n = 80) | Gemcitabine + Docetaxel (n = 42)
Median (95% CI) 5.6 mo (4.2–7.4) | 1.0 mo (0.7–2.3)
HR (95% CI) 0.30 (0.19–0.50)
PFS (%)
Time since randomisation (mo)
Number at risk
Ris-Rez
Gemcitabine + Docetaxel
Investigator-assessed ORR
Odds Ratio (95% CI): 7.1 (0.9–56.4)
ORR: 15% PR Ris-Rez (n = 80)
ORR: 2% PR Gemcitabine + Docetaxel (n = 42)
Investigator-assessed DCR
Odds Ratio (95% CI): 10.4 (4.3–24.8)
DCR: 83% PR SD Ris-Rez (n = 80)
DCR: 31% PR SD Gemcitabine + Docetaxel (n = 42)
[illegible] 17 June 2026. Symbols show censoring. No patient had a complete response
[illegible] blinded independent central review; CI, confidence interval; CR, complete response; DCO, data cutoff; DCR, disease control rate; mo, month; ORR, objective response rate; PFS, progression-free survival;
[illegible]artial response; Ris-Rez, risvutatug rezetecan; SD, stable disease
[illegible]nted by: Lu Xie, MD, PKUPH
Survival table
Endpoint: PFS, investigator-assessed
Arm | N | Median | Median CI
Ris-Rez | 80 | 5.6 mo | 4.2–7.4
Gemcitabine + Docetaxel | 42 | 1.0 mo | 0.7–2.3
HR: 0.30
HR CI: 95% CI 0.19–0.50
📢Check out the full list of #ESMO2026 Annals of Oncology concomitant publications at
https://t.co/yURtlYhlor https://t.co/pZJa9o2Usc
ARTEMIS-011: Simultaneous publication as pre-proof in Annals of Oncology
ANNALS OF ONCOLOGY
DRIVING INNOVATION IN ONCOLOGY
Efficacy and safety of risvutatug rezetecan versus gemcitabine plus docetaxel in relapsed/refractory advanced osteosarcoma: Primary results from the ARTEMIS-011 phase 3 trial
DOI: 10.1016/j.annonc.2026.10.1284
URL: https://www.annalsofoncology.org/article/S0923-7534(26)08076-2/fulltext
Presented by: Lu Xie, MD, PhD
IMA203CD8 (PRAME TCR-T)
IMA203CD8, PRAME-directed TCR-T cell therapy (Immatics) · Heavily pretreated HLA-A*02:01+ PRAME+ solid tumors (Phase 1; ESMO26; investigational)All posts →
🔥 #ESMO26 IMA203CD8: PRAME-directed TCR therapy
Phase I in heavily pretreated HLA-A*02:01+, PRAME+ solid tumors.
💥ORR 51% | cORR 41%
-Melanoma: ORR 52%
-Synovial sarcoma: 67%
-Higher-dose gynecologic tumors: ORR 60%, cORR 55%
Responses ongoing beyond 2.5 years 👀
Is PRAME ready for PRIME time?
@OncoAlert @OncoReporte @myESMO @_SEOM @GrupoMelanoma
[Slide 1]
Phase 1 Multicenter Trial of IMA203CD8 in PRAME+ Solid Tumors
Patient Journey
SCREENING/MANUFACTURING | TREATMENT/OBSERVATION | FOLLOW UP
HLA-A*02:01 Testing (blood)
PRAME Testing – Biopsy or archived tissue – No longer required for indications with high PRAME prevalence, including ovarian and uterine cancer, melanoma, and synovial sarcoma
Leukapheresis
IMA203CD8 Manufacturing (~2 weeks)
Lymphodepletion: Fludarabine 30 mg/m² Cyclophosphamide 500 mg/m² days -6 to -3
IMA203CD8 one-time infusion
± Low Dose IL-2ª: 1M IU SUBQ QD, days 3-5, then 1M IU SUBQ BID, days 6-10
Key Objectives
Primary: • Tolerability • Determination of RP2D
Secondary: • Efficacy • Pharmacokinetics
Key Eligibility Criteria
• Advanced or metastatic solid tumors
• Age ≥18 years
• ECOG PS 0-1
• HLA-A*02:01 positive
• PRAME positive
• No available SOC treatment options
• Measurable disease (RECIST 1.1)
• Adequate organ function
Dose Escalation Scheme ± Low Dose IL-2ª
DL3 (n=7) 0.44-1.00×10⁹ total TCR T cells
DL4a (n=38) 0.93-1.86×10⁹ total TCR T cells
DL4b (n=4) 1.49-2.05×10⁹ total TCR T cells
DL4c (n=9) 1.15-3.06×10⁹ total TCR T cells
DL5 (n=7) 1.95-4.30×10⁹ total TCR T cells
DL6 (n=15) 3.55-8.22×10⁹ total TCR T cells
DL7 (n=17) 4.26-12.50×10⁹ total TCR T cells
Dose escalation completed
Enrichment at relevant DLs (≥DL4c): ~1.2–12.5 billion total TCR T cells
Data cutoff: August 7, 2026
[Footnotes small/partly illegible: IMA203-101: NCT03686124; ... ªDose level ≥DL4c is evaluated ±IL-2 ...; anzu-cel, anzutresgene autoleucel ... [illegible]]
Prof. Dr. med. Antonia Busse, abstract #7231
[ESMO Congress Madrid 2026 logo] 4
[Slide 2]
Tolerability in Advanced Solid Tumors
TEAEs in ≥20% of Patients (N=98ª)
Preferred term, n (%) | Any grade | Grade ≥3
Patients with any adverse event | 98 (100) | 97 (99)
Neutropenia | 88 (90) | 87 (89)
Anemia | 78 (80) | 54 (55)
Thrombocytopenia | 71 (72) | 36 (37)
Nausea | 64 (65) | 2 (2)
Lymphopenia | 45 (46) | 45 (46)
Rash | 39 (40) | 5 (5)
Fatigue | 37 (38) | 6 (6)
Transaminase elevation | 37 (38) | 12 (12)
Hypokalemia | 34 (35) | 2 (2)
Constipation | 33 (34) | 0
Vomiting | 28 (29) | 0
Abdominal pain | 26 (27) | 3 (3)
Leukopenia | 25 (26) | 23 (23)
Hyponatremia | 23 (23) | 2 (2)
Pyrexia | 23 (23) | 0
Hypophosphatemia | 21 (21) | 3 (3)
Diarrhea | 20 (20) | 3 (3)
Headache | 20 (20) | 1 (1)
All TEAEs occurring in at least 20 patients (≥20%) are presented. Grades were determined according to National Cancer Institute Common Terminology Criteria for Adverse Events, version 5.0. Grades for CRS and ICANS were determined according to CARTOX criteria (Neelapu et al, 2018 before protocol v11.0; Neelapu et al, from protocol v11.0 onward)
Adverse Events of Special Interest (N=98ª)
CRS, any grade, n (%) | 94 (96)
Grade 1 | 38 (39)
Grade 2 | 47 (48)
Grade 3 | 8 (8)
Grade 4 | 1 (1)
HLH, any grade, n (%) | 7 (7)
Grade 1 | 0
Grade 2 | 4 (4)
Grade 3 | 2 (2)
Grade 4 | 1 (1)
ICANS, any grade, n (%) | 8 (8)
Grade 1 | 5 (5)
Grade 2 | 1 (1)
Grade 3 | 2 (2)
Late N- ICAHT Beyond Day 28* (N=87)
ICAHT, any grade, n (%) | 20 (23)
Grade 1-2 | 15 (17)
Grade 3-4 | 5 (6)
Late neutropenia-based Immune Effector Cell-Associated Hematotoxicity (N-ICAHT) grade was based on the second-lowest absolute neutrophil count between days 28-100 postinfusion and required ≥2 neutropenic measurements during this period, including ≥1 between days 35-60. Measurements before the day 28 visit were not used for late ICAHT grading but were considered when determining neutropenia onset and duration. Day 28 visits could have occurred ±3 days before or after day 28. Assessments were available for n=87 patients.
• Most frequent TEAEs were cytopenias associated with lymphodepletion
• CRS was mostly grade 1-2
• DLTs in 4 of 98 patients:
1. DL4b: grade 4 neurotoxicity/CRS with grade 3 HLH
2. DL4b: grade 3 CRS
3. DL5: grade 3 ICANSᵇ
4. DL7: grade 4 skin infectionᵇ
• Late grade 3-4 N-ICAHT in 5 patients was manageable with supportive treatment; all improved to grade ≤2 at a median of 69 days postinfusion (range, 42–121)
• No IMA203CD8-related grade 5 eventᶜ
• MTD not reached with doses up to 12.5 billion IMA203CD8 cells
ª All patients who started lymphodepletion, including 1 patient who did not receive IMA203CD8 cells. ᵇ 2 events met DLT criteria but did not limit dose escalation: 1 in an enrichment cohort at DL5 and 1 at highest dose, DL7 (1/6 patients), both within protocol-defined dose-finding rules). ᶜ Possibly related grade 5 event as previously reported was determined by the PI to be unlikely related to IMA203CD8 after complete assessment. Patient died from sepsis that was aggravated by immunosuppression from fludarabine/cyclophosphamide (possibly related), a grade 4 HLH event, the toxicity management, and rapidly progressing disease. CARTOX, CAR T-cell therapy–associated toxicity; CRS, cytokine release syndrome; DL, dose level; DLT, dose-limiting toxicity; ICAHT, immune effector cell–associated hematotoxicity; HLH, hemophagocytic lymphohistiocytosis; ICANS, immune effector cell–associated neurotoxicity syndrome; PI, principal investigator; MTD, maximum tolerated dose; TEAE, treatment-emergent adverse event.
Data cutoff: August 7, 2026
Prof. Dr. med. Antonia Busse, abstract #7231
[Slide 3]
Tumor Reduction Across Dose Levels and Indications During Dose Escalation
Objective responses across all dose levels and biologically distinct tumor types, including ovarian and uterine cancer, melanoma, and synovial sarcoma
[Waterfall plot: Best % Change in Sum of Longest Diameter of Target Lesions from Baseline (RECIST 1.1); per-patient tumor-type labels on x-axis (ovarian, uterine, melanoma, uveal melanoma, synovial sarcoma, NSCLC, breast, etc.) - too small to transcribe individually]
N | 90
ORR | 51% (46/90)
cORR | 41% (36/87)
DCR (at week 6) | 82% (74/90)
Tumor shrinkage | 83% (71/86)
BOR (RECIST 1.1): PD, SD, PR, cPR, CR, cCR
▶ Ongoing response/disease control
* Confirmed response based on prior PR that deepened to CR
Data cutoff: August 7, 2026
[Footnotes small, partly illegible]
Prof. Dr. med. Antonia Busse, abstract #7231
[Slide 4]
Tumor Reduction Across Dose Levels During Dose Escalation by Indication
| | Gynecologic Indications (N=27) | Melanoma (N=44) | Synovial Sarcoma (N=12) | Other (N=7) |
| Median dose [×10⁹ total TCR T cells] | 3.55 | 1.67 | 1.59 | 1.95 |
| ORR | 48% (13/27) | 52% (23/44) | 67% (8/12) | 29% (2/7) |
| cORR | 41% (11/27) | 41% (17/42) | 67% (8/12) | 0% (0/6) |
| DCR | 70% (19/27) | 82% (36/44) | 100% (12/12) | 100% (7/7) |
| Tumor shrinkage | 68% (17/25) | 88% (37/42) | 92% (11/12) | 86% (6/7) |
[Waterfall plots by indication: Best % Change in Sum of Longest Diameter of Target Lesions from Baseline (RECIST 1.1)]
BOR (RECIST 1.1): PD, SD, PR, cPR, CR, cCR
▶ Ongoing response/disease control
* Confirmed response based on prior PR that deepened to CR
Data cutoff: August 7, 2026
[Footnotes small, partly illegible]
Prof. Dr. med. Antonia Busse, abstract #7231
[ESMO Congress Madrid 2026 logo] 11
💉IMA203CD8, a co-transduces a CD8αβ co-receptor alongside the PRAME TCR showing impressive ORR 51% in 90 and durability in heavily pre-treated patients of >3L including melanoma, gynaecological, sarcomas. Well tolerated with CRS mostly G1-2.
Many congratulations to Antonia Busse, investigators and Immatics 👏🏼
#ESMO26
#TCRTherapy
#CellTherapy
@myESMO
[Slide 1]
Targeting PRAME+ Tumors with IMA203CD8, a PRAME-directed TCR T-cell Therapy: Results from a Phase 1 Study
Antonia Busse1, Dejka M. Araujo2, Winfried Alsdorf3, Oladapo Yeku4, Tobias A.W. Holderried5,6, Leonel F. Hernandez-Aya7, Sarah Taylor8, Dirk Jaeger9, Manik Chatterjee10, Anthony J. Olszanski11, Eva M. Wagner-Drouet12, Peter Herhaus13, Katrin Wetzko14, Apostolia M. Tsimberidou2, Friederike Schmitz8, Diwakar Davar15, Karine Pozo16, Liane Preussner17, Cedrik M. Britten17, Martin Wermke18
1Charité Medical University Hospital, Berlin, Germany;
2The University of Texas MD Anderson Cancer Center, Houston, TX, USA;
3Department of Hematology and Oncology, University Hospital Hamburg Eppendorf, Hamburg, Germany;
4Massachusetts General Hospital, Boston, MA, USA;
5University of Bonn, University Hospital Bonn, Medical Clinic and Polyclinic III Internal Medicine with a focus on Oncology, Hematology, and Rheumatology, Bonn, Germany;
6Clinical Division of Hematology, Department of Internal Medicine, Medical University of Graz, Graz, Austria;
7University of Miami, Miami, FL, USA;
8University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA;
9University Hospital Heidelberg, Heidelberg, Germany and Translational Oncology/Early Clinical Trial Unit (ECTU);
10Comprehensive Cancer Center Mainfranken, University Hospital Würzburg, Würzburg, Germany;
11Department of Hematology/Oncology, Fox Chase Cancer Center, Philadelphia, PA, USA;
12University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany;
13TUM School of Medicine and Health, Department of Internal Medicine III, University Medical Center, Technical University of Munich, Germany;
14University Hospital Dresden, Dresden, Germany;
15University of Pittsburgh Medical Center (UPMC), Hillman Cancer Center, Pittsburgh, PA, USA;
16Immatics US, Houston, TX, USA;
17Immatics Biotechnologies GmbH, Tuebingen, Germany;
18TU Dresden, Carl-Gustav-Carus Faculty of Medicine, NCT/UCC Early Clinical Trial Unit, Dresden, Germany.
Prof. Dr. med. Antonia Busse
Proffered paper presentation, abstract #7231
[Stage photo: presenter at ESMO podium (MADRID SPAIN 23-27 OCTOBER 2026), two chairs seated]
[Slide 2]
Tumor Reduction Across Dose Levels and Indications During Dose Escalation
Objective responses across all dose levels and biologically distinct tumor types, including ovarian and uterine cancer, melanoma, and synovial sarcoma
N 90
ORR 51% (46/90)
cORR 41% (36/87)
DCR (at week 6) 82% (74/90)
Tumor shrinkage 83% (71/86)
[Waterfall plot; y-axis: Best % Change in Sum of Longest Diameter of Target Lesions from Baseline (RECIST 1.1), 25 to -100; per-patient bars labelled with % change from +24 to -100; x-axis labels = tumor types per patient (uterine cancer, acral melanoma, ovarian cancer, uveal melanoma, synovial sarcoma, lung cancer (NSCLC), cutaneous melanoma, breast cancer, mucosal melanoma, melanoma (UNK), etc.)]
BOR (RECIST 1.1): PD; SD; PR; cPR; CR; cCR
▶ Ongoing response/disease control * Confirmed response based on prior PR that deepened to CR
Data cutoff: August 7, 2026
n=2 patients with ovarian cancer and n=1 patient with melanoma died before first postbaseline scan and n=1 additional patient with melanoma had a non-evaluable target lesion; these patients are not depicted in the plot but were included in the ORR, cORR and DCR calculation. ORR: according to RECIST 1.1 at any postbaseline scan, PD or death at any prior timepoint; Confirmed ORR for patients with ≥2 postbaseline scans per RECIST 1.1, PD or death at any prior timepoint, those with ongoing unconfirmed PR/CR were excluded. For patients achieving a (c)CR with <100% change from baseline, target lesions were lymph nodes that resolved to <10 mm per RECIST 1.1. BOR, best overall response; (c)CR, (confirmed) complete response; DCR, disease control rate; NSCLC, non-small cell lung cancer; (c)ORR, (confirmed) objective response rate; PD, progressive disease; (c)PR, (confirmed) partial response; SD, stable disease; UNK, unknown.
Prof. Dr. med. Antonia Busse, abstract #7231
[MADRID 2026 ESMO congress logo] 10
[Slide 3]
Tumor Reduction Across Dose Levels During Dose Escalation by Indication
| Gynecologic Indications (N=27) | Melanoma (N=44) | Synovial Sarcoma (N=12) | Other (N=7)
Median dose [×10^9 total TCR T cells]: 3.55 | 1.67 | 1.59 | 1.95
ORR: 48% (13/27) | 52% (23/44) | 67% (8/12) | 29% (2/7)
cORR: 41% (11/27) | 41% (17/42) | 67% (8/12) | 0% (0/6)
DCR: 70% (19/27) | 82% (36/44) | 100% (12/12) | 100% (7/7)
Tumor shrinkage: 68% (17/25) | 88% (37/42) | 92% (11/12) | 86% (6/7)
[Waterfall plots per indication; y-axis: Best % Change in Sum of Longest Diameter of Target Lesions from Baseline (RECIST 1.1), 25 to -100; Baseline line]
BOR (RECIST 1.1): PD; SD; PR; cPR; CR; cCR
▶ Ongoing response/disease control
* Confirmed response based on prior PR that deepened to CR
Data cutoff: August 7, 2026
n=2 patients with ovarian cancer and n=1 patient with melanoma died before first postbaseline scan and n=1 additional patient with melanoma had a non-evaluable target lesion; these patients are not depicted in the plot but were included in the ORR, cORR and DCR calculation. ORR: according to RECIST 1.1 at any postbaseline scan, PD or death at any prior timepoint; Confirmed ORR for patients with ≥2 postbaseline scans per RECIST 1.1, PD or death at any prior timepoint, those with ongoing unconfirmed PR/CR were excluded. For patients achieving a (c)CR with <100% change from baseline, target lesions were lymph nodes that resolved to <10 mm per RECIST 1.1.
BOR, best overall response; (c)CR, (confirmed) complete response; DCR, disease control rate; (c)ORR, (confirmed) objective response rate; PD, progressive disease; (c)PR, (confirmed) partial response; SD, stable disease.
Prof. Dr. med. Antonia Busse, abstract #7231
[MADRID 2026 ESMO congress logo] 11
[Slide 4]
Changes in Tumor Size Over Time
All dose levels: Deep and durable responses observed across all indications with ongoing responses beyond 2.5 years (mFU time of mPFS: 12.8 months)
[Spider plot; y-axis: Change in Sum of Longest Diameter of Target Lesions from Baseline [%], 100 to -100; x-axis: Months post T-cell infusion 0-45 (axis break between 15 and 24); reference lines PD, Baseline, PR]
BOR (RECIST 1.1): PD; SD; PR; cPR; CR; cCR
▶ Ongoing response/disease control
▶ Ongoing
Data cutoff: August 7, 2026
BOR, best overall response; (c)CR, (confirmed) complete response; mFU, median follow-up; PD, progressive disease; (c)PR, (confirmed) partial response; SD, stable disease
Prof. Dr. med. Antonia Busse, abstract #7231
[MADRID 2026 ESMO congress logo] 12
🧬 Great talk by #ESMOAmbassadors @DoniaMarco from @CCITdk 🇩🇰 on TCR-T vs TIL toxicities.
One key point: did the TCR already exist in the patient?
➡️ TIL: yes. Predictable toxicity, though can be severe (IL-2-sparing regimens should help)
➡️ Engineered TCRs: no → off-target risk hard to anticipate
Understand the biology, anticipate the toxicity.
@myESMO @_SEOM @oncodaily
#TIL #CellTherapy #ESMO26
[Slide 1]
Key Messages: where does the toxicity come from?
1 TIL - Primarily the platform, not the cells
Surgery, chemotherapy and especially high-dose IL-2 account for almost all of the toxicity.
Timing is predictable
2 TCR-T - The distinctive toxicity comes from the cells
What the cells recognise, and how potent they are, primarily determine the toxicity.
Safety belongs to the product
What is shared - Chemotherapy
Cytopenia in nearly every patient, and infection risk, are shared
Marco Donia, M.D., Ph.D.
5/26
[Slide 2]
TCRs
1. Lymphodepleting Chemotherapy
Cyclophosphamide lighter than in TILs
Product | Fludarabine | cumulative | Cyclophosphamide | cumulative | Days of conditioning
Conventional TIL (lifileucel) | 25 mg/m² × 5 | 125 mg/m² | 60 mg/kg × 2 | 120 mg/kg | 7
afami-cel | 30 mg/m² × 4 | 120 mg/m² | 600 mg/m² × 3 | 1,800 mg/m² | 4
lete-cel, reduced | 30 mg/m² × 3 | 90 mg/m² | 600 mg/m² × 3 | 1,800 mg/m² | 3
lete-cel, standard | 30 mg/m² × 4 | 120 mg/m² | 900 mg/m² × 3 | 2,700 mg/m² | 4
anzu-cel and IMA203CD8 | 30 mg/m² × 4 | 120 mg/m² | 500 mg/m² × 4 | 2,000 mg/m² | 4
mg/kg and mg/m² are not interchangeable; Cyclophosphamide 120 mg/kg is higher than in the engineered regimens depending on which one and on body size.
Sources: D'Angelo et al., J Clin Oncol 2025; Hong et al. Nat Med 2023; Davar et al., ASCO 2026; Busse et al., ESMO IO 2025; Tecelra FDA Product Information; Amtagvi FDA Product Information
Marco Donia, M.D., Ph.D.
20/26
[Slide 3]
TILs and TCR-T: Where is the Toxicity?
Platform Toxicity | Receptor Toxicity
| Classical TIL | Engineered TCR-T
Procurement | Surgery. 17% complications, 2 of 83 delayed | Leukapheresis. No surgical step
Conditioning | Cy 60 mg/kg × 2 + Flu 25 mg/m² × 5. Cytopenia in all. | Reduced Cy compared to the TIL regimen. Cytopenia in all
The cells | Few transient infusion reactions. No CAR-T-like CRS or ICANS | CRS 72 to 100%, grade ≥3 up to 18%. HLH-like up to 9%. Normal-tissue recognition when the antigen is shared
Cytokine support | High-dose IL-2, up to 6 doses. Drives most acute toxicity | None or one million IU subcutaneously
Late | Cytopenia, slow CD4 recovery, rare melanocyte autoimmunity | Less characterized (likely similar chemo-induced), plus gene-therapy surveillance*
* required by regulatory agencies, insertional oncogenesis risk
Marco Donia, M.D., Ph.D.
23/26
[Slide 4]
TILs
Democratizing TIL therapy
IL-2 free products/reduced chemo may improve tolerability
OBX-115: regulatable membrane-bound IL-15 TIL
Low Dose Lymphodepletion, NO IL-2
ORR 67% (10/15)
[waterfall and AE (All-grade / Grade ≥3) charts - labels illegible]
Betof et al., ASCO 2026
GC101 TIL (IL-2 free expansion)
Low Dose Lymphodepletion, NO IL-2
GC101 TIL VS ICC
Event/N: 30/50 | 42/49
mPFS(95%CI): 4.3(3.0-5.6) | 1.6(1.3-2.7)
HR(95%CI): 0.43(0.26-0.68)
P value: 0.0002
PFS Rate(%) at 6 month 26.18 VS 10.36
Progression-free survival rate(%) / Months
NO.at Risk
GC101 TIL 50 35 24 7 4 2 1 0
ICC 49 20 10 3 2 1 0
FAS
Si et al., ASCO 2026
Classical TIL
Lower Dose Lymphodepletion
Key inclusion criteria: Age ≥70 years; Recently treated brain metastases ≤ 6 months; History of bleeding or bowel metastases requiring surgical resection ≤ 6 months; Acute deep venous thrombosis ≤3 months requiring continuation of anticoagulation; Coronary artery disease requiring recent percutaneous coronary intervention and continuation of antiplatelet therapy ≤3 months; Toxicity warranting Cy discontinuation after the first day of administration
Day-5 Cy 30mg/kg Flu 25mg/m² | Day-4 Cy 30mg/kg Flu 25mg/m² | Day-3 Flu 25mg/m² | Day-2 Flu 25mg/m² | Day-1 Flu 25mg/m² | Day 0 | Days 0-3 IL-2 IV q8-12hr up to 6 doses
Treatment Response (N=16): Response (RECIST v1.1) N (%); ORR 7 (44); PR 7 (44); SD 3 (18); PD 6 (38); Disease Control Rate No. (%) 10 (62)
Karapelyan et al., Transpl Cell Ther 2026
Marco Donia, M.D., Ph.D.
24/26
Survival table
Endpoint: PFS, GC101 TIL vs ICC (FAS)
Arm | N | Median | Median CI
GC101 TIL | 50 | 4.3 | 3.0-5.6
ICC | 49 | 1.6 | 1.3-2.7
HR: 0.43
HR CI: 0.26-0.68
P: 0.0002
Landmark rates:
6 month: GC101 TIL 26.18% | ICC 10.36%
QoLATI-DAHANCA34
Primary transoral robotic surgery + neck dissection vs (chemo)radiotherapy · Early-stage oropharyngeal squamous cell carcinoma, swallowing QoL (randomized, NCT04124198, Rigshospitalet / DAHANCA; LBA45)All posts →
What is the best treatment for early stage HPV+ OPC?
QoLATI/DAHANCA34 and Best-of trial: oncologic equipoise, signals of different QoL profiles.
Eliciting patient preferences is key imo.
Congratulations Dr Channir and Simon and teams @ DAHANCA and @EORTC #ESMO26 #HNSCC https://t.co/bM8sA2Gb4b
[Slide 1]
Clinicaltrials.gov NCT04124198
DAHANCA.dk Danish Head and Neck Cancer Group
Quality of Life After primary TORS vs IMRT for patients with early-stage oropharyngeal squamous cell carcinoma(QoLATI/DAHANCA34): a multicenter, open-label, randomised phase 2 trial
Hani I. Channir, MD, PhD
Dept. of Otorhinolaryngology, Head And Neck Surgery & Audiology, Rigshospitalet, Copenhagen University Hospital Copenhagen, Denmark
25. October 2026
[Slide 2]
Future recommendations
Both TORS and (chemo)radiotherapy should be offered to selected patients, with treatment decisions individualized through multidisciplinary discussion, considering differences in treatment-related toxicity and patient preferences.
Hani I. Channir
[Slide 3]
Transoral surgery versus dysphagia-optimised intensity-modulated radiotherapy for early-stage oropharyngeal, supraglottic, and hypopharyngeal carcinoma (EORTC 1420 Best-of): a multicentre, open-label, randomised, phase 3 trial
Primary results · EORTC–GORTEC–NCRI–IAG/KHT · NCT02984410
Christian Simon
CHUV / University of Lausanne, Switzerland
on behalf of the Best-of investigators — EORTC, NCRI, GORTEC, SAKK, IAG-KHT
J Bourhis · JP Klussmann · C Fortpied · J Cabrieto · A-S Govaerts · K Tsechilidou · M Ansarin · M Broglie Daeppen · M Evans · R Giger · W Golusinski · K Hunter · R Leemans · F López · Nuyts · J Patterson · S Singer · E Willemse · V Grégoire
EORTC European Organisation for Research and Treatment of Cancer
[Slide 4]
Conclusions
1 Primary endpoint: no evidence of a difference in swallowing-related quality of life
3.9 points (90% CI −2.7 to 10.5) at 12 months; point estimate well below the 10-point MCID; consistent across sensitivity analyses.
2 Swallowing function and oncological outcomes consistent
No significant difference in PSS-HN or water swallow test; no feeding tube at 12 months in either arm; no evidence of a difference in survival (2-year OS 97% vs 100%)
3 Signals of different toxicity profiles, clinician-rated and patient-reported
After DO-IMRT
An early mucosal and salivary burden (adjusted risk differences 18–35 percentage points, all periods), mirrored by patient-reported dry mouth and sticky saliva at 4.5 and 6 months.
After transoral surgery
Feeding tube none at 12 months; 31% vs 14% during the first year (no information for the 25% of DO-IMRT patients who did not start it). Adjuvant RT in 15 (36%), CRT in 8 (19%).
No evidence of a difference in the other key QoL endpoints; no treatment-related deaths in either arm.
4 Implication for practice
Neither modality was shown to be functionally superior at 12 months; the choice depends on which pattern of burden suits the patient — a benchmark for shared decision making.
EORTC 1420 'Best-of' · NCT02984410 · C. Simon
TANGENT
Emactuzumab vs placebo · Tenosynovial giant cell tumor (Phase 3, NCT05417789, SynOx Therapeutics)All posts →
#ESMO26 🚀 TANGENT | Phase III
👥 136 pts | TGCT
💊 Emactuzumab (anti-CSF-1R) vs placebo
💉 5 infusions over 8 weeks
🎯 6-mo ORR (RECIST): 30% vs 2%
📈 ORR (TVS): 54% vs 7%
✅ Improved pain, stiffness & function (p<0.001)
⚠️ G≥3 TRAEs: 48% vs 2%
💡 Effective short-course therapy!
@OncoAlert
Same slide also posted by @PerezFidal
[Slide 1]
Objective Response Rate (RECIST v1.1) at Month 6 (Primary Endpoint)
Emactuzumab (n=91) — Objective response at Month 6: CR 2 (2%); PR 25 (27%); SD 54 (59%); PD 4 (4%); Missing data/not evaluable 6 (7%)
Placebo (n=45) — Objective response at Month 6: CR 0 (0%); PR 1 (2%); SD 42 (93%); PD 0; Missing data/not evaluable 2 (4%)
[Waterfall plots: Change from baseline, %; Patients; legend PD, SD, PR, CR]
| Emactuzumab (n=91) | Placebo (n=45)
ORRᵃ by RECIST v1.1, n (%) | 27 (30) | 1 (2)
Difference (95% CI)ᵇ | 28% (16, 39); p<0.001
At Month 6, emactuzumab demonstrated a statistically significant improvement in ORR by RECIST v1.1 compared with placebo (30% vs 2%). Most emactuzumab responders (70%) had responded by Week 6 (first MRI assessment)
ᵃCR or PR according to RECIST v1.1 at 6-month assessment. ᵇCommon risk difference stratified by prior TKI use; CI calculated using the Miettinen and Nurminen method; p value calculated using the Cochran-Mantel-Haenszel test stratified by prior TKI use.
CI, confidence interval; CR, complete response; MRI, magnetic resonance imaging; ORR, objective response rate; PD, progressive disease; PR, partial response; RECIST, Response Evaluation Criteria in Solid Tumors; SD, stable disease; TKI, tyrosine kinase inhibitor.
[Slide 2]
Change at Month 6 in Pain, Stiffness, and Quality of Life
Emactuzumab | Placebo
Worst Pain NRS — LSM (SE) change from baseline; Visit BL, W2, W4, W6, M2, M3, M4, M5, M6
Month 6: Emactuzumab −2.5; Placebo −0.4
Difference in LSM (95% CI): −2.2 (−3.0, −1.4); p<0.001ᵃ
Worst Stiffness NRS
Month 6: Emactuzumab −2.4; Placebo −0.3
Difference in LSM (95% CI): −2.1 (−3.0, −1.3); p<0.001ᵃ
Regimen: 5 infusions over 8 weeks
• QoL (EQ-5D-5L VAS) showed a numerically greater improvement with emactuzumab (+2.0) compared with placebo (−0.4) at Month 6 (LSM difference [95% CI]: 2.4 [−4.2, 9.1]; p=0.238)ᵃ
Emactuzumab was associated with rapid and durable clinically meaningful reductions in pain and joint stiffness. Differences versus placebo were statistically significant by Week 2 (after one dose) onwards
ᵃEstimates are from a mixed model for repeated measures with fixed effects for treatment, visit, and the interaction between treatment and visit, and covariates for prior TKI use (yes/no) and baseline score.
BL, baseline; CI, confidence interval; EQ-5D-5L, EuroQol 5 Dimension, 5 Level questionnaire; LSM, least-squares mean; M, Month; NRS, numerical rating scale; QoL, quality of life; SE, standard error; TKI, tyrosine kinase inhibitor; VAS, visual analogue scale; W, Week.
[Slide 3]
Most Common AEs Considered to be Related to Treatment
AE by preferred term in ≥15% of patients in the emactuzumab group, n (%) | Emactuzumab (n=91) All grades | Grade 3/4 | Placebo (n=45) All grades | Grade 3/4
Any treatment-related AE, n (%) | 91 (100) | 44 (48) | 31 (69) | 1 (2)
Pruritus | 69 (76) | 3 (3) | 10 (22) | 0
Periorbital oedema | 63 (69) | 1 (1) | 3 (7) | 0
Fatigue | 38 (42) | 2 (2) | 9 (20) | 0
Oedema peripheral | 38 (42) | 0 | 0 | 0
Face oedema | 35 (38) | 1 (1) | 1 (2) | 0
Blood CPK increased | 28 (31) | 22 (24) | 1 (2) | 0
AST increased | 22 (24) | 2 (2) | 0 | 0
Eyelid oedema | 22 (24) | 0 | 6 (13) | 0
Rash | 21 (23) | 1 (1) | 2 (4) | 0
Rash maculo-papular | 20 (22) | 2 (2) | 2 (4) | 0
Nausea | 19 (21) | 0 | 7 (16) | 0
Asthenia | 17 (19) | 1 (1) | 4 (9) | 0
Dermatitis acneiform | 16 (18) | 0 | 0 | 0
Lacrimation increased | 16 (18) | 0 | 0 | 0
Lichen myxoedematosus | 16 (18) | 2 (2) | 0 | 0
Blood lactate dehydrogenase increased | 14 (15) | 0 | 0 | 0
Hypertension | 14 (15) | 8 (9) | 1 (2) | 1 (2)
• The most common Grade 3 or 4 treatment-related AE was blood CPK increased, observed in 24% of patients in the emactuzumab group
Post-treatment AEs: any AE with onset or worsening of a pre-existing condition on or after the first administration of study treatment in the double-blind phase and before the first administration of study treatment in the open-label phase.
Events were considered by the investigator to be definitely, probably, or possibly related to treatment.
AE, adverse event; AST, aspartate aminotransferase; CPK, creatine phosphokinase.
[Slide 4]
Conclusions
• A planned course of 5 infusions of emactuzumab over 8 weeks provided statistically significant reductions in tumour size at Month 6 compared with placebo
• Most responders at Month 6 had responded by Week 6 (first MRI assessment) based on both RECIST v1.1 and TVS criteria
• Clinically meaningful improvements in physical function and range of motion with emactuzumab were observed early and were sustained over time, with statistically significant differences versus placebo emerging from Week 4 onwards
• Improvements in pain and stiffness were statistically significant with emactuzumab compared with placebo by Week 2, after the first infusion
• Emactuzumab had a manageable safety profile consistent with Phase 1 findings and expectations of CSF-1R inhibition
Emactuzumab demonstrated radiographic and functional efficacy and manageable safety in patients with TGCT, and has the potential to be the first short-course, potent treatment option for TGCT
CSF-1R, colony-stimulating factor-1 receptor; MRI, magnetic resonance imaging; RECIST, Response Evaluation Criteria in Solid Tumors; TGCT, tenosynovial giant cell tumour; TVS, tumour volume score.
Cross-trial comparisons & roundups
Slides that compare or list several trials
Early report of #T_DXd in #DSRCT from the #FrenchSarcomaGroup presented @MehdiBrahmi. Small number of patients (n=12) but definitely an approach that worth considering in this otherwise devastating disease.
More publications on this topic to follow by other groups 😃.
#Sarcoma #ESMO26 @myESMO #ESMOAmbassadors @ctosociety
[Slide 1]
08:30 - 10:00 Rapid oral: Sarcoma
CHAIRS: MARK DICKSON, PALMA DILEO, CESAR SERRANO
Trastuzumab deruxtecan in patients with desmoplastic small round cell tumors
A retrospective analysis from the French Sarcoma Group
Mehdi Brahmi, Maud Toulmonde, Aymeric de Montfort, Perrine Vuagnat, Clément Korenbaum, Audrey Monneur-Miramon, Lucy Metayer, Yves Reguerre, Justine Gantzer, Margaux Dupont, Benjamin Verret, Jean-Yves Blay
26th October 2026
Mehdi Brahmi
Trastuzumab deruxtecan in patients with desmoplastic small round cell tumors (DSRCT): A retrospective analysis from the French Sarcoma Group
MALAGA AUDITORIUM - HALL 3
[Slide 2]
08:30 - 10:00 Rapid oral: Sarcoma
CHAIRS: MARK DICKSON, PALMA DILEO, CESAR SERRANO
INTRODUCTION
Bulk RNA Sequencing & HER2 expression level
ERBB2 expression in 13 DSRCT vs 1725 sarcomas
T-test, p = 7.8e-08
ERBB2 expression log2(TPM+1)
DSRCT
sarcomas
Top 5 lower/higher ERBB2 sarcoma subtype expressors
GIST (n=32)
Pleomorphic LPS (n=11)
Phosphaturic mesenchymal tumor (n=10)
Angiosarcoma (n=40)
TGCT (n=42)
GLI1-altered mesenchymal tumors (n=16)
SMARCA4-DTS (n=15)
Perineurioma (n=26)
Clear cell sarcoma (n=13)
DSRCT (n=16)
Mehdi Brahmi, MD PhD
Zhang et al. Clin Cancer Res 2024
Brahmi et al., ESMO Open 2025
Mehdi Brahmi
Trastuzumab deruxtecan in patients with desmoplastic small round cell tumors (DSRCT): A retrospective analysis from the French Sarcoma Group
MALAGA AUDITORIUM - HALL 3
[Slide 3]
08:30 - 10:00 Rapid oral: Sarcoma
CHAIRS: MARK DICKSON, PALMA DILEO, CESAR SERRANO
RESULTS
Patients
Demographics/Characteristics | N = 12
Age, median (range), y | 33 (13, 56)
Sex, n (%)
Male | 9 (75)
Female | 3 (25)
Number of previous lines, median (range) | 3 (1, 4)
IHC HER2
0 (null) | 4
0 (ultra-low) | 1
+ | 6
++ | 1
+++ | 0
Best reponse
CR | 1 (8)
PR | 9 (75)
SD | 2 (18)
PD | 0
Safety
Grade 1 fatigue | 2
Grade 1 diarrhea | 2
ILD | 0
Mehdi Brahmi, MD PhD
Mehdi Brahmi
Trastuzumab deruxtecan in patients with desmoplastic small round cell tumors (DSRCT): A retrospective analysis from the French Sarcoma Group
MALAGA AUDITORIUM - HALL 3
🚨 One of those #ESMO26 presentations I knew nothing about (and ended up loving)
SL-28: a novel off-the-shelf, non-genetically modified allogeneic leukocyte therapy in heavily pretreated solid tumors (n=12)!
💥 ORR 66.7% (4 CR, 4 PR), DCR 100%, with responses across multiple tumor types and mDoR not reached!
🚨 mPFS: 24.7 mo. Importantly, the observed deaths were non-cancer related, so the OS curve should be interpreted in that context.
✅ No GVHD. No CRS. No ICANS.
A very early n=12 dataset, but definitely one to watch 👀
@OncoAlert @OncoReporte #ESMO26
@OncoAlert @OncoReporte @myESMO @_SEOM
[Slide 1]
RESULTS: Treatment-emergent adverse events
Event | ANY Grade, n (%) | Grade 1-2, n (%) | Grade 3-4, n (%)
Any | 11 (91.7%) | 11 (91.7%) | 0 (0%)
Pyrexia | 10 (83.3%) | 10 (83.3%) | 0 (0%)
Anemia | 0 (0%) | 0 (0%) | 0 (0%)
WBC count decreased | 0 (0%) | 0 (0%) | 0 (0%)
Leukopenia | 0 (0%) | 0 (0%) | 0 (0%)
Neutropenia | 0 (0%) | 0 (0%) | 0 (0%)
Platelet count decreased | 0 (0%) | 0 (0%) | 0 (0%)
ALT/AST increased | 1 (8.3%) [?] | 1 (8.3%) [?] | 0 (0%)
Nausea | 1 (8.3%) [?] | 1 (8.3%) [?] | 0 (0%)
Vomiting | 0 (0%) [?] | 0 (0%) [?] | 0 (0%)
Hypotension | 0 (0%) | 0 (0%) | 0 (0%)
Fatigue | 0 (0%) | 0 (0%) | 0 (0%)
Headache | 0 (0%) | 0 (0%) | 0 (0%)
GVHD-linked TEAEs (all) | 0 (0%) | 0 (0%) | 0 (0%)
CRS-linked TEAEs (all) | 0 (0%) | 0 (0%) | 0 (0%)
ICANS-linked TEAEs (all) | 0 (0%) | 0 (0%) | 0 (0%)
[Slide 2]
RESULTS: Outcomes
Radiologic response
Y-axis: Change in Lesion Diameters (%) 25 0 -25 -50 -75 -100
Bars (left to right): PDAC* | GC | LLC | ACC | FL | BLCA | NB | PDAC | PCa | PCa | PCa | NSCLC
According to RECIST 1.1:
CR, n=4 (33.3%)
PR, n=4 (33.3%)
SD, n=4 (33.3%)
PD, n=0 (0%)
ORR: 8/12 (66.7%)
DCR: 12/12 (100%)
ACC Adenoid cystic carcinoma (salivary gland)
BLCA Bladder Urothelial Carcinoma
FL Follicular lymphoma
GC Gastric cancer
LCC Large-cell lung carcinoma
NB Neuroblastoma
NSCLC Non-small cell lung cancer
PCa Prostate cancer
PDAC Pancreatic ductal adenocarcinoma
*Tumor doubling time increased from 22 to 358 days, representing a 16.3-fold prolongation.
[Slide 3]
RESULTS: Duration of Disease Control
Rows (top to bottom): FL | PCa | PCa | NSCLC | NB | PCa | PDAC | BLCA | LCC | ACC | GC | PDAC
X-axis: Duration (months) 0 5 10 15 20 25 30 35
OS STATUS column (x = Death, o = Censored)
According to RECIST 1.1:
CR, n=4 (33.3%)
PR, n=4 (33.3%)
SD, n=4 (33.3%)
PD, n=0 (0%)
→ Ongoing
X Death (non-cancer related)
ACC Adenoid cystic carcinoma (salivary gland)
BLCA Bladder Urothelial Carcinoma
FL Follicular lymphoma
GC Gastric cancer
LCC Large-cell lung carcinoma
NB Neuroblastoma
NSCLC Non-small cell lung cancer
PCa Prostate cancer
PDAC Pancreatic ductal adenocarcinoma
Median duration of response in patients with CR/PR has not been reached
[Slide 4]
RESULTS: OS and PFS
OS (n=12)
Preliminary median OS 24.7 mo
12-month OS 83.3%
Estimated survival probability
Y-axis: Probability of Survival 0 25 50 75 100
X-axis: OS time (months) 0 10 20 30 40
PFS (n=12)
Preliminary median PFS 24.7 mo
12-month PFS 83.3%
24-month PFS 69.4%
Y-axis: Probability of PFS
X-axis: Latest progression-free CT/MRI assessment (months) 0 10 20 30 40
No radiographic PD; PFS events were deaths from any cause
Survival table
Endpoint: OS and PFS (single arm, n=12)
SL-28 (OS) | 12 | 24.7 mo (preliminary)
SL-28 (PFS) | 12 | 24.7 mo (preliminary)
Landmark rates:
12 months: OS 83.3% | PFS 83.3%
24 months: PFS 69.4%
‼️ #ESMO26 | ADC toxicities with Yeon Hee Park
💥Key pearls:
• Toxicity depends on the payload, linker, target & patient of course!!
• Different ADCs, different profiles! T-DXd: ILD | SG: myelosuppression/diarrhea | Dato-DXd: stomatitis/ocular
• Timing matters: toxicities can emerge from days to months…
With ADCs, the construct tells you what to watch for
@OncoAlert
@OncoReporte @myESMO @_SEOM @Lung_Cancers @gecp_org
[Slide 1]
Linker stability is a trade-off, not a target to maximize; determinant of ADC toxicity
less stable in plasma -> more stable in plasma
Hydrolysable CL2A - Sacituzumab govitecan (pH-dependent hydrolysis) - PH-dependent: bystander effect, systemic toxicities
Tetrapeptide GGFG - Trastuzumab deruxtecan (enzymatic cleavage) - Protease-dependent: bystander effect, target-dependent toxicities
Thioether, non-cleavable - Trastuzumab emtansine - Non-cleavable: no bystander effect
[Structure labels: SN38 (camptothecin); DXd (camptothecin); DM1 (maytansinoid); Hydrolysable CL2A linker (pH); Tetrapeptide linker (cathepsin B protease); Thioether linker]
Unstable linker
• More free payload in the circulation
• Higher rates of neutropenia
• Less ocular toxicity
• Payload reaches tumour tissue that the antibody itself penetrates poorly
Stable linker
• Less free payload in the circulation
• Lower rates of neutropenia
• More ocular toxicity
• Release depends more heavily on efficient internalisation
Conjugation chemistry & DAR
• Stochastic lysine/cysteine conjugation -> heterogeneous DAR, variable toxicity
• T-DM1: lysine conjugation, average DAR 3.5 at variable sites
• T-DXd, SG: cysteine conjugation at 8 sites, DAR up to 8, more homogeneous
• All approved ADCs still stochastic; site-specific conjugation in development
Observed in MMAE-based ADCs: the same molecule redesigned for greater linker stability shifts the toxicity profile rather than removing it.
Colombo R, et al. Cancer Discov 2024;14(11):2089-2108. Tarantino P, et al. Nat Rev Clin Oncol. 2023;20:558-576.
Yeon Hee Park
[Slide 2]
Determinants of the toxicities of ADCs
• Payload: class sets the expected AE spectrum; potency and DAR scale the severity of toxicity
• Linker: less stable -> higher free-payload peaks and chemotherapy-like AEs; very stable -> sometimes ocular, neuro- or hepatotoxicity
• Antibody: on-target, off-tumour effects (HER2 -> cardiotoxicity; Trop2 -> rash, mucositis; nectin 4 -> rash, dysgeusia; tissue factor -> bleeding) and FcγR uptake by immune cells
• Patient: organ function, comorbidities, pharmacogenomics, body composition, ethnicity
Pharmacodynamic determinants
Uptake into non-malignant cells | Fc/lectin receptors, endocytosis, passive diffusion
Bystander effect | Payload released from apoptotic cells
Deconjugation / linker instability | Premature payload release in circulation
High drug-to-antibody ratio | Increased total payload dose
Limited tumour penetration | Increased systemic toxicity
Pharmacokinetic determinants
Limited target-specific binding | Increased non-target exposure
↑ Absorption, ↓ catabolism | Increased systemic concentration
↑ Half-life, ↓ excretion, albumin binding | Prolonged exposure
Lipophilic payload | Higher tissue penetrance
[Figure: Linker stability (non-cleavable; cleavable enzyme labile; cleavable chemically labile) - Stability vs Chemotherapy-like toxicities; Payload mechanism of action (microtubule inhibitors: DM1 thrombocytopenia, hepatotoxicity; DM4 ocular toxicity; MMAE peripheral neuropathy, myelotoxicity; MMAF ocular toxicity; topoisomerase I inhibitors: diarrhoea, neutropenia; calicheamicins, duocarmycins, pyrrolobenzodiazepines: neutropenia); Antibody on-target toxicities (HER2 cardiotoxicity; Trop2 rash, mucositis; Nectin 4 rash, dysgeusia; Tissue factor bleeding); Binding to Fc receptors on immune cells (off-target toxicities, immune activation); Patient-related factors]
Yeon Hee Park
Tarantino et al. Nature Reviews Clinical Oncology | Volume 20 | August 2023 | 558–576 (Fig. 2; Table 2)
[Slide 4]
Time to first onset differs by TEAE
Median days to first onset (log scale) ■ 5.4 mg/kg ■ 6.4 mg/kg
Axis: 1, 10, 100, 1000
TEAE | 5.4 mg/kg | 6.4 mg/kg
Nausea | 3 | 4
Fatigue | 12 | 7
Vomiting | 9 | 7
Neutropenia | 43 | 16
ILD (adjudicated) | 168 | 85
Interpreting dose-pool differences
Caution in comparison: Pools differ in size, age, sex, tumor type and treatment duration; no statistical comparison was made.
Sex and tumor effects: Vomiting higher in the 5.4 mg/kg pool (94.7% female); mGC symptoms may overlap with GI TEAEs.
Older patients: ≥65 years had more grade 3–4 AEs at 5.4 mg/kg (mainly mBC); similar by age at 6.4 mg/kg.
Renal impairment: Moderate renal impairment linked to higher low-grade ILD/pneumonitis — warrants closer monitoring.
Days - Nausea, vomiting, fatigue — first cycle
Weeks - Neutropenia — cycles 1–3
Months - ILD — monitor throughout treatment
Park YH, et al. The Oncologist. 2026;31:oyal396 (Results; Tables S5–S8; Table 2; Discussion)
Yeon Hee Park
TRIDENTE phase II: encorafenib + binimetinib + cetuximab rechallenge in BRAF V600E mCRC (n=21).
Met the study primary endpoint
ORR 19% (3/4 responses unconfirmed)
DCR 76%
#ESMO26 #ESMOAmbassadors https://t.co/uES7dA9CLz
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What is the frequency of PIK3CA mutations across cancer types in the TCGA PanCancer Atlas studies?
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PIK3CA Mutation Frequency Across TCGA PanCancer Atlas Cancer Types
PIK3CA mutations show striking variation across cancer types in the TCGA PanCancer Atlas, ranging from 0.8% to 48.6% at the sample level:
Top 10 Cancer Types by PIK3CA Mutation Frequency
Cancer Type | Mutated Samples | Profiled Samples | Frequency
Endometrial Cancer | 279 | 574 | 48.6%
Breast Cancer | 347 | 1,066 | 32.6%
Cervical Cancer | 83 | 291 | 28.5%
Colorectal Cancer | 147 | 534 | 27.5%
Bladder Cancer | 90 | 410 | 22.0%
Head and Neck Cancer | 90 | 515 | 17.5%
Esophagogastric Cancer | 88 | 618 | 14.2%
Glioblastoma | 38 | 397 | 9.6%
Glioma | 42 | 514 | 8.2%
Non-Small Cell Lung Cancer | 81 | 1,050 | 7.7%
Bottom 5 Cancer Types
PIK3CA mutations are rare or absent in: Renal Non-Clear Cell Carcinoma (0.9%), Adrenocortical Carcinoma (1.1%), Prostate Cancer (2.0%), Pleural Mesothelioma (2.3%), and Pancreatic Cancer (2.8%).
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Explore the Data
View PIK3CA mutations across all TCGA PanCancer Atlas studies on OncoPrint — shows sample-by-sample mutation status with integrated clinical tracks and copy number data.
Amazing work by @nikolausschultz , his lab & the cBioPortal team! Making cancer genomics accessible and now queryable with cBioChat.
https://t.co/7kMyCfRxeB
#ESMO26 #ESMOAmbassadors https://t.co/zc1XQ75Xo0
[Slide 2]
cBioPortal for Cancer Genomics
New feature: cBioChat – chat.cbioportal.org
Ability to connect your LLM of choice to cBioPortal MCP server
Immunotherapy Patients Over Time (2015–2024)
Year | Total Sequenced Patients | Received Immunotherapy
2015 | 7,234 | 852
2016 | 6,252 | 947
2017 | 8,174 | 1,157
2018 | 9,231 | 1,278
2019 | 11,426 | 1,703
2020 | 9,468 | 1,529
2021 | 10,448 | 1,739
2022 | 10,316 | 1,702
2023 | 11,449 | 1,907
2024 | 11,632 | 1,913
Top Immunotherapy Agents & Their Trends
Agent | Class | 2015 Patients | 2024 Patients | Trend
Pembrolizumab | PD-1 inhibitor | 386 | 1,070 | Strong growth
Nivolumab | PD-1 inhibitor | 424 | 520 | Moderate growth
Ipilimumab | CTLA-4 inhibitor | 193 | 208 | Relatively stable
Durvalumab | PD-L1 inhibitor | 7 | 269 | Rapid rise
Atezolizumab | PD-L1 inhibitor | 49 | 60 | Relatively flat
[Slide 3]
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1 Ask cBioChat
"Survival by KEAP1 in KRAS-mutant lung adeno on pembrolizumab"
Cancer: Lung adeno | KRAS
Treatment: Pembrolizumab
Overall Survival - 538 patients
[KM plot: not mutated vs KEAP1 mutated; 100% to 0%; Months 0 to 105]
KEAP1-mutated patients do worse: median 9 vs 25 mo, p = 1.5×10^-8
2 Refine query via user interface
Clicks Stage IV in the stage chart
filter added Stage: IV
Stage (Highest Recorded)
I–III 176
IV 362
The chat sees the new filter and uses it for follow-ups.
3 Ask a follow-up
"Does KEAP1 still matter?"
Cancer: Lung adeno | KRAS
Treatment: Pembrolizumab | Stage: IV
Overall Survival - 362 patients
[KM plot: not mutated vs KEAP1 mutated; Months 0 to 105]
Yes, still worse: median 8 vs 21 mo, p = 4×10^-6
[Slide 4]
OncoKB updates
Debyani Chakravarty, Sarah Suehnholz, Moriah Nissan, Ritika Kundra, Nicole Fernandez, Kelly Cavender, Kinisha Gala
John Konecny, Calvin Lu, Benjamin Preiser, Reshma Ramaiah, JJ Gao
1033 Genes
11515 Alterations
143 Cancer Types
171 Drugs
Level 1 - FDA-approved drugs - 59 Genes
Level 2 - Standard care - 33 Genes
Level 3 - Clinical evidence - 38 Genes
Level 4 - Biological evidence - 32 Genes
Level R1 - Standard care - 8 Genes
Level R2 - Clinical evidence - 11 Genes
Automated annotation of MSK-IMPACT reports
Integrated into cBioPortal
Free academic licenses, fee for commercial
New: Integration into Open Evidence
New: Annotation of germline variants (also in cBioPortal)
Diana Mandelker, Zsofia Stadler
Bo Kim (UI/UX in DigITs)
[Screenshot: BRCA2 gene page]
BRCA2 Also known as FANCD1, XRCC11, FAD1
Tumor Suppressor
NCBI Gene: 675 | Show additional gene information
BRCA2, a tumor suppressor involved in the DNA damage response, is mutated in various cancer types. Pathogenic germline mutations in BRCA2 cause autosomal dominant BRCA2-associated Hereditary Breast and Ovarian Cancer and confer an increased risk for female and male breast, ovarian, pancreatic, and prostate cancers, as well as other cancer types.
Somatic | Germline
Gene Overview | Genomic Indicators | Annotated Variants
Genetic Risk - Penetrance: High
Annotated Variants - Pathogenic: 282 | Likely Pathogenic: 28
Genomic Indicators
Genomic Indicator | Inheritance | Associated Variants | Description
BRCA2-associated hereditary breast and ovarian cancer syndrome | Autosomal Dominant | Pathogenic Variants | A single variant in BRCA2 causes hereditary breast and ovarian cancer (HBOC) syndrome, which is associated with an increased risk for breast, ovarian, prostate, pancreatic, and other cancers.
Well done @BrahmiMedhi @jeanyvesblay #ESMO2026 #ESMOAmbassadors #desmoplasticroundcellsarcoma https://t.co/I7qPWkKS1g https://t.co/4ep8AaNETg
INTRODUCTION
Bulk RNA Sequencing & HER2 expression level
ERBB2 expression in 13 DSRCT vs 1725 sarcomas
T-test, p = 7.8e-08
ERBB2 expression log2(TPM+1)
DSRCT
sarcomas
Top 5 lower/higher ERBB2 sarcoma[illegible]
GIST (n=32)
Pleomorphic LPS (n=11)
Phosphaturic mesenchymal tumor (n=10)
Angiosarcoma (n=40)
TGCT (n=42)
GLI1-altered mesenchymal tumors (n=16)
SMARCA4-DTS (n=15)
Perineurioma (n=26)
Clear cell sarcoma (n=13)
DSRCT (n=16)
[illegible]hdi Brahmi, MD PhD
Zhang et al. Clin Canc[illegible]
📌 #ESMO26 e-poster spotlight
“Are we measuring the symptoms that matter most to patients? Our analysis shows that existing @EORTC questionnaires capture most common treatment-related symptoms in #HeadNeckCancer.”
Congrats to @mkmoutafi et al. 👏
#GivingVoice2Patients @myESMO https://t.co/m3iBLa9wXG
Coverage of Treatment-Related Toxicities by EORTC QLQ-C30 and QLQ-H&N43 in Head and Neck Cancer
POSTER: #6481
Myrto Moutafi1, Daniel Portik1, Claire Piccinin1, Hayat Hamzeh2, Katherine J. Taylor3,4, Pierluigi Bonomo5, Jose Pais Silva1, Ana Joaquim1, Madeline Pe1, Lotte van der Weijst1
1. European Organisation for Research and Treatment of Cancer (EORTC) Headquarters, Brussels, Belgium, 2. Leeds Institute of Medical Research, University of Leeds, Leeds, UK, 3. Division of Epidemiology and Health Services Research, Institute of Medical Biostatistics, Epidemiology, and Informatics (IMBEI), University Medical Centre of Johannes Gutenberg University, Mainz, Germany, 4. Division of Quality of Life, University Medical Center Rostock, Comprehensive Cancer Center Mecklenburg-Vorpommern, Rostock, Germany, 5. Radiation Oncology, Azienda Ospedaliero - Universitaria Careggi, University of Florence, Florence, Italy
Contact: Myrto Moutafi
Email: myrto.moutafi@eortc.org
BACKGROUND
- Clinician reported toxicity grading has limitations for subjective adverse events (AEs).
- The health-related quality of life (HRQOL) questionnaires EORTC QLQ-C30 and QLQ-H&N43 capture patient-reported symptoms and treatment burden.
- This study their coverage of common treatment-related symptomatic AEs in head and neck cancer (HNC).
METHODS
- Treatment regimens were extracted from ESMO and NCCN guidelines
- AEs from EMA SmPC and radiotherapy literature were mapped to QLQ-C30 and QLQ-H&N43 domains.
- Symptomatic AEs were analysed separately from laboratory based or diagnostically defined AEs.
Table 1. Top 20 AEs (coverage summary)
Type | N (%)
Total AEs | 20
Symptomatic | 15 (75%)
Diagnostic/lab | 5 (25%)
Captured by QLQ-C30/H&N43 | 13/15 (87%)
Partially captured * | 2/15
*Partial PRO capture indicates indirect assessment through related domains rather than a dedicated item (e.g. alopecia through appearance/body image items or pyrexia through its impact on fatigue and functioning).
RESULTS
- Forty regimens were analysed. Among frequent AEs, 75% were symptomatic and 25% diagnostic/laboratory-based (Table 1). Across systemic therapies, nausea/vomiting and diarrhoea occurred in 85%, anorexia in 73%, rash in 70%, constipation/alopecia in 63%, and fatigue in 58%.
- Radiotherapy-related AEs were predominantly symptomatic, including near-universal fatigue, mucositis (>30-50%), xerostomia (≈20-30%), and dysphagia (≈5-20%), and aligned with HRQoL domains. Structural complications (e.g. osteoradionecrosis, plexopathy) and laboratory AEs were not PRO-captured.
- Among the 20 most frequent clinician-graded AEs analysed, 15 (75%) were symptomatic and 13/15 (87%) were directly captured by QLQ-C30 and/or QLQ-H&N43, while the remainder were only partially represented. Table 2 illustrates the 10 most frequent AEs.
Table 2. Top 10 Most Frequent Clinician-Graded Adverse Events and Coverage
Rank | Adverse Event | Symptomatic / Diagnostic | QLQ-C30 | QLQ-H&N43 | Coverage Comment
1 | Diarrhoea | Symptomatic | Captured | Not applicable | Directly captured (QLQ-C30 item)
2 | Nausea / vomiting | Symptomatic | Captured | Not applicable | Directly captured (QLQ-C30 scale)
3 | Anaemia | Diagnostic (laboratory) | Not captured | Not captured | Laboratory-based
4 | Anorexia / decreased appetite | Symptomatic | Captured | Not applicable | Directly captured
5 | Rash | Symptomatic | Not applicable | Captured | Captured as skin problems
6 | Alopecia | Symptomatic (visible) | Not applicable | Captured | Limited symptom granularity
7 | Neutropenia | Diagnostic (laboratory) | Not captured | Not captured | Laboratory-based
8 | Thrombocytopenia | Diagnostic (laboratory) | Not captured | Not captured | Laboratory-based
9 | Constipation | Symptomatic | Captured | Not applicable | Directly captured
10 | Hepatic enzymes increased | Diagnostic (laboratory) | Not captured | Not captured | Laboratory-based
CONCLUSION
The EORTC QLQ-C30 and QLQ-H&N43 capture most common symptomatic adverse events (AEs) in head and neck cancer. Although radiotherapy-related AEs are often less frequently reported than systemic therapy AEs, some may persist as late effects, highlighting the value of long-term PRO assessment. AEs not captured by the PRO measures were mainly laboratory-based or structural and therefore generally require clinical assessment. Together, these findings support the use of PROs to assess core treatment burden, complemented by clinician-based evaluation of toxicities requiring clinical, laboratory, or diagnostic assessment..
ACKNOWLEDGEMENTS/FUNDING
This work was supported by Kom op tegen Kanker (Stand up to Cancer), the Flemish cancer society from Belgium.
Myrto Moutafi's fellowship was supported by the EORTC Cancer Research Fund (ECRF).
Discover more
www.eortc.org
1622eP
Slides not tied to a tracked trial
Not tied to a single tracked trial
Hey @PTarantinoMD ! I guess we can say this passes the truck test?
glad to see #sarcoma at the plenaries both at @ASCO and @myESMO https://t.co/Cz2xBngOCd
Primary Endpoint: BICR-assessed PFS with Ris-Rez vs Gemcitabine + Docetaxel
• At data cutoff date, there were 41 PFS events per BICR (41/80; 51%) in the Ris-Rez arm and 31 (31/42; 74%) in the Gemcitabine + Docetaxel arm
• Ris-Rez demonstrated a statistically significant and clinically meaningful improvement in BICR-PFS vs Gemcitabine + Docetaxel
4-mo rate
Ris-Rez | 65%
Gemcitabine + Docetaxel | 33%
Ris-Rez (n = 80) | Gemcitabine + Docetaxel (n = 42)
Median, mo (95% CI) | 5.5 (4.1–7.4) | 1.4 (0.8–2.7)
HR (95% CI) | 0.33 (0.20–0.55)
P-value | <0.0001
PFS (%)
Time since randomisation (mo)
Number at risk
DCO: 17 June 2026.
BICR, blinded independent central review; CI, confidence interval; DCO, data cutoff; HR, hazard ratio; mo, months; NR, not reached; PD, progressive disease; PFS, progression-free survival; Ris-Rez, risvutatug rezetecan
Presented by: Lu Xie, MD, PKUPH
Survival table
Endpoint: BICR-assessed PFS (primary)
Arm | N | Median | Median CI
Ris-Rez | 80 | 5.5 mo | 4.1–7.4
Gemcitabine + Docetaxel | 42 | 1.4 mo | 0.8–2.7
HR: 0.33
HR CI: 0.20–0.55
P: <0.0001
4-mo PFS rate: 65% vs 33%
Ooo, supportive care. Easy win for patients.
Looks like swapping olanzapine out for mirtazapine significantly reduces nausea. Relevant to every oncologist.
Randomized trial from India at #ESMO26. 120 chemo-naive patients starting highly emetogenic chemo, randomized 1:1. Both arms got fosaprepitant + palonosetron + dex. Fourth drug was mirtazapine 15 mg vs olanzapine 5 mg, days 1–4.
Mirtazapine vs olanzapine:
Acute 78.5% vs 56.4%, p=0.01
Delayed 52.3% vs 25.5%, p=0.003
Overall 46.2% vs 21.8%, p=0.005
Major differences
120 patients? Minimal risk? I'm sold. The day after the paper comes out, I'll swap.
@realbowtiedoc thoughts?
@OncoAlert @TheGutOncLab @Onco_Nexus
[Slide 1]
Proportion of patients achieving total control in the acute, delayed, and overall phases
FDP-M FDP-O
Acute 78.5% 56.4% P=0.01
Delayed 52.3% 25.5% P=0.003
Overall 46.2% 21.8% P=0.005
Phase | Total (N=120) | FDP-M (N=65) | FDP-O (N=55) | P value
Acute | 82 (68.3%) | 51 (78.5%) | 31 (56.4%) | 0.01
Delayed | 48 (40%) | 34 (52.3%) | 14 (25.5%) | 0.003
Overall | 42 (35%) | 30 (46.2%) | 12 (21.8%) | 0.005
Dr Anusha Mruthyunjaya Swamy
[Slide 2]
1:1 block randomisation and opaque envelope allotment
• Chemotherapy naive
• HPE proven solid organ malignancy
• Need to be initiated on HEC
• Willing to consent
• Fulfilling all the eligibility criteria
ARM- A (FDP-M)
Inj Fosaprepitant 150mg IV on D1
Inj Dexamethasone 8-12mg IV on D1 followed by Tab Dexamethasone 4mg PO bd from D1-D4
Inj Palonosetron 0.25mg IV on D1
Tab Mirtazapine 15mg PO D1-D4
ARM- B (FDP-O)
Inj Fosaprepitant 150mg IV on D1
Inj Dexamethasone 8-12mg IV on D1 followed by Tab Dexamethasone 4mg PO bd from D1-D4
Inj Palonosetron 0.25mg IV on D1
Tab Olanzapine 5mg PO D1-D4
DAY 2 DAY 6 4 WEEKS
• Diary record of nausea, vomiting, use of rescue medication and their doses
• Adverse events and their severity (CTCAE v5.0)
• FLIE questionnaire to be answered
Treatment emergent adverse events and their severity (CTCAE v5.0)
• Statistical analysis was performed using the Statistical Package for Social Sciences (SPSS) software for Windows (version 29).
• Proportions and percentages were used for categorical variables, while mean ± standard deviation was used for numerical variables.
• The association between categorical variables was assessed using the Chi square test.
• For normally distributed data, between group comparisons were carried out using the unpaired t test.
• A 'p' value of less than 0.05 was considered statistically significant.
These Kaplan-Meier curves finally separate… by about the width of a pixel...
The curves ride on top of each other for years before a modest late subatomic divergence, and then the blue arm takes a dramatic vertical plunge at the far righ, right about the time the numbers at risk collapse to single digits. Truly a triumph of statistical significance over clinical drama.
Novartis is already calling a ~20% relative reduction “clinically meaningful.” Somewhere a health economist is quietly calculating the cost per life-year for treating 5,100 patients to avert ~27 deaths.@5_utr
93.9% (Δ=1.2%) 91.9% (Δ=2.1%a)
92.7% 89.7%
Overall survival (%)
Median follow-up: 66.5 months
RIB + NSAI (n = 2549) | NSAI alone (n = 2552)
No. of OS events(b): 178 | 205
HR (95% CI): 0.809 (0.661-0.989)
Nominal P value (1-sided)(c): 0.019
Time since randomization (Months)
No. of patients at risk
RIB + NSAI: 2549 2404 2336 2299 2258 2219 2184 2132 2086 2047 1982 1521 761 85 2 0
NSAI alone: 2552 2301 2254 2208 2159 2117 2064 2012 1981 1936 1866 1426 730 81 3 0
Survival table
Endpoint: Overall survival
RIB + NSAI | 2549
NSAI alone | 2552
HR: 0.809
HR CI: 0.661-0.989
P: 0.019 (nominal, 1-sided)
Landmark rates:
60 months: RIB + NSAI 93.9% | NSAI alone 92.7%
72 months: RIB + NSAI 91.9% | NSAI alone 89.7%
#ESMO26
Optimal duration of adjuvant endocrine therapy: 5, 7–8, or 10 years?
From Dr. Fumikata Hara’s excellent discussion👇 https://t.co/BHXSGesayf
CLINICAL APPLICATIONS
HOW LONG? COMPARE THE RANDOMIZED TREATMENT DURATIONS
TRIAL | COMPARE | SHORTER / LONGER ET | HR (95% CI)
B-42 | 5 vs 10 y (Placebo vs LET 5 y) | Prior AI 5 y or TAM <=3 y -> AI (total 5 y) | DFS 0.85 (0.76-0.94)
AERAS | 5 vs 10 y (Stop vs ANA 5 y) | Prior ANA 5 y or TAM 2-3 y -> ANA 2-3 y | DFS 0.61 (0.46-0.82)
GIM4 | 5 vs 7-8 y (LET 2-3 y vs 5 y) | Prior TAM 2-3 y | iDFS 0.78 (0.65-0.93)
DATA | 5-6 vs 8-9 y (ANA 3 y vs 6 y) | Prior TAM 2-3 y | Adapted DFS 0.86 (0.72-1.01)
IDEAL | 7.5 vs 10 y (LET 2.5 y vs 5 y) | Prior ET 5 y (TAM / AI / sequence) | DFS 0.92 (0.74-1.16)
ABCSG-16 / SALSA | 7 vs 10 y (ANA 2 y vs 5 y) | Prior ET 5 y (TAM / AI / sequence) | DFS 0.99 (0.85-1.15); SALSA: 10 y had more fractures (6.3% vs 4.7%); HR 1.35
[Bar diagram legend: Prior ET; AI in both arms; Additional AI in longer arm; R = Randomization]
Extension beyond 5 years can help, but 10 years is not necessary for everyone
B-42: Mamounas et al. ESMO 2026, LBA24. AERAS: J Clin Oncol. 2023;41:3329-3338. GIM4: Lancet Oncol. 2021;22:1458-1467. DATA: EClinicalMedicine. 2023;58:101901. IDEAL: J Natl Cancer Inst. 2018;110:40-48. SALSA: N Engl J Med. 2021;385:395-405. DFS definitions and analysis populations differ across trials. Bars approximate where prior TAM was 2-3 y.
🇮🇳 Promising practice-changing data from @TataMemorial India 🇮🇳 at #ESMO2026!
Phase III trial (n=475) in technically unresectable oral cancer:
Weekly paclitaxel-carboplatin + oral metronomic therapy (PCm) vs DCF
✅ Higher response rates
✅ Greater conversion to resectability
✅ Significantly less toxicity
✅ Non-inferior overall survival
✅ Outpatient-friendly, without central line
2-year OS: 38.9% vs 29.4%, favouring PCm.
An innovative, pragmatic, potentially more accessible and cost effective regimen from India!
👏 Congratulations @VanitaNoronha and the entire team from @TataMemorial
#ESMO26 @OncoAlert @oncodaily @myESMO @montypal @neerajaiims
[Slide 2]
Multicentric phase III randomized non-inferiority study in technically unresectable oral cancers
ELIGIBILITY CRITERIA
• Age ≥ 18 years
• Oral cavity cancers
• Tumors deemed technically unresectable in MDT*
• ECOG PS 0-1
• Normal organ and marrow functions
R 1:1
DCF arm (n=236): Docetaxel 75mg/m2 IV day 1; Cisplatin 75 mg/m2 day 1; 5-FU 750 mg/m2 CIVI days 1-5 (all pts were admitted, and had central line inserted); Cycles administered every 3 weeks for 2-3 cycles
PCm arm (n=239): Paclitaxel 80 mg/m2 IV day 1; Carboplatin AUC 1.5 IV day 1; Celecoxib 200mg PO twice daily; Erlotinib 150 mg PO daily; Methotrexate 9 mg/m2 PO wkly; Cycles administered every week for 6-9 cycles
REASSESSMENT: • Clinical assessment • Radiologic • MDT discussion
If resectable → surgery, followed by adjuvant therapy
If unresectable, plan decided in MDT: -Radical CRT, or -Radical RT alone, or -Palliative therapy, or -Best supportive care
*MDT=multidisciplinary tumor board
Examples of technically unresectable tumors:
▪ Buccal mucosa primaries and soft tissue involvement or edema extending to zygomatic arch
▪ Oral tongue primaries with soft tissue involvement up to oropharynx or hyoid
▪ Extensive skin or nodal involvement
▪ Involvement of high infratemporal fossa.
Primary endpoint: OS; Secondary endpoints: EFS, ORR, safety, QoL
[Slide 3]
CONCLUSIONS
• PCm is a novel regimen of weekly pacli-carbo with triple oral metronomic chemotherapy
• In patients with technically unresectable oral cancers, PCm leads to
• Significantly higher response rate than DCF
• Significantly higher conversion to resectability than DCF
• Significantly fewer toxicities than DCF
• Non-inferior overall survival as compared to DCF
• The PCm regimen can be administered as an outpatient without the need for a central line or an infusion pump, reducing logistic issues
• PCm thus represents a novel safe and effective regimen for patients with technically unresectable oral cancer
• Given the low toxicity, there is scope to intensify the PCm regimen, and we are exploring the addition of immunotherapy to PCm
Vanita Noronha, Tata Memorial Hospital (Mumbai)
[Slide 4]
Kaplan–Meier Overall Survival Curves for DCF and PCm Regimens
Regimen: DCF, PCm
Arm | Event/total | Median OS | HR (one sided 95% CI) | one-sided NI P value
DCF | 134/236 | 14.0 (12.0 - 16.7) | 1 (Reference) | 0.0002
PCm | 122/239 | 13.7 (12.4 - 18.3) | 0.84 (0.68 - 1.03) |
12 months: PCm 58.1%; DCF 56.4%
24 months: PCm 38.[illegible]%; DCF 29.4%
Number at risk (months 0, 4, 8, 12, 16, 20, 24, 28, 32, 36, 40) — at risk (cumulative events)
DCF: 236 (0) 208 (0) 153 (17) 97 (44) 64 (59) 42 (68) 21 (83) 13 (90) 5 (97) 1 (101) 0 (102)
PCm: 239 (0) 224 (1) 174 (15) 104 (44) 67 (62) 47 (73) 29 (90) 15 (102) 9 (108) 1 (116) 1 (116)
Survival table
Endpoint: Overall survival (primary, non-inferiority)
Arm | N | Median | Median CI
DCF | 236 | 14.0 mo | 12.0–16.7
PCm | 239 | 13.7 mo | 12.4–18.3
HR: 0.84
HR CI: 0.68–1.03 (one-sided 95% CI)
P: 0.0002 (one-sided non-inferiority)
Landmark rates:
12 months: PCm 58.1% | DCF 56.4%
24 months: DCF 29.4%
A true tour de force by the amazing @DrJNaidoo at #ESMO26 Presidential Symposium! 👏🔥
A masterclass in how to discuss a negative trial: sharp, insightful, and extracting every important message for our oncology community.
And doing it all while waiting for the new member of the family! ❤️ A powerful #WomenForOncology role model! Absolutely WOW! 🌟💪💪
#ESMO2026 #W4O @myESMO
Methods and Purpose of 'De-intensification'
Reduce Dose of Therapy
Shorten Duration of Therapy
Reduce Frequency of Therapy
Reduce number of agents
Avoid other parts of treatment plan
Patient
Efficacy
Toxicity
- Adapted from Pal et al, ESMO 2022-
Back in Japan from #ESMO26
An exciting meeting with many practice-changing results across various cancer types.
I'm delighted to have presented the results of the TRIDENTE trial in a rapid oral session! Grateful to the TRIDENTE study group!
@myESMO @OncoAlert https://t.co/UVsJEMVpNU
Objective response rate
N = 21
Complete response | 0
Partial response | 4 (19.0%)
Stable disease | 12 (57.1%)
Progressive disease | 4 (19.0%)
Not evaluable | 1 (4.8%)
Objective response rate (90% CI) | 19.0% (6.8-38.4%)*
Disease control rate (95% CI) | 76.2% (52.8-91.8%)
* Lower bound of the 90% CI (6.8%) exceeded the pre-specified threshold of 3.0%.
PR SD PD NE
Best percentage change in target lesion from baseline (%)
The ORR includes one confirmed and three unconfirmed partial responses.
ORR did not differ significantly by prior regimen (EC vs EC + BINI: 7.7% vs 37.5%, p = 0.121) or ENCO-free interval (<6 months vs ≥6 months: 37.5% vs 7.7%, p = 0.121).
Daisuke Kotani, MD, PhD
My first ESMO oral! 🇪🇸
Our study: immunotherapy around cancer surgery becomes standard of care before we know if patients live longer, mature survival data should come first.
Grateful to my mentors and my family ❤️ #ESMO26 @oncology_bg @dr_rajapramanik @gupta_aarushi https://t.co/PykpnULhPi
Background
Why does mature OS data matter for perioperative ICI trials?
• Perioperative immune checkpoint inhibitors have become standard of care across a variety of solid tumors based on large phase three studies
• All studies use EFS/DFS as primary end point- validation of these surrogate end points for overall survival (OS) in this setting is unknown
• ICI's can have permanent long-term toxicity which is especially relevant in the curative intent setting
• Mature survival data is essential to gauge improvement in cure rates with ICI's and counsel patients on risks vs benefits
Abhenil Mittal
Exciting emerging data in 1L R/M #HNSCC at #ESMO26!
🔹 OrigAMI-4: Amivantamab (EGFR×MET) + pembrolizumab + carboplatin: ORR 77% in HPV-unrelated disease (n=22), CR 14%.
🔹 Iza-bren (EGFR×HER3 bispecific ADC) + pembrolizumab: ORR 58–63% across two dose cohorts, mDoR 13.6–17.8 months.
Two different approaches to EGFR targeting: dual receptor blockade versus dual targeting + cytotoxic payload delivery.
Key questions:
🔬 How do HPV status, PD-L1 CPS and EGFR/MET/HER3 expression influence benefit?
🔬 What is the incremental contribution of each component?
🔬 Can we identify who needs an ADC payload versus receptor blockade alone?
Promising early signals, but small cohorts, different populations and no head-to-head comparisons.
The next challenge is moving beyond response rates towards biomarker-guided treatment selection.
Great discussion by @BrigetteMa2
#HeadNeckCancer #ADC #bispecific #PrecisionOncology
[Slide 1]
ORR and Best Response
OrigAMI-4 1L R/M HNSCC
Among the 29 participants in the efficacy population, the confirmed ORR was 66% (95% CI, 46–82), meeting the prespecified statistical hypothesis
INV-assessed response(a) | HPV-unrelated (n=22) | HPV-related(b) (n=7)
Confirmed ORR, % (95% CI) | 77 (55–92) | 29 (4–71)
Confirmed response, n (%)
CR | 3 (14) | 0
PR | 14 (64) | 2 (29)
SD | 4 (18) | 2 (29)
PD | 1 (5) | 2 (29)
NE | 0 | 1 (14)
Time to first response, wk (range)(c) | 9.4 (8.3–28.0) | 18.1 (9.1–27.1)
Clinical benefit rate, % (95% CI)(d) | 82 (60–95) | 57 (18–90)
• All participants (100%) with HPV-unrelated disease had tumor shrinkage of their target lesions
• Among confirmed responders with HPV-unrelated disease (n=17), median DoR was NR (95% CI, 4.0–NR), with 65% ongoing
Best Response for HPV-unrelated (n=22) [waterfall and spider plots]
[footnotes small, partially illegible]
[Slide 2]
Depth & Duration of Response
Iza-bren 2.5 mg/kg D1D8Q3W + pembrolizumab: ORR = 57.9%; mDOR = 13.6 mo; median treatment cycles = 8.5
Iza-bren 2.75 mg/kg D1D8Q3W + pembrolizumab: ORR = 62.5%; mDOR = 17.8 mo; median treatment cycles = 6.0
[waterfall and spider plots; legend: Confirmed Complete Response, Complete Response, Confirmed Partial Response, Partial Response, Stable Disease, Progressive Disease]
□ Iza-bren 2.5 mg/kg D1D8Q3W + pembrolizumab: 81.6% of patients (31/38) with tumor shrinkage and the median (range) shrinkage (%) was -61.5 (-100, -4.7).
□ Iza-bren 2.75 mg/kg D1D8Q3W + pembrolizumab: 85.0% of patients (34/40) with tumor shrinkage and the median (range) shrinkage (%) was -48.2 (-88.7, -10.8).
Data cutoff: July 3[illegible], 2026
[Slide 3]
Bispecific ADC vs Bispecific antibody against EGFR
• Bispecific antibody
1. Dual blockade of compensatory pathways (eg EGFR + MET or EGFR + HER3).
2. Immune cell engagement + receptor inhibition
3. Minimal bystander effect
4. Resistance: TME, target heterogeneity
5. Toxicity: Infusion reactions, skin. Predictable PK. Allows independent dose adjustment of chemo/ PD1i/ TKI partners
6. Administration & Costs
• Bispecific ADC
1. Dual blockade of compensatory pathways (eg EGFR + MET or EGFR + HER3).
2. + Payload delivery.
3. More Bystander effect
4. Resistance: Payload (drug efflux pumps or TOPO1 alterations), target heterogeneity
5. Toxicity: Payload-related (e.g marrow, ILD), skin, affinity-attenuation and linker stability
6. Administration & Costs
[Slide 4]
Selected studies in 1L R/M HNSCC (CPS>=1/ unselected)
Phase 3 & Phase I/II trials. Cross trial comparison not intended
Kn048 Ph3, n = 281 (FU 68m) | Burtness 2019/ Tahara 2025 | All comers HPV CPS (subgp) | ORR: 37% (CR 7.1%) | mPFS: 4.9m | OS: 13m | DOR: 6.7m
Extreme, ph3 N = 442 | Vermorken 2008 | - | 36% | 5.6m | 10.1m | 5.6m
Ami+pembro+carbo (Origami4 co.5) n = 22 | Swiecicki 2026 (ESMO) | CPS unselected HPV unrelated | 77% (CR 14%) | 7.7m | NR | NR
Iza-Bren + pembro (2.5mg/kg) n = 38 | Ji 2026 (ESMO) | Two dose levels ? HPV/ CPS | 57.9% (CR 2.6%) | 8.5m | NR | 13.6m
Petosemtamab (ph2) n = 45, FU 14.3m | Van Herpen 2025 | CPS >=1 HPV all comers | 63% | 9m | 79% OS rate 1yr | NR
Ficerafusp-Alfa (FORTIFI-HN01) Ph1b, n = 30, FU 36m | Wong 2026 | CPS>=1 Not in OPSCC HPV+ | 54% (CR 25%) | 9.9m | 21.3m (3yr OS 31%) | 21.7m
Other 1L studies early phase: BNT113-01 in HPV+ve, PDL1+ HNSCC (E6/E7 mRNA vaccine) (Ottensmeier 2024); Ivonescimab (PD1-VEGF)-Ligufalimab (CD47): CPS>=1 Chen 2024. n=20, ORR 60%. mPFS 7.1m
💡What’s cool is the power of #ctDNA on multiple levels in CLOVER☘️Trial
1. It acted as a surrogate to early response
2. We were looking at 2 doses - we saw dose response
3. We were able to collaborate @NateraGenetics to find real world comparator
📈drug development @OncoAlert https://t.co/hAlyvC63Bo
[Slide 1]
CLOVER – ctDNA % Change at Week 2 Based on Signatera Exome*
CYTODYN
Patients with Data Available in September 2026
350 mg Cohort (n=14): -100% | -99% | -99% | -89% | -88% | -87% | -85% | -74% | -73% | -70% | -69% | -64% | -39% | -26% - Median decrease: 80%
700 mg Cohort (n=14): -97% | -97% | -96% | -94% | -93% | -92% | -90% | -90% | -82% | -79% | -78% | -72% | -54% | -34% - Median decrease: 90%
Percent Change in ctDNA from Baseline
*Analysis includes all available Signatera Exome ctDNA measurements within seven days of starting treatment
CYTODYN.COM 11
[Slide 2]
CLOVER – ctDNA responses, Natera's real-world comparator cohorts
CYTODYN
0-4 Weeks, Molecular Residual Disease (MRD) Change from Baseline
p = 0.01 | p = 0.0005
Lonsurf (n = 30) | Lonsurf + Bev (n = 75) - Natera Real-world Cohorts
Lonsurf + Bev + Leronlimab (n = 12) - CLOVER Study
MRD Change from Baseline
CYTODYN.COM 13
Promising data presented by @AndreaNecchi at #ESMO26 #GDFather-NEO.
Nivo + Visugromab
• Higher response (pCR and ORR)
• At median F/U 15.7 mo: no recurrence observed after pCR
• No new safety signal
Paper out in @NatureMedicine. Congrats Andrea and co-authors !
@myESMO @OncoAlert
[Slide 2]
Conclusions
Main conclusions
• Trial context
Exploratory, stratified phase 2 trial; first evaluation of GDF-15 neutralization in a checkpoint-inhibitor-naïve neoadjuvant setting
• Higher response with N+V
Approximately fourfold higher locally assessed pCR and ORR, confirmed by central blinded review
• No recurrence after pCR · bladder preservation
At a median follow-up of 15.7 months, no recurrence was observed after pCR; four N+V patients with pCR retained their bladder after re-TURBT alone
• Exploratory biomarker signal
Response to N+V was associated with a pre-existing proliferative CD8+ T-cell state; PD-L1 CPS and baseline serum or tumor GDF-15 did not distinguish responders from non-responders
• No new safety signal
Grade 3–4 TRAEs and immune-related AE rates were similar between arms; no treatment-related discontinuation, death or surgical delay occurred with N+V
These findings support further randomized evaluation of visugromab with checkpoint inhibition across MIBC and other urothelial cancer settings
We thank all participating patients and their families, and all investigators and site staff.
Prof. Andrea Necchi
Ongoing visugromab clinical development
GDFATHER-NSCLC-01 (NCT[illegible]) Treatment-naive non-squamous NSCLC, randomized phase 2b
GDFATHER-NSCLC-02 (NCT[illegible]) Checkpoint-inhibitor-refractory NSCLC, randomized phase 2b
GDFATHER-HCC-01 (NCT[illegible]) Checkpoint-inhibitor-refractory HCC, randomized phase 2b
VINCIT (NCT[illegible]) Cancer cachexia, placebo-controlled phase 2/3
[Slide 3]
nature medicine
Article
https://doi.org/10.1038/s41591-026-04740-9
Neoadjuvant nivolumab with or without visugromab in muscle-invasive bladder cancer: the phase 2a GDFATHER-NEO trial
Received: 7 September 2026
Accepted: 6 October 2026
Andrea Necchi, Chiara Mercinelli, Brigida A. Maiorano, Michela Piacentini, Antonio Cigliola, Roberto Iacovelli, Chiara Ciccarese, Chiara Ligato, Patrizia Giannatempo, Alessandro Rametta, Paolo Gontero, Francesco Soria, Christine Schuberth-Wagner, Joerg Wischhusen, Bernhard Rössler, Michael Metterlein, Stefan Ries, Thorsten Ross, Aasim Amin, Tobias Dreker, Frank Hermann, Lena Lemke, Kathrin Klar, Olga Mitina, Ana Kamova, Petra Fettes, Alexandra Auckenthaler, Sujata Rao, Eugen Leo & Felix S. Lichtenegger
e-mail: necchi.andrea@hsr.it
DOI: 10.1038/s41591-026-04740-9
URL: https://www.nature.com/articles/s41591-026-04740-9
QR code:
MADRID 2026 ESMO congress
When OS Is Not Enough: The Emerging Need for Context-Sensitive Endpoint Frameworks in Oncology in @ESMO_Open presented at #ESMO2026. Context-sensitive frameworks are needed when OS is immature/confounded/not demonstrable with RTC. https://t.co/RjDvD8m9Sk https://t.co/iDl88j538l
ESMO OPEN - Science for optimal cancer care
REVIEW · Articles in Press, 108644, October 25, 2026 · Open Access
When Overall Survival Is Not Enough: The Emerging Need for Context-Sensitive Endpoint Frameworks in Oncology
Antonella Cardone 1 · Frank Griesinger 2 · Åslaug Helland 3 · Daniel Gladwell 4 · Jose Diaz 5
1 Cancer Patients Europe, Brussels, Belgium
2 Department of Hematology and Oncology, Pius-Hospital Oldenburg, Oldenburg, Germany
3 Institute of Clinical Medicine, University of Oslo, Oslo, Norway
4 Health Economics and Outcomes Research, Lumanity, London, United Kingdom
5 Global HEOR, Bristol Myers Squibb, Uxbridge, United Kingdom
Disease biology and natural history | Prognosis and post-progression survival | Treatment intent | Feasibility of mature OS | Salvage availability
OS DECISIVE - Short post-progression survival (e.g. previously treated metastatic pancreatic cancer)
Treatment Switching (Crossover and imbalances in Post Study Anticancer Therapies: confounded OS)
OS IMMATURE, CONFOUNDED OR NOT DEMONSTRABLE - Disease-control endpoints may need to carry decision weight
Long post-progression survival or curative intent; OS immature at decision time (e.g. nmCRPC; adjuvant oesophageal cancer; newly diagnosed myeloma)
OS, overall survival; nmCRPC, non-metastatic castration-resistant prostate cancer.
Opening Ceremony at @myESMO #ESMO26 with the ESMO Award Ceremony
#NoemiReguart, chair of Nomination Committee presents all awardees
Congrats to all 👏🏻👏🏻👏🏻
#ESMOAmbassadors https://t.co/g2tMu7XVHP
2026 ESMO SOCIETY AWARDS
ESMO Award — Rebecca Fitzgerald
ESMO Award for Translational Research — Dan A. Landau
ESMO Women for Oncology Award — Pilar Garrido
ESMO Lifetime Achievement Award — Antoni Ribas
Very promising randomized results with the CDK4 selective inhibitor atirmociclib presented by @antgiorda. Next gen CDKs are here! #ESMO26 #ESMOAmbassadors https://t.co/XuIiabKA5H https://t.co/YuDTbHahRg
Same slide also posted by @DrBarbiOnc, @E_de_Azambuja
Investigator-Assessed PFS
Atirmociclib arm (n = 126) | ICT arm (n = 137)
Median follow-up, months | 13.7 | 13.6
Events | 72 | 93
Median PFS, months (95% CI) | 9.4 (7.3–13.6) | 6.6 (3.8–7.8)
Stratified HR (95% CI) | 0.60 (0.440–0.825)
one-sided P value | 0.0007
Landmark labels: Atirmociclib 82.5% (3 mo), 62.3% (6 mo), 44.8% (12 mo); ICT 68.9% (3 mo), 51.9% (6 mo), 22.5% (12 mo)
No. at risk
Atirmociclib arm 126 120 100 98 83 83 72 71 64 63 55 49 34 32 13 12 12 3 3 2 0
ICT arm 137 127 90 84 66 65 58 54 45 45 31 25 17 16 7 7 6 1 0 0 0
CI, confidence interval; HR, hazard ratio; ICT, investigator's choice of therapy; PFS, progression-free survival.
Presenter: Antonio Giordano
Survival table
Endpoint: Investigator-assessed PFS
Arm | N | Median | Median CI
Atirmociclib arm | 126 | 9.4 | 7.3–13.6
ICT arm | 137 | 6.6 | 3.8–7.8
HR: 0.60 (stratified)
HR CI: 0.440–0.825
P: 0.0007 (one-sided)
Landmark rates:
3 mo: Atirmociclib 82.5% | ICT 68.9%
6 mo: Atirmociclib 62.3% | ICT 51.9%
12 mo: Atirmociclib 44.8% | ICT 22.5%
#ESMO2026 | Drugging the Undruggable: A New Era in Precision Oncology
“Undruggable” was never about the target. It was about our tools.
An inspiring presentation by Dr. Vivek Subbiah (@VivekSubbiah) at ESMO 2026, highlighting how previously untargetable cancer drivers are becoming therapeutically actionable.
From KRAS inhibition and p53 reactivation to MYC targeting, protein degradation, synthetic lethality, and AI-driven drug discovery, precision oncology is entering a new era.
The next challenge is not only developing new drugs, but identifying the right molecular target in the right patient.
Comprehensive genomic profiling and ctDNA testing will play an increasingly important role in this transformation.
#ESMO26 @myESMO @VivekSubbiah #PrecisionOncology #UndruggableTargets #KRAS #TP53 #GenomicTesting #LiquidBiopsy @Dr_R_Kurzrock
MADRID 2026 ESMO congress
The undruggable journey is the journey of Odyssey
From bold ideas to breakthrough therapies: the evolution of KRAS inhibitors
Matt Damon in The Odyssey
Photograph: Landmark Media/Alamy
Timeline of KRAS Inhibitors
Discovery -> Development
1964 • Retroviral isolates were identified (also in 1967, 1974 and 1978)
1969 • Oncogene
1972 • DNA transfection to convert normal cells to cancer cells
1982 • The first human transforming gene was cloned • The human HRAS oncogene was found to be activated by point mutation • Human oncogenes were found to be related to v-ras oncogenes
1995 • Farnesyltransferase inhibitors were found to block Ras-induced tumours in mice
2013 • KRAS mutation becomes druggable
2019 • KRAS G12C inhibitors in clinical trials (Sotorasib, Adagrasib)
2021 • The first KRAS G12C inhibitor approved by US FDA (Sotorasib)
2022 • KRAS G12C, KRAS G12D and other KRAS inhibitors in trials
Vivek Subbiah, MD | X/Twitter @VivekSubbiah
J Hematol Oncol 17, 108 (2024)
simultaneously published in NEJM https://t.co/cksTgfNMeF https://t.co/IMG0z3UtoC
Thank you everyone who attended our proffered paper policy session yesterday. Thankful to the scientific session for selecting our abstract for oral. Thank you to the chairs and discussants for creating this fantastic session and for putting our results into context. @myESMO #ESMO26
Cancer Medicine Approvals in the US
JAMA
Brian Shkabari, BHSc1; Nicole I. Vorko, BHSc1,2; Wesley M. Geerlinks, BHSc1,3; Elizaveta Purh, BHSc1; Claire M. Diana-Gonsalves, BHSc1; Svasti Sutaria, BSc1; Bishal Gyawali, MD, PhD1,2,4
Table. Cancer Medicines Approved by the US Food and Drug Administration for Adult Solid Cancer Indications, 2006-2025 (N = 385)
Category | No. (%) 2006-2010 (n = 30) | 2011-2015 (n = 64) | 2016-2020 (n = 136) | 2021-2025 (n = 155) | Total (n = 385)
Trial phase
3 | 26 (83.9) | 53 (79.1) | 77 (58.3) | 94 (64.8) | 250 (66.7)
2 | 5 (16.1) | 10 (14.9) | 49 (37.1) | 45 (31.0) | 109 (29.1)
1 | 0 | 4 (6.0) | 6 (4.5) | 6 (4.1) | 16 (4.3)
Trial design
Randomized clinical trial | 27 (87.1) | 55 (82.1) | 80 (60.6) | 91 (62.8) | 253 (67.5)
Single-arm trial | 4 (12.9) | 12 (17.9) | 52 (39.4) | 54 (37.2) | 122 (32.5)
Trial primary efficacy end pointc
Overall survival | 12 (40.0) | 28 (43.8) | 33 (24.3) | 29 (18.7) | 102 (26.5)
Progression-free survival | 11 (36.7) | 28 (43.8) | 53 (39.0) | 51 (32.9) | 143 (37.1)
Objective response rate | 3 (10.0) | 15 (23.4) | 62 (45.6) | 66 (42.6) | 146 (37.9)
Other curative setting end pointsd | 2 (6.7) | 3 (4.7) | 12 (8.8) | 29 (18.7) | 46 (11.9)
Other unique end pointse | 2 (6.7) | 1 (1.6) | 1 (0.7) | 0 | 4 (1.0)
Prof. Bishal Gyawali
BG LAB BISHAL GYAWALI ONCOLOGY
Thank you very much @myESMO for the opportunity to present on how to read and interpret cancer clinical trials today at the MCBS session. I was encouraged with the excellent turn out and hope that these lessons can be applied to the trials coming out of #ESMO26. https://t.co/Blk44RdIAu
Editorial
Improved adverse event reporting: it's about time
Laure-Anne Teuwen, MD, PhD(1,2), Nathan Cherny, MD(3), Bishal Gyawali, MD, PhD*(4,5,6)
Box: Recommendations for improved adverse event reporting in clinical trials
1. Avoid the use of subjective downplaying terms to describe toxicities.
2. Capture toxicity grades, ideally using the Patient-Reported Outcomes version of the Common Terminology Criteria for Adverse Events.
3. Report maximum severity as well as onset, duration, and adverse event load.
4. Report dose reductions and treatment interruptions.
5. Report incidence of serious and fatal adverse events.
6. Report quality-of-life impact based on validated tools.
More efficacy and safety here: https://t.co/ILWsLDx8u0
14:45 - 16:15 Proffered paper: Developmental therapeutics
CHAIRS: VALENTINA BONI, FUNDA MERIC-BERNSTAM
Manageable safety profile
No DLTs were observed during dose escalation, and there were no drug-related Grade 5 events as assessed by the investigator; the incidence of TRAEs leading to discontinuation related to both study drugs was 3.5%
Elfe-D / Pumitamig | 3 mg/kg / 20 mg/kg DL1 (N=2) | 6 mg/kg / 10 mg/kg DL1-1 (N=14) | 6 mg/kg / 20 mg/kg DL2 (N=72) | 6 mg/kg / 30 mg/kg DL3 (N=54) | Total (N=142)
Median (range) treatment duration, months | 1.7 (1.3, 2.1) | 4.8 (1.4, 9.7) | 5.5 (0.7, 11.5) | 6.3 (1.3, 10.3) | 5.5 (0.7, 11.5)
TEAEs, n (%) Any | 2 (100.0) | 14 (100.0) | 69 (95.8) | 54 (100.0) | 139 (97.9)
TEAEs, n (%) Grade ≥3 | 1 (50.0) | 5 (35.7) | 37 (51.4) | 34 (63.0) | 77 (54.2)
TRAE, n (%) Any | 2 (100.0) | 13 (92.9) | 68 (94.4) | 52 (96.3) | 135 (95.1)
TRAE, n (%) Grade ≥3 | 0 | 4 (28.6) | 25 (34.7) | 26 (48.1) | 55 (38.7)
TRAEs leading to discontinuation, n (%) Both study drugs | 1 (50.0) | 2 (14.3) | 2 (2.8) | 0 | 5 (3.5)
TRAEs leading to discontinuation, n (%) Elfe-D | 1 (50.0) | 2 (14.3) | 3 (4.2) | 2 (3.7) | 8 (5.6)
TRAEs leading to discontinuation, n (%) Pumitamig | 1 (50.0) | 2 (14.3) | 3 (4.2) | 1 (1.9) | 7 (4.9)
TRAEs leading to dose reduction, n (%) Elfe-D* | 0 | 0 | 7 (9.7) | 10 (18.5) | 17 (12.0)
One grade 5 event of dyspnea (HNSCC) was considered unrelated to treatment by the investigator.
*Dose reduction was not allowed for pumitamig per protocol.
Data cutoff date: September 4, 2026
Ye Guo
Elfetabart drozuntecan (Elfe-D; DB-1311/BNT324 [B7H3 ADC]) + pumitamig (PD-L1 x VEGF-A bsAb) in patients with advanced solid tumors: First results from a global phase 2 trial
BURGOS AUDITORIUM - HALL 3
We at @getne should be very proud of what the up-and-coming young generation is achieving. A magnificent presentation of the #CABOTHYROID study findings by @JHernando3 at #ESMO26
@myESMO @OncoAlert https://t.co/O4KoXuAFN9
[partially cropped] ...2216 / CABOTHYROID Trial
STUDY DESIGN
Baseline: Advanced RAIR DTC after PD to standard MKIs, N = 41
Treatment Phase (cycles Q4W): Cabozantinib 60 mg QD (24 weeks)
EOT: Safety visit 30 d after last dose
New treatment - Follow-up: until PD Q12W
Long-term follow-up: until withdrawal, death, or end of study
Survival status, Safety
CT or MRI scan and tumor markers Q12W
Blood sample cfDNA (baseline, during treatment, EOT, new treatment)
QoL → QoL Q12W and PD
Blood sample cfDNA → Methylation → Sequencing (EM-seq) → Methylation-pattern analysis (Machine Learning (ML) analysis) → Subgroup efficacy analysis
[Stage photo: three panel chairs seated, presenter at podium]
Full house for the opening of #ESMO26 with @myESMO president @FAndreMD…looking forward to important days of science, networking and above all progress in #cancer care ! 💪
@OncoAlert @UniGenova https://t.co/uHFJDtL5yA
[Wide photo of packed main hall; multiple screens show the presidential address slide alongside the speaker]
Supporting better policy and healthcare systems
Revision of In Vitro Diagnostic Medical Devices Regulation (IVDR)
EU Biotech Act
Discussions on healthcare workforce challenges
Advocating for equitable access to financial services for cancer survivors (Right to be forgotten)
Very interesting work, present for @oncology_bg #ESMO26
"Drugs approved based on phase 2 evidence: Do FDA and EMA always agree?"
It's conclusions should make us a reflection https://t.co/0BONY78zUM
[Slide 1]
Discussion
BG LAB
• 17% of accelerated approval indications based on P2 have been withdrawn.
• 8 (7%) haven't had any regulatory decision until 5 years!
• More than half of these FDA approved indications did not have matching EMA authorization, highlighting more stringent standards at EMA
• Enthusiasm for approvals, specially RA, based on ORR from P2 should be curtailed.
• P2 based approvals should be AA with the requirement for timely completion of confirmatory trials.
Prof. Bishal Gyawali
[Slide 2]
Discussion
BG LAB
• Proportion of approvals based on P2 trials is increasing in recent years.
• The mORR remains quite modest: 36% , with less than a quarter having an ORR of > 50%.
• RCT was feasible for most of these indications based on sample size as well as future conduct of RCT, arguing against rarity.
• mORR was lower with increasing sample size.
• No difference in ORR between AA versus upfront RA.
Prof. Bishal Gyawali
Preliminary clinical results of QTX3034, an oral G12D-preferring KRAS inhibitor with cetuximab ± mFOLFOX6 in KRASG12D-mCRC
#ESMO26 #ESMOAmbassadors
👉ORR: 25% vs 50%, DCR: 75 vs 90%
👉 no new safety signals
🧐Supports the combination with CTx
@myESMO @ASCO https://t.co/4KrcgfdNU2
Same slide also posted by @EvelynWongYT
[Slide 1]
Introduction
• KRASG12D-mutated mCRC remains an important unmet need
• QTX3034 is an investigational KRASG12D-preferring oral multi-KRAS inhibitor
• EGFR inhibitors +/- chemotherapy may improve response and delay onset of resistance to KRAS inhibition
• The initial Phase 1 monotherapy and combination data with cetuximab was previously presented, showing a combinable safety profile and no evidence of rash at QTX3034 monotherapy RP2D
• We present the pooled results of patients with mCRC who received QTX3034 at the RP2Ds of 1200mg BID + cetuximab and 800/1200 mg BID + cetuximab + FOLFOX
[Diagram] Cetuximab | EGFR | GRB2 | SOS1/2 | Upstream EGFRi boosts efficiency of RAS(OFF) trapping | OFF: Inactive RAS (GDP) | KRAS | ON: Active RAS (GTP) | QTX3034 | MAPK signaling | Blocking RAS(ON)-MAPK signaling releases compensatory feedback via EGFR
Dose-escalation: QTX3034 + cetuximab: 150 mg BID -> 1200 mg BID; QTX3034 + cetuximab + FOLFOX: 800 mg BID -> 1200 mg BID
Dose-expansion: QTX3034 + cetuximab 1200 mg BID
3
[Slide 2]
Efficacy – QTX3034 + cetuximab
QTX3034 + cetux demonstrated anti-tumor activity
QTX3034 1200 mg BID + cetuximab (N=20), N of responses (%)1
Legend: PD | SD | uPR | PR | CR | ▶ Ongoing
ORR | 5 (25)
PR | 5 (25)
CR | 0
DCR | 15 (75)
Rows under waterfall: Prior oxaliplatin | Prior irinotecan | Prior bevacizumab | Prior LOT
QTX3034 + cetuximab [spider plot: Difference in SLD from baseline vs Study day; 1200 mg]
• QTX3034 + cetuximab exhibited encouraging ORR, with 2.7-5.5 months duration
• Majority of responders had received prior FU, oxaliplatin, and irinotecan
1One patient non-evaluable due to withdrawal of consent, not related to study drug or disease
6
Clinical Cut-Off: Aug 28th, 2026
[Slide 3]
Efficacy – QTX3034 + Cetuximab + FOLFOX
Early signal of clinical activity in chemo-refractory and naïve patients
QTX3034 (800 / 1200 mg) + cetuximab + FOLFOX (N=10), N (%)1
Legend: PD | SD | uPR | PR | CR | ▶ Ongoing
ORR | 5 (50)
PR | 4 (40)
CR | 1 (10)
DCR | 9 (90)
QTX3034 dose | 1200 | 1200 | 800 | 1200 | 800 | 800 | 1200 | 1200 | 800 | 1200
Prior oxaliplatin | Prior irinotecan | Prior bevacizumab (shaded grid)
Prior LOT | 1 | 1 | 1 | 0 | 1 | 1 | 0 | 1 | 1 | 0
QTX3034 + cetuximab + FOLFOX [spider plot: % Change in TL size vs Study day; 800 mg, 1200 mg]
• Encouraging ORR, in a predominantly chemo-refractory population and responses of 1.4 - 3.9 m
◆ Ongoing uPR was confirmed after clinical cut-off date
• *Complete Response confirmed in chemotherapy-naïve patient who subsequently elected for definitive surgery
1One patient non-evaluable due to poor compliance and subsequent study withdrawal not related to drug toxicity
7
Clinical Cut-Off: Aug 28th, 2026
[Slide 4]
Best change in ctDNA
Clinical responses supported by deep reductions in ctDNA
QTX3034 + cetuximab | N with ctDNA clearance > 90% | 9 (56%)
QTX3034 + cetuximab + FOLFOX | N with ctDNA clearance > 90% | 7 (70%)
Y-axis: KRASG12D VAF best change from baseline
Legend: 800 mg BID | 1200 mg BID
Study day | 43 | 15 | 43 | 15 | 15 | 15 | 15 | 15 | 15 | 43 | 43 | 15 | 15 | 15 | 15 | 15 | 43 | 43 | 15 | 43 | 43 | 43 | 43 | 43 | 43 | 43
BOR | SD | PD | SD | PD | PD | SD | SD | PD | PR | SD | PR | SD | SD | PR | SD | PR | SD | PD | CR | PR | SD | PR | PR | SD | SD | PR
8
Clinical Cut-Off: Aug 28th, 2026
Cancer Immunotherapy- what's next ? Nice slide to explain progress so far by Dr Vinod Balachandran @myESMO #esmo26 https://t.co/TbS6xFT4je
15:15 - 16:00 What oncologists should know about mRNA vaccines
CHAIRS: YELENA JANJIGIAN, JAMES LARKIN
Cancer Immunotherapy – What's Next?
1893 — Infection as a way to fight cancer (William Coley)
1957 — The immune system can see and destroy abnormal cells (Thomas & Burnet)
1959 — BCG (TB vaccine) triggers immune response against tumors in mice (Old & Clarke)
1975 — Tumor necrosis factor (TNF) discovered (Old, Carswell, et al.)
1976 — IL-2 discovered (Gallo)
1986-1990 — First Cancer Immunotherapies BCG IFN-a2
1992 — Discovery of PD-1 (Honjo)
1996 — CTLA-4 blockade rejects murine tumors (Allison)
2011 — First immune checkpoint inhibitor FDA approved (Wolchok)
2014 — First PD-1/PD-L1 inhibitors FDA approved
2017 — First CAR T cells FDA approved (Sadelain, June)
What's next?
Why NOT Cancer Vaccines??
[OCCV logo — The Olayan Center for Cancer Vaccines, Memorial Sloan Kettering Cancer Center]
[Speaker panel] Vinod Balachandran — RNA vaccines for cancer: Principles to practice
ALICANTE AUDITORIUM - HALL 6
#ESMO2026
Compelling data from investigators of KN412 on ctDNA to prognosticate
Baseline and rapid clearance of ctDNA were highly prognostic in HPV- HNSCC
More evidence supporting #PrecisionOncology in #HeadNeckCancer 💪🏻💪🏻💪🏻 https://t.co/LUZcBm3rnD
[Slide 1]
Machiels KN412 ESMO [illegible]
Baseline ctDNA Levels Are Prognostic in Both Pembro + CRT (OS) and Placebo + CRT (EFS and OS) Arms in the HPV-Negative Subgroup
EFS
Pembro + CRT: MSAF <median (n = 106); MSAF ≥median (n = 95) | 58.9% | 51.2% | P = 0.086
Placebo + CRT: MSAF <median (n = 96); MSAF ≥median (n = 108) | 48.1% | 38.1% | P = 0.002*
OS
Pembro + CRT: MSAF <median (n = 106); MSAF ≥median (n = 95) | 70.5% | 55.8% | P = 0.009*
Placebo + CRT: MSAF <median (n = 96); MSAF ≥median (n = 108) | 58.3% | 49.5% | P = 0.01*
Months
No. at risk
EFS Pembro + CRT: 106 79 68 62 55 48 17 0 / 95 64 54 48 44 39 14 0
EFS Placebo + CRT: 96 70 59 53 50 37 15 0 / 108 56 47 43 39 33 18 0
OS Pembro + CRT: 106 95 90 84 75 73 40 7 / 95 78 65 58 56 53 35 2
OS Placebo + CRT: 96 89 79 71 65 55 30 5 / 108 86 71 66 56 52 32 1
Cox proportional hazards model with adjustment for baseline ECOG PS was used. *Indicates statistical significance (prespecified nominal α = 0.05). Hypothesis: negative association. Clinical data cutoff: August 21, 2024.
Survival table
Endpoint: EFS and OS by baseline ctDNA (MSAF <median vs ≥median), HPV-negative subgroup
Pembro + CRT, MSAF <median | 106
Pembro + CRT, MSAF ≥median | 95
Placebo + CRT, MSAF <median | 96
Placebo + CRT, MSAF ≥median | 108
P: EFS pembro 0.086; EFS placebo 0.002; OS pembro 0.009; OS placebo 0.01
Landmark rates:
dotted-line landmark (timepoint not printed; line at ~60 mo): EFS Pembro MSAF <median 58.9%
same: EFS Pembro MSAF ≥median 51.2% | EFS Placebo MSAF <median 48.1% | EFS Placebo MSAF ≥median 38.1% | OS Pembro MSAF <median 70.5% | OS Pembro MSAF ≥median 55.8% | OS Placebo MSAF <median 58.3% | OS Placebo MSAF ≥median 49.5%
[Slide 2]
Machiels KN412 ESMO [illegible]
HPV-Negative Subgroup: ctDNA Clearance at C3D1 in the Pembro Arm is Higher Than in the Placebo Arm and is Associated With a Greater Improvement in OS Compared With the Placebo Arm
EFS
Pembro + CRT: ctDNA clearance rate 76.8% (119/155); ctDNA not cleared (n = 36); ctDNA cleared (n = 119) | 63.1% | 38.2% | P = 0.001*
Placebo + CRT: ctDNA clearance rate 66.3% (110/166); ctDNA not cleared (n = 56); ctDNA cleared (n = 110) | 48.4% | 35.5% | P = 0.011*
OS
Pembro + CRT: ctDNA clearance rate 76.8% (119/155); ctDNA not cleared (n = 36); ctDNA cleared (n = 119) | 72.9% | 38.9% | P <0.001*
Placebo + CRT: ctDNA clearance rate 66.3% (110/166); ctDNA not cleared (n = 56); ctDNA cleared (n = 110) | 58.6% | 48.2% | P = 0.075
Months
No. at risk
EFS Pembro + CRT: 36 21 16 14 14 10 2 0 / 119 93 80 73 66 61 22 0
EFS Placebo + CRT: 56 30 24 21 20 15 5 0 / 110 72 64 61 55 43 22 0
OS Pembro + CRT: 36 29 24 19 16 14 9 0 / 119 110 98 92 88 85 53 6
OS Placebo + CRT: 56 46 39 36 30 27 15 2 / 110 101 87 78 70 62 34 2
[illegible]...predictive value was independent of ECOG PS and other prognostic markers, including
Survival table
Endpoint: EFS and OS by ctDNA clearance at C3D1, HPV-negative subgroup
Pembro + CRT, ctDNA cleared | 119
Pembro + CRT, ctDNA not cleared | 36
Placebo + CRT, ctDNA cleared | 110
Placebo + CRT, ctDNA not cleared | 56
P: EFS pembro 0.001; EFS placebo 0.011; OS pembro <0.001; OS placebo 0.075
Landmark rates:
dotted-line landmark (timepoint not printed; ~60 mo): EFS Pembro cleared 63.1%
same: EFS Pembro not cleared 38.2% | EFS Placebo cleared 48.4% | EFS Placebo not cleared 35.5% | OS Pembro cleared 72.9% | OS Pembro not cleared 38.9% | OS Placebo cleared 58.6% | OS Placebo not cleared 48.2%
Proud to be part of the Women for Oncology (W4O) session at #ESMO26 peters_solange @Piuchagarrido @ElinardouHelena highlighting barriers and opportunities for women in oncology. Inspiring call to challenge inequalities, break down barriers and empower women to thrive and lead!!! https://t.co/hwsbSEWqFJ
EDUCATION LEADERSHIP NETWORKING
A solid education to acquire competence and expertise
❖ Oncology training
❖ Fellowship opportunities
❖ Participation to international events
Time and ways to develop as a leader
❖ Leadership skills
❖ Communication skills
❖ Self-awareness
Opportunities for advancement
❖ Mentors & sponsors
❖ Real-life experiences
❖ National and international networks
WOMEN FOR ONCOLOGY An ESMO Initiative
#ESMO26 🧬 Rapid Oral | DSRCT
💊 Trastuzumab deruxtecan (T-DXd)
👥 French retrospective series
🎯 ORR: 82% (9/11)
📈 Updated mPFS: 22 mo (n=12)
⏳ 12-mo OS: 69%
🔬 Responses despite HER2 IHC 0/1+
⚠️ 1 treatment-related ILD death
💡 Remarkable activity! Prospective validation needed.
@OncoAlert
[Slide 1]
08:30 - 10:00 Rapid oral: Sarcoma
CHAIRS: MARK DICKSON, PALMA DILEO, CESAR SERRANO
METHODS
NetSarc-ResOs Réseaux de référence Clinique Sarcomes - GIST - Desmoïdes
• Multicentre retrospective study
• NETSARC+ (https://expertisesarcome.org/)
• Pediatric and adult patients
• Pathological and molecular confirmation of the diagnosis
• Metastatic, relapsed or refractory DSRCT with documented progression after ≥ 1 previous line of therapy
• ≥ 1 dose of T-DXd and ≥ 1 tumor assessment following treatment initiation
• T-DXd intravenously at a dose of 5.4 mg/kg every three weeks
Mehdi Brahmi, MD PhD
Mehdi Brahmi
Trastuzumab deruxtecan in patients with desmoplastic small round cell tumors (DSRCT): A retrospective analysis from the French Sarcoma Group
MALAGA AUDITORIUM - HALL 3
[Slide 2]
08:30 - 10:00 Rapid oral: Sarcoma
CHAIRS: MARK DICKSON, PALMA DILEO, CESAR SERRANO
RESULTS
Survival
Progression free survival
Median PFS 22 months (3.0-NE)
Event/Total | Median (95% CI)KM | Survival Estimates (95% CI)KM
6/12 | 22.0 (3.0-NE) | 12m : 0.51 (0.2-0.76)
Overall survival
12 months OS 69% (30-89)
Event/Total | Median (95% CI)KM | Survival Estimates (95% CI)KM
3/12 | NE (4.0-NE) | 12m : 0.69 (0.3-0.89)
KM Kaplan-Meier method;
Survival
Time (Months)
Mehdi Brahmi
Trastuzumab deruxtecan in patients with desmoplastic small round cell tumors (DSRCT): A retrospective analysis from the French Sarcoma Group
MALAGA AUDITORIUM - HALL 3
Survival table
Endpoint: PFS and OS (single-arm retrospective)
Arm | N | Median | Median CI
T-DXd - PFS | 12 | 22.0 months | 3.0-NE
T-DXd - OS | 12 | NE | 4.0-NE
12-month PFS: 0.51 (0.2-0.76)
12-month OS: 0.69 (0.3-0.89); slide text '12 months OS 69% (30-89)'
[Slide 3]
08:30 - 10:00 Rapid oral: Sarcoma
CHAIRS: MARK DICKSON, PALMA DILEO, CESAR SERRANO
CONCLUSION
• Multicentre retrospective cohort of patients with relapsed or refractory DSRCT treated with T-DXd
• Substantial antitumor activity, with marked objective responses and disease control achieved in all patients
• Responses despite the absence of HER2 overexpression by IHC
• Need to better understand the biological determinants of sensitivity
• T-DXd is a promising therapeutic strategy for patients with DSRCT and support prospective evaluation of HER2-directed ADCs
Baseline
After 25 cycles of T-DXd
23 yo female patient with R/R DSRCT HER2 IHC 1+
Mehdi Brahmi, MD PhD
Mehdi Brahmi
Trastuzumab deruxtecan in patients with desmoplastic small round cell tumors (DSRCT): A retrospective analysis from the French Sarcoma Group
MALAGA AUDITORIUM - HALL 3
💙 Oncologist wellbeing matters too.
📍 Our RESILIENCE-@_SEOM poster at #ESMO26, presented by @DrVilmaPBarcia: a structured program to prevent burnout in early-career oncologists across 7 Spanish centres 🇪🇸
🙌 Proud to co-lead this one
@myESMO https://t.co/chM3K7mPX3
Same slide also posted by @DrVilmaPBarcia
[Slide 1]
3914P Implementing a structured intervention to prevent and mitigate burnout among early-career medical oncologists: Baseline data and initial feasibility from the RESILIENCE-SEOM study
V. Pacheco-Barcia1, Y. Garitaonaindía2, S. Martínez Morante3, L. León Mateos4, L. Punti Brun5, B. García Paredes6, B. Obispo7, P. Llanes Barragan5, M.M. Sánchez del Corral8, A.S. Cortegoso Mosquera4, E. Ceballos Barbancho9, S. de la Cruz10, E. García Asencio11, A.I. Martín Quesada12, R. Sánchez Bayona13, A. Lecumberri10, D. Sánchez14, C.A. Rodríguez Sánchez15, J. de Castro16, E. Elez17.
[Background and Methods panels partially obscured by presenter]
RESULTS
Figure 1. Baseline characteristics (Percentage %)
Female | 86%
≤35 years | 46%
University hospital | 96%
Previous burnout | 50%
Poor work-life balance | 79%
Previous treatment with antidepressants/anxiolytics | 14%
A total of 42 participants were included (86% female; 46% aged ≤35 years). Baseline characteristics are shown in Figure 1.
The mean CIPS score was 63.8 (SD 18.5), indicating frequent experiences of impostor phenomenon.
Baseline MBI-HSS scores revealed a burnout profile characterized by high emotional exhaustion, moderate depersonalization, and low personal accomplishment (Figure 2).
Figure 2. Baseline MBI-HSS scores [partially obscured]: Emotional exhaustion 28.2 | ... 12.[?] | ... 30.9
[Feasibility and Conclusions panels partially obscured by presenter]
[Slide 2]
3914P Implementing a structured intervention to prevent and mitigate burnout among early-career medical oncologists: Baseline data and initial feasibility from the RESILIENCE-SEOM study
V. Pacheco-Barcia1, Y. Garitaonaindía2, S. Martínez Morante3, L. León Mateos4, L. Punti Brun5, B. García Paredes6, B. Obispo7, P. Llanes Barragan5, M.M. Sánchez del Corral8, A.S. Cortegoso Mosquera4, E. Ceballos Barbancho9, S. de la Cruz10, E. García Asencio11, A.I. Martín Quesada12, R. Sánchez Bayona13, A. Lecumberri10, D. Sánchez14, C.A. Rodríguez Sánchez15, J. de Castro16, E. Elez17.
BACKGROUND
The prevalence of burnout among medical oncology trainees in Europe is estimated to exceed 70%, posing a significant threat to both healthcare professionals' well-being and the quality of patient care.
Early-career oncologists are particularly vulnerable due to high workloads and limited psychological support.
We evaluated a structured intervention combining individual and group-based strategies aimed at addressing burnout and improving emotional regulation.
METHODS
This prospective, multicenter cohort study included medical oncology residents and oncologists with ≤7 years of experience from seven Spanish hospitals. Baseline assessment included demographic data, the Maslach Burnout Inventory–Human Services Survey (MBI-HSS), and the Clance Impostor Phenomenon Scale (CIPS). The intervention consists of eight sessions delivered in a hybrid format, combining individual coaching and progressive group workshops. Follow-up assessments are planned at program completion and at 6 and 12 months.
RESULTS
Figure 1. Baseline characteristics (Percentage %)
Female | 86%
≤35 years | 46%
University hospital | 96%
Previous burnout | 50%
Poor work-life balance | 79%
Previous treatment with antidepressants/anxiolytics | 14%
A total of 42 participants were included (86% female; 46% aged ≤35 years). Baseline characteristics are shown in Figure 1.
The mean CIPS score was 63.8 (SD 18.5), indicating frequent experiences of impostor phenomenon.
Baseline MBI-HSS scores revealed a burnout profile characterized by high emotional exhaustion, moderate depersonalization, and low personal accomplishment (Figure 2).
Initial feasibility was assessed based on attendance at the first in-person session across four centers: 71.4% (10/14), 66.7% (4/6), 100% (7/7), and 66.7% (10/15), respectively, resulting in an overall initial attendance rate of 73.8% (31/42 scheduled participants).
Figure 2. Baseline MBI-HSS scores
MBI-HSS baseline (Mean score)
Emotional exhaustion | 28.2
Depersonalization | 12,0
Personal accomplishment | 30,9
CONCLUSIONS
Baseline findings confirm high levels of psychological vulnerability and burnout among early-career oncologists in Spain.
Although initial attendance rates suggest promising feasibility, high clinical workloads remain a major barrier to participation. These findings highlight the urgent need for structured institutional interventions.
Acknowledgments: Gratitude to the SEOM's Resilience-SEOM group and +MIR section.
Author COIs: speaker honoraria from Pierre Fabre, Nutricia, Servier, Pfizer, AstraZeneca, Leo Pharma; consultancy or advisory board from Advanced Accelerator Applications, a Novartis company, Pfizer, Nutricia, Servier; travel support from Amgen, Servier, Pfizer, Nutricia, Merck.
Funding: SEOM grant 2025.
Author contact: [email omitted]
A valuable session on mentorship and career development at #ESMO26 @myESMO
Thanks to @FerMosele @AndresC27622123 @LoiSher for sharing their insights
@OncoAlert https://t.co/uFd8yHjPzR
[Slide 1]
Domain 3: Effective Mentoring Practices
Bases and foundations
- Provide both content-focused and character focused mentoring -
- Mix of "carpenter and gardener"approaches (ie, provide both structured mentoring and an environment for thriving)
- Parallels to parenting: Give and take, mutually beneficial, reciprocal relationship
- Tailor strategies to the mentor: more joy in thei rsuccess than your own
• Parallels to primary care
- One primary mentor, others for specific needs
- Have a primary mentor for life
- End mentorship relationship if not a good fit
Ameling J, et al. JAMA Network Open 2026
Andres Cervantes
[Slide 2]
MY PERSONAL JOURNEY
POSITIVE
Learn translational and also clinical research
Expand networking
To work in the first cancer research center of Europe
Learn from your mentors
Multidisciplinary work
NEGATIVE
Family and personal life disruption
Learn a new language
Cultural barrier
You always will be a foreign person
Foreign degree validation
M. Fernanda MOSELE, MD
🇪🇸 #ESMO26 🧬 SETHY | Phase II – Spanish GETNE study
💊 Sacituzumab govitecan (TROP2 ADC)
🔬 DTC (n=24):
🎯 ORR 4.4% | mPFS 5.5 mo
🔬 ATC (n=13):
🎯 ORR 16.7% | mPFS 2.9 mo
💡 Preliminary activity in ATC. TROP2 biomarker analysis awaited!
👏 Great work by @GrupoGetne
@OncoAlert
Same slide also posted by @GrupoGetne
[Slide 1]
10:15 - 11:45 Proffered paper: NETs and endocrine tumours
CHAIRS: JAYDIRA DEL RIVERO, ENRIQUE GRANDE
Primary Results from the SETHY Trial
GETNE Grupo Español de Tumores Neuroendocrinos y Endocrinos
STUDY DESIGN & OBJECTIVES
Baseline | EOT | PD
Advanced radioactive iodine refractory DTC after PD to 1-3 prior systemic
Advanced ATC on 1st line or after 1 prior systemic treatment
Treatment Phase (cycles Q3W): Sacituzumab govitecan 10 mg/Kg days 1 & 8* Until progression, death, study withdrawal, or unacceptable toxicity.
Safety visit 30 days after last dose of study treatment
Follow-up: until PD CT or MRI scans Q12W
Long-term follow-up: until withdrawal, death, or end of study
Survival status, Safety
PFS follow-up: CT or MRI scan and tumor markers Q12W
QoL (EORTC QLQ-C30) Q12W and PD
n = 21 per cohort
Tumor biopsy
Simon Two-Stage Statistical Design
Stage I: Futility assessment (12 pts)
EXPAND IF ≥1 RESPONSE
Stage II: Cohort expansion (total 21 pts)
Primary Endpoint: Objective Response Rate (ORR) per RECIST 1.1
Secondary Endpoints: Disease Control Rate (DCR); Duration of Response (DoR); Progression-Free Survival (PFS); Overall Survival (OS); Safety/Tolerability; Quality of Life
Exploratory Endpoints: TROP-2 expression levels linked to clinical efficacy.
Presented by Dr. Alejandro García-Álvarez
Alejandro Garcia-Alvarez
Primary results from the SETHY trial: Sacituzumab govitecan (SG) in advanced/metastatic differentiated thyroid carcinoma (DTC) and anaplastic thyroid carcinoma (ATC)
MURCIA AUDITORIUM - HALL 3
[Slide 2]
10:15 - 11:45 Proffered paper: NETs and endocrine tumours
CHAIRS: JAYDIRA DEL RIVERO, ENRIQUE GRANDE
Primary Results from the SETHY Trial
RESULTS: ORR (PRIMARY ENDPOINT)
Max Change from baseline (%)
DTCs | ATCs
20% | -30%
| DTCs (n=24) | ATCs (n=13)
Confirmed ORR (95% CI) | 4.2 (0.1-21.1) | 15.4 (1.9-45.5)
Best response; n (%) CR | 0 (0.0) | 0 (0.0)
PR | 1 (4.2) | 2 (15.4)
SD | 18 (75.0) | 4 (30.8)
PD | 4 (16.6) | 6 (46.1)
NE | 1 (4.2) | 1 (7.7)
Histology; TROP2; BRAF; RAS; TERT; RET; Previous Treatments
Genes: Mutated, Native
TROP2 H Score: 201-300, 101-200, 0-100
Histology: Papillary, Poorly diff., Follicular, Hürthle cell
Prev. Treatments: 2-3, 1, 0
Presented by Dr. Alejandro García-Álvarez
MURCIA AUDITORIUM - HALL 3
[Slide 3]
10:15 - 11:45 Proffered paper: NETs and endocrine tumours
CHAIRS: JAYDIRA DEL RIVERO, ENRIQUE GRANDE
Primary Results from the SETHY Trial
RESULTS: PFS
Survival Probability (%)
Time (months)
Median PFS (95% CI) DTCs: 5.5 m (5.0-NR)
Median PFS (95% CI) ATCs: 2.9 m (2.3-NR)
Number at risk (censored)
DTCs: 6m PFS 40.2% (22.8-71.1); 12m PFS 33.5% (17.1-65.6)
ATCs: 6m PFS 20.5% (6.5-64.3); 12m PFS 10.3% (1.7-61.8)
The median follow-up was 7.9 m (95% CI: 4.7-11.8) for DTCs and 4.1 m (95% CI: 2.8-8.7) for ATCs.
Presented by Dr. Alejandro García-Álvarez
MURCIA AUDITORIUM - HALL 3
Survival table
Endpoint: PFS by cohort (single-arm cohorts)
Arm | N | Median | Median CI
DTCs | 24 | 5.5 | 5.0-NR
ATCs | 13 | 2.9 | 2.3-NR
DTC 6m PFS 40.2% (22.8-71.1); 12m 33.5% (17.1-65.6)
ATC 6m PFS 20.5% (6.5-64.3); 12m 10.3% (1.7-61.8)
[Slide 4]
10:15 - 11:45 Proffered paper: NETs and endocrine tumours
CHAIRS: JAYDIRA DEL RIVERO, ENRIQUE GRANDE
Primary Results from the SETHY Trial
RESULTS: SAFETY
Most common grade 3-4 toxicities were diarrhea (16%), asthenia (11%) and neutropenia (8%).
Dose reductions and delays were required in 19% and 49%, respectively.
Toxicities (N=37)
Anaemia 19 | 1
Asthenia 14 | 4
Diarrhoea 12 | 6
Alopecia 17
Neutropenia 11 | 3
Fatigue 5
Vomiting 5
Rash 4
Decreased Appetite 2 | 1
Constipation 3
Headache 2
Hypomagnesaemia 2
Grade 1-2 | Grade 3-4
Patients (%)
Presented by Dr. Alejandro García-Álvarez
MURCIA AUDITORIUM - HALL 3
Impressive session from Cascal Herrle (Zurich, Switzerland) in #ESMO26. "Treatment costs for essential cancer medicines in 82 countries"
Pacients in low-income countries WAIT LONGER and PAY MORE for cáncer medicines.
The world upside down😱. Need to act. https://t.co/J6kMGJg8MT
Beyond Price: The Full Dimension of Access Inequity
Price 3–5×
higher relative cost in low-income countries as a proportion of per capita income
No compensatory pricing mechanisms
Longer access time
from first global regulatory approval – real availability in LMICs
Disproportionately affects WHO EML medicines
Patients in low-income countries wait longer AND pay more
Wouters & Kuha, Health Affairs 2024
Bruna David, MD [rest of footer illegible] Policy Session · 24 October 2026
#ESMO26 #HNSCC
Nice presentation from Dr Even about the systemic approach of HPV+ HNSCC
My take: Is time to end with antiEGFR agents in HPV+ HNSCC? or shall we keep it as a last resource in latter lines
None of the major guidelines (ASCO, ESMO and NCCN) do make any clear recommendation against/disadvice
@OncoAlert @myESMO @brunolarvol
@DavidSherMD
CONCLUSIONS
✓ HPV-related HNSCC are biologically, clinically, and prognostically distinct from HPV-unrelated cancers and should be considered as separate disease entities in future research, requiring dedicated clinical development.
✓ The underlying molecular biology, TME, and host immune response in HPV-associated HNSCC still need to be investigated to identify novel therapeutic targets
✓ Whether recurrent disease relies upon the same viral oncogenic machinery, immune environment and molecular alterations as in localized disease requires further study, which may help guide the appropriate setting in which to apply the therapies
Great to present the results of the @GrupoGetne SPAINTRK study at #ESMO2026!
Our real-world data in spanish population support the efficacy and durability of larotrectinib across NTRK fusion-positive solid tumors.
Proud of this collaborative effort! https://t.co/dxJDljN9op
Real-world outcomes of Larotrectinib in Solid Tumors with Tropomyosin Receptor Kinase Fusion (GETNE S2411 / SPAINTRK)
Jorge Hernando 1,2, Carlos Lopez 3, Alejandro Garcia-Alvarez 1,2, Santiago Aguín Losada 4, Olga Martínez-Sáez 5, Carlos Gonzalez-Perez 6, Ricardo López-Almaraz 7, Raúl Sánchez Morillas 8, Joseba Rebollo Liceaga 9, Laura Ferreira Freire 10, Miriam Pavon-Mengual 11, María Ruiz Vico 12, Miriam López-Gómez 13, Idoia Morilla 14, Delvys Rodriguez-Abreu 15, Jaume Capdevila 1,2
1070P
[Affiliations: Vall d'Hebron (Barcelona), Valdecilla (Santander), Santiago de Compostela, Hospital Clínic (Barcelona), La Paz (Madrid), Cruces/Biobizkaia (Barakaldo), Son Espases (Palma), Quirón Salud Torrevieja, Lucus Augusti (Lugo), Sant Joan de Déu (Barcelona), 12 de Octubre (Madrid), Infanta Sofía (San Sebastián de los Reyes), Navarra (Pamplona), Insular de Gran Canaria — small print]
[GETNE logo] Grupo Español de Tumores Neuroendocrinos y Endocrinos
INTRODUCTION
NTRK gene fusions have been described as oncogenic drivers in diverse adult and paediatric cancers, promoting cell survival and proliferation 1,2. Larotrectinib is a first-in-class selective tropomyosin receptor kinase (TRK) inhibitor with proven activity in a broad range of solid tumors 3. This study aimed to describe the effectiveness of larotrectinib in patients with solid tumors harbouring NTRK fusions in Spain 4.
METHODS
SPAINTRK (NCT06837090) was a retrospective observational study including adult and pediatric patients with solid neoplasms bearing NTRK fusions, treated with larotrectinib through compassionate use program, between European Medicines Agency (EMA) approval and commercialization in Spain (Oct 19-Sept 23) (Figure 1). Larotrectinib as part of clinical trials was excluded. TRK fusions were determined as part of standard care using next-generation sequencing (NGS), fluorescence in situ hybridization and/or immunohistochemistry, along with confirmatory molecular test.
The primary endpoint was duration of response (DoR). The secondary endpoints were objective response rate (ORR) and safety. No formal sample size was calculated.
Figure 1. Study Schedule & Milestones [timeline 4Q 2024 – 1Q 2026]
OBJECTIVES
Primary
- Description of the effectiveness of larotrectinib treatment in tumors with NTRK fusion in Spanish patients as a clinical series.
Secondary
- Describe duration of treatment, dose reductions, interruptions, and reasons for such modifications.
- Description of the efficacy of larotrectinib according to previous lines of therapy.
- Line of treatment at which molecular testing for NTRK was performed.
- Safety assessment of larotrectinib.
Exploratory
- The potential prognostic value of clinical and/or histological variable regarding the effectiveness and tolerability of larotrectinib.
REFERENCES
1. Cocco et al. Nt Rev Clin Oncol 2018 2. Bazhenova et al. Target Oncol 2021 3. Drilon et al. N Engl J Med 2018 4. Hernando et al. EJC 2026
Clinicaltrials.gov: NCT06837090 [QR code]
RESULTS
Table 1. Patient characteristics (n=20)
Age at treatment start, Median (range); years: 37 (0.83-81)
Sex; n (%): Male 10 (50); Female 10 (50)
Race; n (%): Caucasian 14 (70); Latin 3 (15); Asian 1 (5); North African 1 (5); Unknown 1 (5)
ECOG-PS n (%): 0 7 (35); 1 9 (45); 2 3 (15); Unknown 1 (5)
Tumor type; n (%): Infantile fibrosarcoma 3 (15); Infant desmoplastic ganglioglioma 1 (5); Glioblastoma 5 (25); Lung* 5 (25); Breast tumor 2 (10); Thyroid tumor 2 (10); Neuroendocrine Carcinoma 1 (5); Head and neck tumor 1 (5)
Disease status at enrollment; n (%): Locally advanced 9 (45); Metastatic 11 (55)
NTRK fusion gene; n (%): NTRK1 8 (40); NTRK2 5 (25); NTRK3 7 (35)
Previous systemic treatment lines**; n (%): 0 6 (30); 1 7 (35); 2 4 (20); ≥3 3 (15)
*Four patients had NSCLC and one patient had lung-NET. **Includes adjuvant
Table 2. Overall Response Rate (ORR)
Full dataset ORR; % (95% CI): 60 (36.1-80.9)
Best response; n (%): Complete response 4 (20); Partial response 8 (40); Stable disease 4 (20); Progressive disease 3 (15); Not evaluable 1 (5)
Figure 2. Duration of response among 12 patients with a Response calculated from the time of first response [KM curve: labels 83.3%, 66.7%, 50%; Number at risk 12, 10, 8, 6, 5, 4, 3, 3, 3, 2, 2, 1 at 0–66 months]
Table 3. Treatment-related adverse events (AEs). No patient presented grade 4-5 AE
Event; n (%) — Grade 3 / Any grade
Transaminitis 2 (10) / 3 (15); Neutropenia 2 (10) / 3 (15); Anaemia 0 (0) / 2 (10); Fractures 1 (5) / 2 (10); Dysgeusia 0 (0) / 1 (5); Skin toxicity 0 (0) / 1 (5); Acute hepatic failure 0 (0) / 1 (5); Dizziness 0 (0) / 1 (5); LDH increased 0 (0) / 1 (5); ALP increased 0 (0) / 1 (5)
Between Feb-Jun25, 20 pts from ten months to 81 years were included, 15 adults and 5 paediatrics, with eight different solid tumor types. NTRK fusions were reported in NTRK1 gene (40%), NTRK2 (25%) and NTRK3 (35%), 65% of pts were diagnosed using NGS Table 1. Larotrectinib was administered for a median of 13 months (95% CI: 8-21) and 70% had received previous treatments.
After a median follow-up of 24.4 months (95% CI: 13.2-35), the median DoR was 24.5 months (95% CI: 11.1- not reached) (Figure 2) and ORR was 60% (95% CI: 36.1-80.9) (Table 2). ORR was higher among pediatric pts (80%; 95% CI: 28.4-99.5). The highest ORR were seen among pts with infant fibrosarcoma (100%; 95% CI: 29.2-100) and lung tumors (80%; 95% CI: 28.44-99.5). After 1 year of treatment, 60% of pts remained progression-free and 75% maintained response (Figure 3). At data cutoff, 41.7% of the pts with a response were disease-free and/or remained on treatment. Toxicities were uncommon, with neutropenia and transaminitis being the most frequent, reported in 15%, each (Table 3).
Figure 3. Effectiveness of larotrectinib. Left panel shows treatments before larotrectinib. The right panel (squared) shows larotrectinib treatment and outcomes [swimmer plot by NTRK fusion and tumor type: Infant Fibrosarcoma, Head & Neck, Lung, Breast, Infant Desmoplastic ganglioglioma, Thyroid, Glioblastoma, Neuroendocrine]
CONCLUSIONS
❖ Larotrectinib evoked broad and durable antitumor activity in a plethora of solid tumors with NTRK fusions.
❖ Durable responses were observed irrespective of age, tumor type, and NTRK fusion gene.
❖ Safety profile was consistent with that of clinical trials, even after long-term administration.
❖ NGS is implemented in most hospitals and its use should keep expanding.
*Corresponding author: Dr. Jorge Hernando. E-mail: [email], Medical Oncology Department, Vall Hebron University Hospital and Vall Hebron Institute of Oncology (VHIO), Barcelona, Spain. ESMO 2026 Annual Symposium // Conflicts of interest: The presenting author has no conflict of interest regarding this communication // Funding: Grupo Español de Tumores Neuroendocrinos y Endocrinos (GETNE). // Partners: Bayer // Acknowledgement: GETNE acknowledge MFAR Clinical Research staff for their assistance in the development of this poster.
Fantastic to see CNS oncology take centre stage with a keynote lecture at @myESMO meeting in Madrid! Anna Berghoff introducing Wolfgang Wick on glioblastoma, brain metastases and LMD disease: the next frontier in oncology care.
#ESMO2026 #NeuroOncology
@EANOassociation https://t.co/3suPeHbeG8
[ESMO Congress Madrid 2026 stage screen; live video of speaker at left]
Leptomeningeal Metastasis (LM)
• Incidence of LM in advanced malignancies to approximate 9%–25% for small cell and non-small cell lung cancer, 5%–20% for breast cancer, and 6%–18% for melanoma.
• Prognosis of LM is poor but heterogeneous, with certain subgroups of patients (eg, EGFR-mutant NSCLC, HER2-positive breast cancer) demonstrating superior survival.
• Historical survival benchmark of 2–4 months does not apply to all patients
PMID: 38902944
[Figure panels A–C: brain/spinal CSF circulation schematic; B: adherent LM cells, floating LM cells, brain parenchyma; C: choroid plexus, barrier disruption through secreted factors, LM cancer cells]
MADRID SPAIN 23-27 OCTOBER 2026
@YJanjigianMD and #JamesLarkin on the main topics and data that will be presented at @myESMO #ESMO26 Annual Conference
🦠Cancer Vaccine - very hot topic!
💉ADCs in many settings
👀Follow the “What oncologist should know about” special sessions 🆕
#ESMOAmbassadors https://t.co/0IGPRev30q
[Slide 1]
ESMO 2026 IN NUMBERS
[microscope icon]
4,414 Abstracts:
• 12 in Presidential Symposia
• 147 Proffered Papers
• 242 Rapid Oral
• 2,025 Posters
• 1,988 ePosters
[presentation icon]
296 Sessions, of which:
• 230 Programme Sessions
• 66 Industry Satellite Symposia
[people icon]
~ 40,000
Professionals attending
[Slide 2]
FROM DISCOVERY
TO CLINICAL IMPACT
What matters is not simply what is new.
It is what changes outcomes for patients.
1. DISCOVER
The biology that matters
→ 2. VALIDATE
In rigorous clinical trials
→ 3. DELIVER
Meaningful, accessible care
[Slide 3]
THEMES ACROSS THE ESMO 2026 PROGRAMME
[globe icon] GLOBALISATION OF CANCER RESEARCH
[chart icon] TREATMENT OPTIMISATION
[shield icon] INTERCEPTION AND PREVENTION
[link icon] NEXT-GENERATION ADCs
[AI chip icon] ARTIFICIAL INTELLIGENCE
[hands/heart icon] NON-PHARMACOLOGICAL INTERVENTIONS
#ESMO26 🧬 Phase II | Malignant vascular tumors
👥 52 pts | Advanced/unresectable disease
💊 Nab-paclitaxel + pegylated liposomal doxorubicin (PLD)
🎯 ORR: 50% | DCR: 93.8% (n=48 evaluable)
📈 mPFS: 8.0 mo | mOS: 28.4 mo
🔬 Angiosarcoma (n=31 evaluable):
🎯 ORR: 61.3%
⏳ mPFS: 7.5 mo | mOS: 21.4 mo
📍 Cutaneous vs non-cutaneous ORR: 75% vs 41.7% (p=0.046)
⚠️ G≥3 leukopenia: 26.9% | Neutropenia: 17.3%
🚀 Promising activity, particularly in angiosarcoma. Further validation needed!
@OncoAlert
[Slide 1]
08:30 - 10:00 Rapid oral: Sarcoma
CHAIRS: MARK DICKSON, PALMA DILEO, CESAR SERRANO
Study Design
• An open, single-arm, multi-center, phase II study
• To evaluate the efficacy and safety of nab-paclitaxel plus PLD in patients with advanced or unresectable malignant vascular tumors
Key inclusion criteria
• Age ≥18 years, and ≤70 years
• Confirmed advanced or unresectable malignant vascular tumors with no standard therapy or failed from standard therapy
• At least one measurable lesion per RECIST 1.1
• Adequate renal, hepatic and hematologic function
Key exclusion criteria
• Prior taxane therapy within 6 months
• Prior cumulative doxorubicin dose ≥350 mg/m²
• Active CNS metastases, uncontrolled cardiac disease, or active severe infection
Nab-paclitaxel + PLD
Nab-paclitaxel
220 mg/m² IV infusion, Day 1
+
Pegylated liposomal doxorubicin
35 mg/m² IV infusion, Day 1
Q3W
Until disease progression, unacceptable toxicity, or maximum 8 cycles
Primary endpoint
• RECIST1.1 ORR
Secondary endpoint
• PFS
• OS
• DCR
• Safety
Xing Zhang
Xing Zhang
Nab-paclitaxel plus pegylated liposomal doxorubicin in advanced or unresectable malignant vascular tumors: Results from a phase II study
MALAGA AUDITORIUM - HALL 3
[Slide 2]
08:30 - 10:00 Rapid oral: Sarcoma
CHAIRS: MARK DICKSON, PALMA DILEO, CESAR SERRANO
Efficacy: Investigator assessed ORR and DCR
Response-evaluable patients (N = 48)
PR SD PD
Change in target lesion size from baseline (%)
Best overall response | No. of patients
CR | 0
PR | 24 (50.0%)
SD | 21 (43.8%)
PD | 3 (6.3%)
ORR | 50.0%
DCR | 93.8%
Subgroup Analysis: ORR by Histological Subtype, Primary Site, and Previous Treatment
Subgroup | ORR | P
Histological subtype | | 0.090
Angiosarcoma (N=31) | 61.3%
EHE (n=14) | 28.6%
Others (n=3) | 33.3%
Primary site | | 0.046
Cutaneous disease (n = 12) | 75.0%
Non-cutaneous disease (n = 36) | 41.7%
Previous systemic therapy | | 0.365
Yes (n = 17) | 41.2%
No (n=31) | 54.8%
ORR was higher in cutaneous angiosarcoma, with significant differences by primary site
EHE: Epithelioid hemangioendothelioma
Xing Zhang
[Slide 3]
08:30 - 10:00 Rapid oral: Sarcoma
CHAIRS: MARK DICKSON, PALMA DILEO, CESAR SERRANO
Efficacy: PFS and OS in the Overall Cohort and Histological Subgroups
The whole cohort
Angiosarcoma subgroup
EHE subgroup
Progression-free survival (%)
Overall survival (%)
Months
Median: 8.0 months
Median: 7.5 months
Median: 9.5 months
Median: 28.4 months
Median: 21.4 months
Median: not reached
Durable disease control in angiosarcoma and EHE, with favorable survival outcomes
EHE: Epithelioid hemangioendothelioma
Xing Zhang
Survival table
Endpoint: PFS and OS (single-arm, by cohort)
Whole cohort - PFS | 8.0 months
Angiosarcoma subgroup - PFS | 7.5 months
EHE subgroup - PFS | 9.5 months
Whole cohort - OS | 28.4 months
Angiosarcoma subgroup - OS | 21.4 months
EHE subgroup - OS | not reached
Making sense of surrogate endpoints in Oncology, now at the YO Brunch session, by Florian Lordick
#ESMO26 #ESMOAmbassadors @myESMO https://t.co/l7t47lxtkt
Surrogate endpoints for overall survival in oncology
Meta-analysis across tumor types (Sherrill et al., OncoTargets and Therapy 2012)
Surrogate endpoint (number of meta-analyses) | Correlation with overall survival (pooled correlation coefficient, r [95% CI]) | Strength of association
Localized disease (early stages, mainly adjuvant setting)
Disease-free survival (DFS) (n = 5) | 0.71 (0.62-0.80) | Strong
Metastatic disease (stage IV, advanced)
Progression-free survival (PFS) (n = 24) | 0.60 (0.51-0.69) | Moderate
Time to progression (TTP) (n = 11) | 0.59 (0.46-0.72) | Moderate
Objective response rate (ORR) (n = 13) | 0.42 (0.31-0.52) | Weak
Duration of response (DOR) (n = 6) | 0.33 (0.17-0.50) | Weak
Clinical benefit rate (CBR) (n = 3) | 0.46 (0.24-0.68) | Weak
Tumor shrinkage (n = 4) | 0.24 (0.06-0.42) | Very weak
Correlation coefficient (r)
Weaker association / Stronger association
Key findings
1 Disease-free survival in localized (adjuvant) settings shows the strongest correlation with overall survival (r = 0.71).
2 In metastatic disease, progression-free survival and time to progression show moderate correlations (r ≈ 0.60).
3 Other response-based endpoints (ORR, DOR, CBR, tumor shrinkage) show weak correlations with overall survival (r ≤ 0.46).
Strength of association (based on r)
Strong r ≥ 0.70
Moderate r = 0.50 - 0.69
Weak r = 0.30 - 0.49
Very weak r < 0.30
Surrogate endpoints show stronger correlations with overall survival in early-stage (adjuvant) settings, while correlations are only moderate or weak in metastatic disease.
Sherrill B et al. OncoTargets and Therapy. 2012;5;287-303.
MADRID SPAIN 23-27 OCTOBER 2026
Felt like a footballer in the tunnel before kick-off with @OncobitesTv ⚽
🎯 Our #ESMO26 poster 1988P: ADC + PD-1 blockade across solid tumors
14 trials | n=1,017 with initial benefit
Acquired resistance at 18 mo: 39-63%
➡️ CR rate did not predict it, unlike with anti-PD-1
Depth ≠ durability with ADC-IO?
#ADC #Immunotherapy
@_SEOM @OncoAlert @Larvol
@AinhoaMada sharing tips for young investigators on how to conduct academic research, at the YO Forum #ESMO26
Ask. Test. Learn. Repeat.
#ESMOAmbassadors @myESMO https://t.co/89lce3hQNH
Take home messages
Start with a question that matters.
Ask. Test. Learn. Repeat.
Find good mentors, build collaborations & listen to patients.
Match the funding to the next step—not just the final ambition.
Your next clinical trial may already be hiding in your clinic.
Ainhoa Madariaga, MD PhD
🚨 #ESMO26 | Elfe-D + pumitamig across solid tumors
First clinical data beyond lung cancer for the B7-H3 ADC elfetabart drozuntecan + PD-L1×VEGF-A bsAb pumitamig!
📊 N=139 efficacy-evaluable: uORR 48.9% | cORR 39.6% | DCR 87.8%
👀 Melanoma (n=26): uORR 30.8% | cORR 26.9% | DCR 80.8%
Safety appeared manageable, with mainly G1–2 GI/hematologic TRAEs, no DLTs or treatment-related deaths, and 2 investigator-reported ILD cases 👍🏼
One question: is the activity driven by the IO, the antiangiogenic effect, or a synergy between the two?? 🤔
@OncoAlert @OncoReporte @myESMO @_SEOM @GrupoMelanoma
[Slide 1]
Baseline demographics and characteristics
At data cutoff, 142 patients had received elfe-D + pumitamig and 62% were still on treatment; ~60% had received >=2 prior lines of therapy
Elfe-D / Pumitamig | 3 mg/kg / 20 mg/kg DL1 (N=2) | 6 mg/kg / 10 mg/kg DL1-1 (N=14) | 6 mg/kg / 20 mg/kg DL2 (N=72) | 6 mg/kg / 30 mg/kg DL3 (N=54) | Total (N=142)
Age, years, Median (range) | 62.5 (60-65) | 53.5 (34-78) | 60.0 (26-83) | 59.5 (19-83) | 60.0 (19-83)
Sex, n (%) Male | 2 (100.0) | 11 (78.6) | 37 (51.4) | 18 (33.3) | 68 (47.9)
Female | 0 | 3 (21.4) | 35 (48.6) | 36 (66.7) | 74 (52.1)
Race, n (%) Asian | 0 | 8 (57.1) | 41 (56.9) | 35 (64.8) | 84 (59.2)
White | 2 (100.0) | 4 (28.6) | 27 (37.5) | 16 (29.6) | 49 (34.5)
Other | 0 | 2 (14.3) | 4 (5.6) | 3 (5.6) | 9 (6.3)
ECOG PS, n (%) 0 | 2 (100.0) | 5 (35.7) | 30 (41.7) | 17 (31.5) | 54 (38.0)
1 | 0 | 9 (64.3) | 42 (58.3) | 37 (68.5) | 88 (62.0)
Tumor type, n (%) HNSCC | 0 | 14 (100.0) | 24 (33.3) | 3 (5.6) | 41 (28.9)
Melanoma | 1 (50.0) | 0 | 11 (15.3) | 14 (25.9) | 26 (18.3)
HCC | 1 (50.0) | 0 | 11 (15.3) | 10 (18.5) | 22 (15.5)
CC | 0 | 0 | 11 (15.3) | 11 (20.4) | 22 (15.5)
PROC | 0 | 0 | 15 (20.8) | 16 (29.6) | 31 (21.8)
Prior lines of anticancer therapy, Median (range) | 2 (2-2) | 2 (1-4) | 2 (1-4) | 2 (1-5) | 2 (1-5)
>=2 lines, % | 50.0 | 57.1 | 58.3 | 63.0 | 59.9
DL, dose level; ECOG PS, Eastern Cooperative Oncology Group performance status; elfe-D, elfetabart drozuntecan; HCC, hepatocellular carcinoma; HNSCC, head and neck squamous cell carcinoma; CC, cervical cancer; PROC, platinum-resistant ovarian cancer
Data cutoff date: September 4, 2026
[Slide 2]
Most common TRAEs
The safety profile was consistent with the known profiles of the individual agents
TRAEs occurring in >=15% of the overall population (N=142)
Values shown as all-grade (grade >=3) percentages
Nausea 43.0 (1.4)
Fatigue 36.6 (2.1)
Neutrophil count decreased 34.5 (12.0)
WBC count decreased 32.4 (7.7)
Decreased appetite 28.2 (0.7)
Anemia 25.4 (2.8)
Vomiting 21.8 (0.7)
Proteinuria 21.1 (0.7)
Alopecia 18.3 (0)
Weight decreased 17.6 (0.7)
Hypertension 16.2 (7.0)
AST increased 16.2 (0.7)
Platelet count decreased 15.5 (2.1)
Stomatitis 15.5 (0.7)
Legend: Grade 1/2; Grade >=3. Patients (%)
- TRAEs were primarily grade 1/2 gastrointestinal and hematologic events
- Most common grade >=3 TRAEs were neutrophil count decreased, WBC count decreased, and hypertension
- VEGF-related toxicities consisted mainly of proteinuria and hypertension
- There were 2 investigator-reported cases of ILD (1 grade 1 non-ILD per adjudication; 1 grade 1 pending adjudication [0.7%])
Data cutoff date: September 4, 2026
[Slide 3]
Efficacy summary
Encouraging early responses were observed across all tumor types
Efficacy parameter | HNSCC (N=39) | Melanoma (N=26) | HCC (N=21) | CC (N=22) | PROC (N=31) | Total* (N=139)
Prior treatment, median (range), lines | 2 (1-4) | 2 (1-5) | 2 (1-2) | 2 (1-4) | 2 (1-4) | 2 (1-5)
Follow-up duration, median (range), months | 4.8 (0.5-10.0) | 7.4 (3.6-12.5) | 7.7 (1.4-9.3) | 6.1 (4.0-11.4) | 6.5 (2.6-8.6) | 6.3 (0.5-12.5)
Unconfirmed BOR, n (%)
CR | 0 | 0 | 0 | 1 (4.5) | 2 (6.5) | 3 (2.2)
PR | 15 (38.5) | 8 (30.8) | 9 (42.9) | 10 (45.5) | 23 (74.2) | 65 (46.8)
SD | 19 (48.7) | 13 (50.0) | 10 (47.6) | 9 (40.9) | 3 (9.7) | 54 (38.8)
PD | 4 (10.3) | 5 (19.2) | 1 (4.8) | 2 (9.1) | 3 (9.7) | 15 (10.8)
NE/missing | 1 (2.6) | 0 | 1 (4.8) | 0 | 0 | 2 (1.4)
uORR, % (95% CI) | 38.5 (23.4-55.4) | 30.8 (14.3-51.8) | 42.9 (21.8-66.0) | 50.0 (28.2-71.8) | 80.6 (62.5-92.5) | 48.9 (40.4-57.5)
cORR, % (95% CI) | 23.1 (11.1-39.3) | 26.9 (11.6-47.8) | 38.1 (18.1-61.6) | 40.9 (20.7-63.6) | 71.0 (52.0-85.8) | 39.6 (31.4-48.2)
Pending confirmation, n (%)† | 3 (7.7)‡ | 1 (3.8) | 0 | 1 (4.5) | 2 (6.5) | 7 (5.0)
DCR, % (95% CI) | 87.2 (72.6-95.7) | 80.8 (60.6-93.4) | 90.5 (69.6-98.8) | 90.9 (70.8-98.9) | 90.3 (74.2-98.0) | 87.8 (81.1-92.7)
*Efficacy-evaluable participants: received >=1 dose of study drug, baseline efficacy assessment, and >=1 post-baseline assessment or early treatment discontinuation.
†Pending confirmation includes patients with an observed CR/PR whose confirmed BOR was not yet available as of September 4, 2026, excluding those who received new anticancer therapy, died/reached EOS, or had confirmed PD before response confirmation.
‡As of Oct 09, of the 7 responses pending confirmation at the data cutoff, 3 have since been confirmed, while the remaining 4 are awaiting the next tumor assessments.
Data cutoff date: September 4, 2026
[Slide 4]
Efficacy by prior IO and/or bevacizumab
Efficacy in patients previously treated with IO and/or bevacizumab was broadly comparable to the overall population
Efficacy parameter | HNSCC Prior IO* (N=28) | HNSCC All (N=39) | Melanoma Prior IO* (N=26) | Melanoma All (N=26) | HCC Prior IO/Beva (N=19) | HCC All (N=21) | CC Prior IO/Beva (N=20) | CC All (N=22) | PROC Prior IO/Beva (N=27) | PROC All (N=31) | Total Prior IO/Beva (N=120) | Total All (N=139)
uORR, % (95% CI) | 42.9 (24.5-62.8) | 38.5 (23.4-55.4) | 30.8 (14.3-51.8) | 30.8 (14.3-51.8) | 42.1 (20.3-66.5) | 42.9 (21.8-66.0) | 50.0 (27.2-72.8) | 50.0 (28.2-71.8) | 81.5 (61.9-93.7) | 80.6 (62.5-92.5) | 50.0 (40.7-59.3) | 48.9 (40.4-57.5)
cORR, % (95% CI) | 25.0 (10.7-44.9) | 23.1 (11.1-39.3) | 26.9 (11.6-47.8) | 26.9 (11.6-47.8) | 36.8 (16.3-61.6) | 38.1 (18.1-61.6) | 40.0 (19.1-63.9) | 40.9 (20.7-63.6) | 70.4 (49.8-86.2) | 71.0 (52.0-85.8) | 40.0 (31.2-49.3) | 39.6 (31.4-48.2)
Pending confirmation, n (%) | 2 (7.1) | 3 (7.7) | 1 (3.8) | 1 (3.8) | 0 | 0 | 1 (5.0) | 1 (4.5) | 2 (7.4) | 2 (6.5) | 6 (5.0) | 7 (5.0)
DCR, % (95% CI) | 85.7 (67.3-96.0) | 87.2 (72.6-95.7) | 80.8 (60.6-93.4) | 80.8 (60.6-93.4) | 89.5 (66.9-98.7) | 90.5 (69.6-98.8) | 90.0 (68.3-98.8) | 90.9 (70.8-98.9) | 88.9 (70.8-97.6) | 90.3 (74.2-98.0) | 86.7 (79.3-92.2) | 87.8 (81.1-92.7)
*For melanoma and HNSCC, bevacizumab is not a standard treatment option; therefore, the subgroup includes patients with prior IO exposure only. For PROC, 27 patients had prior bevacizumab, of whom 3 also received prior IO.
Data cutoff date: September 4, 2026
Esmo conference is always rich in data and discussion. 👍 @myESMO #esmo26 https://t.co/8nqJAtLmxx
Nice to see the MASTERPLAN study presented #ESMO26 and published in @TheLancetOncol !
Congrats to the authors!
Our new paper :
"A new era in anti-RAS therapy: Unique challenges and opportunities for radiotherapy clinical trials"
with @free_radical28 is out in EJC, open access :
https://t.co/qBMfJOhCAF
Food for thoughts for ongoing and future trials in that space!👇
European Journal of Cancer 249 (2026) 117790
Contents lists available at ScienceDirect
European Journal of Cancer
journal homepage: www.ejcancer.com
[Elsevier logo] [EJC cover thumbnail] [Check for updates badge]
Current Perspective
A new era in anti-RAS therapy: Unique challenges and opportunities for radiotherapy clinical trials
Susannah G. Ellsworth a, Timothée Olivier b,c,*
a Department of Radiation Oncology, University of Pittsburgh Hillman Cancer Center, Pittsburgh, PA, USA
b Department of Medicine, University of Geneva (UNIGE), Geneva, Switzerland
c Department of Oncology, Geneva University Hospital, Geneva, Switzerland
@YukinoriOzaki presents the JCOG1204A1 of ctDNA analysis!
Congrats!
Looking forward to the primary result!
#ESMO26 https://t.co/ckn40jHZlK
Conclusions
• Within a randomized trial across intensive surveillance and standard of care arms, patients who remained ctDNA-negative throughout surveillance had 99.5% 5-year RFS, compared to 53.6% among ctDNA-positive patients
• Among initially ctDNA-negative patients, detection of ctDNA during surveillance preceded recurrence by a median lead time of 7.5 months overall and by 9.5 months in the intensive surveillance arm.
• These findings support integrating ctDNA surveillance into structured follow-up strategies, particularly for ER+/HER2- BC.
Yukinori Ozaki, M.D., Ph.D.
🚨 iNATURE at #ESMO26 (LBA52): Median PFS 10.3 vs 3.1 mo, HR 0.29 in refractory metastatic disease. Striking! But before anyone says "personalized neoantigen vaccine works," let’s be careful on what this design can and can't tell us 🧵 https://t.co/IwjPgikuM1
LBA52 - Personalized neoantigen vaccine combined with precision critical lesion radiotherapy (CLERT) in advanced solid tumors: Updated results from the iNATURE phase II trial
Speakers FengMing P. Kong (Hong Kong, Hong Kong SAR, China)
Lecture Time 08:35 - 08:40
Abstract
Antonella #Cardone CEO of @CancerPatientsE presenting at #ESMO26 on new definitions of clinical #benefit as informed by patients themselves. An impressive work toward person-centric care!
@myESMO
@ESMO_Open
#ESMOAmbassadors https://t.co/K6AkqMUrPu
Manuscript publication
ARTICLE IN PRESS
ESMO OPEN PUBLICATION
When Overall Survival Is Not Enough: The Emerging Need for Context-Sensitive Endpoint Frameworks in Oncology
Antonella Cardone¹ · Frank Griesinger² · Åslaug Helland³ · Daniel Gladwell⁴ · Jose Diaz⁵
¹ Cancer Patients Europe ² Pius-Hospital Oldenburg ³ University of Oslo ⁴ Lumanity ⁵ Global HEOR, Bristol Myers Squibb
DOI: 10.1016/j.esmoop.2026.108644
Read the manuscript: www.esmoopen.com/article/S2059-7029(26)02590-1/fulltext
SCAN TO READ THE ARTICLE
🎉 Proud to present our study at #ESMO2026 in Madrid! 🇪🇸 (3904P)
🦴 In our prospective two-center study of 190 patients, adding loratadine to naproxen showed numerically lower G-CSF-induced bone pain (27.9% vs 32.7%), without statistical significance.
🧠 Greater pain was associated with poorer quality of life, sleep, mood, and anxiety.
💡 Bone pain is more than pain. Supportive care matters!
🏆 Proud to contribute four posters to ESMO as a team!
🙏 Grateful to the International Cancer Foundation for the travel grant and to all our collaborators!
@myESMO @OncoAlert
@uyargalip @kbaskurtt
@osutcuoglu @RyanNipp
#InternationalCancerFoundation #OneGlobalOncologyCommunity
#ESMO26 #ESMO
Helpful summary table on ADC-related eye toxicity #ESMO26
More stable linkers associated with greater toxicity.
Befriend an opthalmologist and have them be part of your toxicity dream team! 👁️ https://t.co/us0Z8b2XvP
14:45 - 16:15 Emerging toxicities induced by antibody-drug conjugates
CHAIRS: CHRISTINA RUHLMANN, FLORIAN SCOTTÉ
ADC Ocular Adverse Events (OAEs)
Off-target toxicity occurring with a wide variety of ADCs
1. Off-target
2. Various linkers
3. Various payloads
ADC | Indication | Antibody | Linker | Payload | DAR | OAE
Belantamab mafodotin (Blenrep)* | Multiple myeloma | BCMA | Non-cleavable | MMAF | 4 | 71%
Mirvetuximab soravtansine (Elahere) | Ovarian cancer | FRα | Cleavable | DM4 | 3.5 | 61%
Tisotumab vedotin (Tivdak) | Cervical cancer | Tissue factor | Enzyme-cleavable | MMAE | 4 | 60%
Datopotamab deruxtecan (Datroway) | Breast cancer | TROP2 | Cleavable | TOP1i | 4 | 51%
Enfortumab vedotin (Padcev) | Bladder cancer | Nectin-4 | Enzyme-cleavable | MMAE | 3.8 | 40%
Trastuzumab deruxtecan (Enhertu) | Breast cancer | HER2 | Enzyme-cleavable | TOP1i | 8 | 11%
Trastuzumab emtansine (Kadcyla) | Breast cancer | HER2 | Non-cleavable | DM1 | 3.5 | 6%
Lindgren ES…Pasricha ND. Incidence and Mitigation of Corneal Pseudomicrocysts Induced by Antibody–Drug Conjugates (ADCs). Curr Ophthalmol Rep. 2024
Neel Pasricha
Eye toxicities
MURCIA AUDITORIUM - HALL 3
🌅Sunday 7:23 am
👀Our poster is already there for you to come and have a look - 130P
👉Message: #MedicalDevices as a reliable tool vs #PatientReported #QualityOfLife specially for some specific aspects, such as #fatigue
@myESMO #ESMO26 @TheSTARTCenter @Hospital_FJD https://t.co/nWR7oIwkd2
130P
Physical activity measured by wearable devices and its correlation with patient reported outcomes (PRO) in EORTC Q30 Quality of Life (QoL) questionnaires: prospective observational study in patients entering phase I clinical trials
Angela Lamarca1; Eva Ruiz2; Tatiana Hernandez-Guerrero3,4; Bernard Doger De-Speville4; Daniel Morillo4; Ignacio Mahillo-Fernaandez5; Jesus Garia-Foncillas1; Victor Moreno4
1 Department of Medical Oncology, Fundacion Jimenez Diaz University Hospital; Health Research Institute-Fundación Jimenez Diaz University Hospital (IIS-FJD); Universidad Autónoma de Madrid (UAM), Madrid, Spain; 2 Department of Medical Oncology, Fundacion Jimenez Diaz University Hospital; Health Research Institute-Fundación Jimenez Diaz University Hospital (IIS-FJD), Madrid, Spain; 3 Early Phase Clinical Trials Unit, START Barcelona Nou Delfos, Spain; 4 Early Phase Clinical Trials Unit, START Madrid-FJD, Hospital Universitario Fundación Jiménez Díaz, Madrid, Spain; 5 Biostatistics Unit, Health Research Institute-Fundación Jimenez Díaz University Hospital (IIS-FJD), Madrid, Spain
INTRODUCTION
- Patient reported outcomes (PROs) such as quality of life questionnaires (EORTC QIQ-C30 being the one most commonly used) may be affected by reporting bias.
- Wearable devices are able to collect objective information associated with patients daily activity, that may help capturing reflect quality of life.
- Prior data supports that good objective performance status (OPS) (defined as walking ≥1200 meters per day) was associated with better outcomes in cancer patients being considered to entry phase I clinical trials (Ruiz et al, JCO Oncology Practice 2025).
METHODS
- The aim of this analysis was to assess if information collected with wearables (such as distance walked per day) could be utilised as a surrogate of quality of live in cancer patients.
- For this purpose, the correlation between OPS (defined as previously described by Ruiz et al, JCO oncology Practice 2025) and QoL EORTC QLQ30 scales and symptoms was assessed utilising spearman correlation (variables did not follow a normal distribution; Bonferroni adjustment for multiple comparisons) and T-student test. The scales/symptoms of interest were further assessed with linear regression, utilising OPS as the dependent variable. P-values of 0.05 were considered statistically significant. Stata v.17 was used for statistical analyses.
RESULTS - PATIENT POPULATION
- A total of 63 patients were eligible; median age 61 years old (range 28-84), majority were male (40; 63.49%); median lines of prior therapies and median number of metastatic sites was 2; all patients were in screening process of phase I clinical trials, for a variety of solid tumours with performance status of 0 (36; 57.14%) or 1 (27;42.86%). None of the patients were receiving active treatment at the time of the assessment.
- Majority (44;69.84%) had died at the time of the analysis, with median follow-up of 6.31 months. Median distanced walked per day was 2488.44 metres (range 182-21223.67); good OPS (≥1200 metres) 16 patients (25.40%), bad OPS (<1200 metres) 47 patients (74.60%).
RESULTS - QoL and DISTANCE (continuous variable)
- Spearman correlation (evaluating walked distance as continuous variable) identified acceptable correlation with Global health status scale (rho 0.38831), physical functioning scale (rho 0.4190), role functioning scale (rho 0.3704) and fatigue (rho -0.4525).
QoL and OPS (DISTANCE binary variable)
- Patients in the good OPS (vs bad OPS) group reported a higher scoring in the Global health status scale (mean 69.33 (61.61-77.03) vs 46.88 (38.79-54.96); t-test mean difference 22.45 points (8.56-36.34); p-value 0.0020), physical functioning scale (85.67 (80.45-90.89) vs 74.58 (66.77-82.39); t-test mean difference 11.09 (1.20-20.97); p-value 0.0285) and role functioning scale (87.23 (79.65-94.82) vs 70.83 (58.48 83.18); t-test mean difference 16.40 (1.81-30.98); p-value 0.0282.
- Patients in the good OPS (vs bad OPS) group reported a lower scoring in the fatigue symptom (24.58 (17.68-31.49) vs 40.28 (30.64-49.92); t-test mean difference -15.69 (-28.59- -2.79); p-value 0.0180).
OTHER FINDINGS
- Linear regression confirmed OPS as a categorical variable (vs contiuous) to be more reliable to predict QoL status: Global health status scale (coefficient -22.45 (95% CI -36.34 - -8.56); p-value 0.002; R2 0.1462; Root MSE 24), physical functioning (coefficient -11.09 (95% CI -20.97 - -1.2); p-value 0.029; R2 0.0762; Root MSE 17.08), role functioning (coefficient -16.40 (95% CI -30-98- -1.82); p-value 0.028; R2 0.0766; Root MSE 25-197) and fatigue (coefficient 15.69 (95% CI 2.79-28.59); p-value 0.018; R2 0.0884; Root MSE 22.29).
- Interestingly, the information collected in terms of sleep by the wearable device (time of total, deep and light sleep and time awake), did not correlate with the insomnia symptom reported by patients in QoL questionnaires (all spearman rho <0.3; all t-test student p-value >0.1)
TABLE: QoL variable | Scale or symptom | Rho coeff (Spearman) | Number of observations | P-value | Group >1200 metres (bad OPS); n=47 Mean (95% CI) | Group <1200 metres (good OPS); n=16 Mean (95% CI) | Mean Difference (95% CI) | P-value (T-student)
QL2 Global health status/QoL (revised) | Scale | 0.3831 | 62 | 1 | 69.33 (61.61-77.03) | 46.88 (38.79-54.96) | 22.45 (8.56-36.34) | 0.0020
PF2 Physical functioning (revised)† | Scale | 0.4190 | 62 | 0.6024 | 85.67 (80.45-90.89) | 74.58 (66.77-82.39) | 11.09 (1.20-20.97) | 0.0285
RF2 Role functioning (revised) | Scale | 0.3704 | 62 | 1 | 87.23 (79.65-94.82) | 70.83 (58.48 83.18) | 16.40 (1.81-30.98) | 0.0282
EF Emotional functioning | Scale | 0.0533 | 62 | 1 | 82.09 (76.09-85-08) | 75.00 (64.62-85.38) | 7.09 (-4.59-18.78) | 0.2295
CF Cognitive functioning | Scale | 0.0908 | 62 | 1 | 89.01 (84.41-93.60) | 79.17 (63.11-95.22) | 9.84 (-1.84-21.53) | 0.0974
SF Social functioning | Scale | 0.2188 | 62 | 1 | 84.39 (76.87-91.92) | 70.83 (55.79-85.87) | 13.56 (-1.65-28.77) | 0.0797
FA Fatigue | Symptom | -0.4525 | 62 | 0.1909 | 24.58 (17.68-31.49) | 40.28 (30.64-49.92) | -15.69 (-28.59- -2.79) | 0.0180
NV Nausea and vomiting | Symptom | -0.2183 | 62 | 1 | 5.32 (2.08-8.56) | 11.46 (3.05-19.86) | -6.14 (-13.30-1.02) | 0.0917
PA Pain | Symptom | -0.2637 | 62 | 1 | 24.47 (16.00-32.93) | 32.29 (19.54-45.05) | -7.82 (-23.86-8.22) | 0.3332
DY Dyspnoea | Symptom | -0.0668 | 62 | 1 | 14.89 (9.19-20.59) | 16.67 (5.43-27.89) | -1.77 (-13.26-9.71) | 0.7586
SL Insomnia | Symptom | -0.1402 | 62 | 1 | 22.69 (15.31-30.08) | 31.25 (19.17-43.33) | -8.55 (-22.78-5.67) | 0.2337
AP Appetite loss | Symptom | -0.3345 | 62 | 1 | 13.47 (6.51-20.44) | 22.92 (8.83-37.01) | -9.44 (-23.58-4.69) | 0.1867
CO Constipation | Symptom | -0.1240 | 62 | 1 | 22.69 (13.54-31.85) | 29.17 (13.44-44.87) | -6.47 (-24.28-11.34) | 0.4702
DI Diarrhoea | Symptom | 0.0723 | 62 | 1 | 5.67 (1.43-9.91) | 6.25 (-0.91-13.41) | -0.56 (-8.79-7.64) | 0.8890
FI Financial difficulties | Symptom | 0.1642 | 62 | 1 | 17.73 (8.87-26.59) | 8.33 (0.39-16.28) | 9.39 (-6.36-25.16) | 0.2377
CONCLUSION
Wearable devices could be utilised as an objective measure of quality of life, especially in terms of global health, physical functioning and role functioning.
On top of this, the correlation identified with patient-reported fatigue could be of much interest for objective assessment and monitoring of such a subjective, underreported and relevant adverse event in the setting of clinical trials.
Further validation of these findings and assessment of other aspects being assessed by wearable devices is underway.
2026 European Society of Medical Oncology Annual Meeting | 23-27 October, Madrid, Spain
Correspondence to: Dr Angela Lamarca angela.lamarca@quironsalud.es
#ESMO26
🚀SETHY (GETNE T2318) is a single-arm, multicenter, phase 2 trial for ATC/DTC with Sacituzumab govitecan
🗣️ @Alej_GarciaMD
Congratulations on an interesting ITT trial
✔️ More efficacy at increasing H-score for #TROP2
☣️No new safety signals
Discussed by Dr. Nunes
@OncoAlert @myESMO @ASCO @_SEOM @VHIO @brunolarvol
👇🏽👇🏽
[Slide 3]
Primary Results from the SETHY Trial
GETNE
RESULTS: PFS
Survival Probability (%)
Time (months)
Median PFS (95% CI)
DTCs: 5.5 m (5.0-NR)
Median PFS (95% CI)
ATCs: 2.9 m (2.3-NR)
Number at risk (censored)
6m PFS | 40.2% (22.8-71.1)
12m PFS | 33.5% (17.1-65.6)
6m PFS | 20.5% (6.5-64.3)
12m PFS | 10.3% (1.7-61.8)
The median follow-up was 7.9 m (95% CI: 4.7-11.8) for DTCs and 4.1 m (95% CI: 2.8-8.7) for ATCs.
Presented by Dr. Alejandro García-Álvarez | 8
Survival table
Endpoint: PFS
Arm | N | Median | Median CI
DTC (RAI-refractory) cohort | 24 | 5.5 m | 5.0-NR
ATC cohort | 13 | 2.9 m | 2.3-NR
DTC 6m PFS 40.2% (22.8-71.1)
DTC 12m PFS 33.5% (17.1-65.6)
ATC 6m PFS 20.5% (6.5-64.3)
ATC 12m PFS 10.3% (1.7-61.8)
[Slide 4]
SETHY: strengths, caveats and its own design
Phase 2
Strengths: an innovative and strong design
• First ADC trial in thyroid cancer, academic and multicentre
• An anaplastic cohort — an unmet need
• Heavily pretreated population, like real life — an unmet need
• Mandatory biopsies — the key to unlocking what comes next
Caveats
• DTC below its 5% null (1 of 24);
• Unselected for TROP2 or histology —DTC is not one disease: is heterogeneity the catch?
• A single H-score as the only biomarker read-out
Simon Two-Stage: H0 5% vs H1 20%; Stage 1 Continue if 1 of 12; Final Rule approximately 3 of 21
RAI-Refractory DTC (n=24)
1 of 24 Confirmed Responses: ORR 4.2%
Endpoint Not Met (Below 5% Null Hypothesis)
Anaplastic Cohort (n=13 of 21)
2 of 13 Confirmed Responses: ORR 15.4%
Needs 1 Response in 8 Remaining Patients
confirmed response | treated, no response | still to enrol
Garcia-Alvarez ESMO 2026 (4209O); Capdevila JCO 2024 TPS6130; Simon Control Clin Trials 1989.
Tiago Lopes Nunes da Silva, MD - IPO Lisboa
#ESMO2026 wang presents first data with an effective B7H3 topo 1 ADC. Patients had not received a prior ADC. Expression did not predict response. @OncoAlert https://t.co/q9IW38uPWE
[Slide 1]
Background
B7-H3, a promising therapeutic target
✓ B7-H3 is highly overexpressed on a wide range of human solid cancers and often correlates with poor prognosis in patients
Bar chart: B7-H3 expression frequency (%) by Tumor type (Neurologic, H&N, Lung, Breast, Esophageal, Gastric, HCC, Biliary, PDAC, CRC, Adrenocortical, Renal cell, Bladder, Ovarian, Endometrial, Cervical, Prostate, Melanoma, Orthopedic, Hematologic, Other, Total)
SYS6043, a new-generation B7-H3 targeting ADC
✓ Designed without Fcγ receptors to reduce off-target toxicity
✓ Payload: topoisomerase I inhibitor
✓ Linger: Cleavable linker
✓ Bystander antitumor effect
✓ DAR ~6
Antibody Fab region: B7-H3 binding
Linker-payload DAR 6: Site-specific conjugation; Payload: topoisomerase I inhibitor
Antibody Fc region: Abrogate FcγR and C1q binding activity with no ADCC and CDC function
Hongxia Wang, MD
[Slide 3]
Safety Cutoff date: June 15, 2026
| N (%) | All patients (n = 139) |
| Any TRAEs | 138 (99.3) |
| Grade ≥ 3 TRAEs | 40 (28.8) |
| Serious TRAEs | 8 (5.8) |
| TRAEs leading to dose reduction | 9 (6.5) |
| TRAEs leading to dose interruption | 34 (24.5) |
| TRAEs leading to treatment discontinuation | 1 (0.7) |
| TRAEs leading to death | 0 |
| Interstitial lung disease (ILD) | 2 (1.4) |
TRAEs, treatment related adverse events
Most common TRAEs (Incidence %)
Hypertriglyceridemia 26.6%
Vomitting 26.6%
Hypercholesterolemia 28.1%
ALT increased 28.1%
AST increased 32.4%
Constipation 39.6%
Decreased appetite 42.4%
Asthenia 51.1%
Anemia 51.1%
Neutropenia 55.4%
Leukopenia 60.4%
Nausea 61.2%
TRAEs 99.3%
Hongxia Wang, MD
PACE-AI: 🏴 PCa pt attitudes towards cancer care & AI technologies #ESMO26 @Ioanna_Nixon @urotoday
📌n=60 respondents
📌72%: Mod confidence using digital tech for healthcare
📌58%: Awareness of AI in healthcare
📌78%: support AI as a tool for clinicians
📌Key benefit: 82% - improved diagnostic accuracy
📌Key concern: 68% - AI-related errors
📌73%: support integration of AI-driven tech in Onc care
Same slide also posted by @urotoday
[Slide 1]
Patient Attitudes Towards AI in oncology
Moderate-to-high awareness of AI in healthcare | 58
Support AI integration into routine oncology care | 73
Comfortable with AI-assisted radiotherapy with clinician oversight | 70
Support AI as a supportive tool for clinicians | 78
% of patients who hold these beliefs
[Slide 2]
Perceived benefits flagged by respondents (%)
Improved diagnostic accuracy | 82
Earlier detection of treatment complications | 76
More personalised cancer care | 74
Perceived benefits flagged by respondents
[Slide 3]
Perceived concerns flagged by respondents (%)
Data privacy/security risk | 63
Reduced human interaction | 57
AI-related errors | 68
Perceived concerns flagged by respondents (%)
Efficacy of bemarituzumab in GC/GEJ by FGFR2 amplification status: Exploratory analysis from FORTITUDE-101 and -102
#ESMO26 #ESMOAmbassadors
👉 Amplification of FGFR2 in 16 -19%
👉 OS benefit in FGFR2 Amp pts for bema with & without Nivo
🧐FGFR2 Amp negative prognostic, potentially predictive for FGFR2🎯
@myESMO @ASCO
[Slide 1]
Background & Study Design
• Bemarituzumab, a monoclonal antibody targeting FGFR2b, was evaluated in the phase 3 FORTITUDE-101 and FORTITUDE-102 studies in FGFR2b-overexpressing advanced GC/GEJ1,2
• Exploratory survival analyses were conducted in the biomarker-evaluable population to determine the outcome by FGFR2 amplification status
FORTITUDE-101
FGFR2b ≥ 10% (N = 324a)
R 1:1
Bema + mFOLFOX6 (n = 159) | Placebo + mFOLFOX6 (n = 165)
FORTITUDE-102
FGFR2b ≥ 10% (N = 425a)
R 1:1
Bema + mFOLFOX6/CAPOX + nivolumab (n = 212) | Placebo + mFOLFOX6/CAPOX + nivolumab (n = 213)
Exploratory biomarker analysis: FGFR2 amplification evaluated by tissue and/or ctDNA NGS in assessable specimensb
n = 88 (55%) | n = 97 (59%) | n = 146 (69%) | n = 150 (70%)
• FGFR2b overexpression was detected by IHC using the investigational VENTANA FGFR2b (FPR2-D) RxDx Assay (Roche Diagnostics, Tucson, AZ)
• Tissue NGS was performed using the Tempus xT panel (FGFR2 amplification threshold ≥ 8 copies; tumor purity ≥ 30%)
• For ctDNA NGS, plasma samples were sequenced using the Guardant360 Liquid assay (Guardant Health; FGFR2 amplification threshold ≥ 2.2 copies)
aPrimary efficacy analysis population. bAssessable specimens excluded patients from China and Brazil. Data cutoff: March 2, 2026.
Bema, bemarituzumab; CAPOX, capecitabine and oxaliplatin; ctDNA, circulating tumor DNA; FGFR2b, fibroblast growth factor receptor 2 isoform IIIb; IHC, immunohistochemistry; mFOLFOX6, modified leucovorin, fluorouracil, and oxaliplatin; NGS, next-generation sequencing; R, randomized; TC, tumor cell.
1. Rha SY, et al. Slides presented at: European Society for Medical Oncology Congress; October 17-21, 2025; Berlin, Germany. Abstract LBA10. 2. ClinicalTrials.gov. https://clinicaltrials.gov/study/NCT05111626. Accessed September 25, 2026.
Presented by: Zev Wainberg, MD
[Slide 2]
FGFR2 Amplification Prevalence and Correlation With FGFR2b Expression
FGFR2 Amplification Status Among FGFR2b+ Patientsa
FORTITUDE-101: 18.9% (n = 35) IHC+ Amp+; 81.1% (n = 150) IHC+ Amp−
FORTITUDE-102: 15.9% (n = 47) IHC+ Amp+; 84.1% (n = 249) IHC+ Amp−
Legend: FGFR2b+/FGFR2Amp− ; FGFR2b+/FGFR2Amp+
Correlation Between FGFR2 Amplification Copy Number and FGFR2b Protein Expressionb
FORTITUDE-101: N = 129, Kendall's τ = 0.12, P = 0.083
FORTITUDE-102: N = 190, Kendall's τ = 0.19, P < 0.001
y-axis: FGFR2b Protein Expression (% 2+/3+ TC); x-axis: FGFR2 Amplification Copy Numbers
Key findings:
• FGFR2 amplification was identified in 19% and 16% of FGFR2b-overexpressing patients in FORTITUDE-101 and FORTITUDE-102, respectively
• FGFR2 amplification was associated with higher FGFR2b protein expression in patients with FGFR2b-overexpressing GC/GEJ
• Correlation between FGFR2b expression levels and FGFR2 copy number was weak (Kendall's τ = 0.12 in FORTITUDE-101 and 0.19 in FORTITUDE-102)
aFGFR2 amplification identified by tissue and/or ctDNA NGS. FGFR2b overexpression (IHC+) defined as ≥ 10% of TCs with 2+/3+ membrane staining by IHC.
bTissue FGFR2 amplification vs tissue FGFR2b protein expression (% 2+/3+, TC) in FGFR2b ≥ 10% population.
Presented by: Zev Wainberg, MD
[Slide 3]
FORTITUDE-101: Overall Survival by FGFR2 Amplification Status
FGFR2 Amplified (Placebo vs Bema)
Median OS, months (95% CI): Bema 19.3 (12.2–NE); Placebo 8.0 (6.0–NE)
OS HR (95% CI): 0.50 (0.22–1.12)
P = 0.086
Number at Risk (0, 6, 12, 18, 24, 30 months)
Placebo 17 11 5 2 2 0
Bema 18 14 13 10 5 1
FGFR2 Non-amplified (Placebo vs Bema)
Median OS, months (95% CI): Bema 12.9 (10.6–19.0); Placebo 12.9 (10.3–17.1)
OS HR (95% CI): 0.94 (0.65–1.37)
P = 0.76
Number at Risk (0, 6, 12, 18, 24, 30, 36 months)
Placebo 80 63 42 21 12 5 0
Bema 70 63 39 21 11 6 0
Key findings:
• In FORTITUDE-101, Bema (bemarituzumab + mFOLFOX6) showed a numerically greater treatment effect vs Placebo (placebo + mFOLFOX6) in FGFR2-amplified vs non-amplified patients for OS (HR 0.50 [95% CI 0.22–1.12] vs 0.94 [0.65–1.37]) and PFS (HR 0.47 [95% CI 0.21–1.02] vs 0.91 [0.63–1.30])
• Results from the placebo arm suggest FGFR2 amplification may confer poor prognosis
FGFR2 amplification identified by tissue and/or ctDNA NGS.
CI, confidence interval; HR, hazard ratio; NE, not estimable; OS, overall survival; PFS, progression-free survival.
Presented by: Zev Wainberg, MD
Survival table
Endpoint: OS by FGFR2 amplification status (exploratory)
Arm | N | Median | Median CI
FGFR2 amplified: Bema + mFOLFOX6 | 18 | 19.3 mo | 12.2–NE
FGFR2 amplified: Placebo + mFOLFOX6 | 17 | 8.0 mo | 6.0–NE
FGFR2 non-amplified: Bema + mFOLFOX6 | 70 | 12.9 mo | 10.6–19.0
FGFR2 non-amplified: Placebo + mFOLFOX6 | 80 | 12.9 mo | 10.3–17.1
HR: 0.50 (amplified); 0.94 (non-amplified)
HR CI: 0.22–1.12 (amplified); 0.65–1.37 (non-amplified)
P: 0.086 (amplified); 0.76 (non-amplified)
The topic of systemic cancer treatment near the end of life is clinically and ethically challenging.
Please have a look at our poster 3113P at #ESMO26.
Paolo Bottalico presents a real world analysis of prevalence and determinants of systemic treatment use near the end of life. https://t.co/RBIiXj5gsG
Prevalence and determinants of systemic anticancer therapy use near the end of life: a real-world analysis of 1418 patients
FPN 3113P | ESMO Congress Madrid, Spain 23-27 October 2026
Paolo Bottalico*1, Noemi Pisetta1, Flavio Salerno1, Marco Audisio2, Sara Bustreo2, Ilaria Depetris2, Laura Fanchini2, Roberto Filippi2, Caterina Mecca2, Enrica Milanesi2, Chiara Paratore2, Giuliana Ritorto2, Maria Antonietta Satolli1, Rosella Spadi2, Tiziana Vavalà2, Massimo Di Maio1
1Department of Oncology, University of Turin, AOU Città della Salute e della Scienza di Torino, Turin, Italy; 2SC Medical Oncology 1U, AOU Città della Salute e della Scienza di Torino, Turin, Italy; *Presenting author
BACKGROUND
Use of systemic anticancer therapy (SACT) near end of life (EOL) remains controversial, raising concerns on appropriateness of care. We evaluated the prevalence and determinants of SACT close to death in a real-world, single-center cohort.
METHODS
Retrospective study of adult patients with advanced solid tumors who started SACT (≥1 line) at the Oncology Unit of a tertiary center in 2020–2024 and died between 1 Jan 2020 and 13 May 2025. Excluded: breast cancer; haematological, neurological, dermatological and head-neck malignancies followed at other centers; treatment continued elsewhere; adjuvant/neoadjuvant therapy only. Primary endpoint: SACT within 30 days before death (L30D); SACT within 14 days (L14D) also assessed. Treatment type refers to the last SACT received: chemotherapy (CT), targeted therapy (TT), immunotherapy (IT), hormonal therapy (HT); categories not mutually exclusive. Associations were explored by chi-square test and multivariable logistic regression (odds ratios [OR], 95% CI), adjusting for treatment type, treatment period, age, sex, treatment line, tumor category and palliative care involvement.
TABLE 1. BASELINE CHARACTERISTICS (N=1,418)
Age at death, median (IQR) | 70 (62–76) years
Sex, male | 908 (64.0%)
Tumor category: Gastrointestinal | 771 (54.4%)
Thoracic | 358 (25.2%)
Genitourinary | 166 (11.7%)
Other | 123 (8.7%)
Palliative care involvement: Yes | 1,099 (77.5%)
No | 319 (22.5%)
Treatment line at last SACT: 1st line | 623 (43.9%)
2nd line | 391 (27.6%)
3rd line | 224 (15.8%)
≥4th line | 180 (12.7%)
Last SACT received*: Chemotherapy | 1,063 (75.0%)
Targeted therapy | 267 (18.8%)
Immunotherapy | 183 (12.9%)
Hormonal therapy | 69 (4.9%)
*Not mutually exclusive. CT, chemotherapy; TT, targeted; IT, immunotherapy; HT, hormonal; GI, gastrointestinal; GU, genitourinary.
RESULTS
1,418 patients (deceased) | 20.0% SACT in last 30 days (284) | 7.7% SACT in last 14 days (109)
Palliative care involvement was documented in 1,099 patients (77.5%). SACT near EOL was less frequent with palliative care: 15.6% vs 35.4% in the last 30 days and 4.7% vs 17.9% in the last 14 days (Figure 1). After adjustment, palliative care remained strongly associated with lower odds of SACT near EOL (OR 0.35, 95% CI 0.26–0.47 at 30 days; OR 0.24, 0.15–0.36 at 14 days; Figure 2).
In the crude analysis, targeted therapy (L30D, L14D) and hormonal therapy (L14D) were associated with higher use of SACT near EOL, but none of these associations remained significant after adjustment (Table 2).
Genitourinary tumors showed independently higher use of SACT (OR 1.89 at 30 days; 2.42 at 14 days), as did thoracic tumors at 14 days (OR 3.05) (Figures 2–3). Treatment period 2023–25 was associated with higher use only in the last 14 days (OR 1.71, 1.12–2.59).
TABLE 2. WHO RECEIVES SACT NEAR EOL?
Last SACT / palliative care | % yes vs no | Crude OR (95% CI) | Adjusted OR (95% CI)
SACT in the last 30 days (L30D)
Palliative care | 15.6 vs 35.4 | 0.34 (0.25–0.45) | 0.35 (0.26–0.47)
Chemotherapy | 17.8 vs 26.8 | 0.59 (0.45–0.79) | 0.73 (0.45–1.20)
Targeted therapy | 26.6 vs 18.5 | 1.60 (1.17–2.17) | 1.25 (0.80–1.96)
Immunotherapy | 21.9 vs 19.8 | 1.14 (0.78–1.66) | 0.79 (0.45–1.38)
Hormonal therapy | 29.0 vs 19.6 | 1.68 (0.98–2.87) | 0.92 (0.42–2.02)
SACT in the last 14 days (L14D)
Palliative care | 4.7 vs 17.9 | 0.23 (0.15–0.34) | 0.24 (0.15–0.36)
Chemotherapy | 5.5 vs 14.4 | 0.34 (0.23–0.51) | 0.54 (0.26–1.12)
Targeted therapy | 13.9 vs 6.3 | 2.41 (1.58–3.67) | 1.64 (0.82–3.29)
Immunotherapy | 7.7 vs 7.7 | 0.99 (0.55–1.78) | 0.46 (0.20–1.07)
Hormonal therapy | 18.8 vs 7.1 | 3.03 (1.60–5.74) | 1.50 (0.51–4.39)
Bold = 95% CI excludes 1. Crude: targeted therapy (L30D, L14D) and hormonal therapy (L14D) are higher; none remains significant after adjustment.
Figure 1. SACT near end of life, by palliative care involvement (each figure = 1% of patients in the group; colored = received SACT). ×2.3 at 30 days · ×3.8 at 14 days more SACT without palliative care (crude ratio)
Palliative care: YES, last 30 days | 15.6% | 171 / 1099 pts
Palliative care: NO, last 30 days | 35.4% | 113 / 319 pts
Palliative care: YES, last 14 days | 4.7% | 52 / 1099 pts
Palliative care: NO, last 14 days | 17.9% | 57 / 319 pts
Figure 1 caption: SACT near EOL by palliative care involvement: last 30 days 15.6% with vs 35.4% without; last 14 days 4.7% vs 17.9% (N=1,418).
MULTIVARIABLE LOGISTIC REGRESSION: ADJUSTED OR (95% CI) (* 95% CI excludes 1; tumor site ref: GI)
SACT in the last 30 days (L30D)
Palliative care | 0.35 (0.26–0.47) *
Chemotherapy | 0.73 (0.45–1.20)
Targeted therapy | 1.25 (0.80–1.96)
Immunotherapy | 0.79 (0.45–1.38)
Hormonal therapy | 0.92 (0.42–2.02)
Period 2023–25 | 1.29 (0.98–1.70)
Age ≥70 y | 0.80 (0.60–1.06)
Female sex | 1.12 (0.84–1.50)
Line of therapy (per line) | 0.99 (0.87–1.14)
Thoracic | 1.42 (0.99–2.04)
GU | 1.89 (1.14–3.14) *
Other tumor | 1.52 (0.95–2.46)
SACT in the last 14 days (L14D)
Palliative care | 0.24 (0.15–0.36) *
Chemotherapy | 0.54 (0.26–1.12)
Targeted therapy | 1.64 (0.82–3.29)
Immunotherapy | 0.46 (0.20–1.07)
Hormonal therapy | 1.50 (0.51–4.39)
Period 2023–25 | 1.71 (1.12–2.59) *
Age ≥70 y | 0.90 (0.58–1.40)
Female sex | 1.41 (0.90–2.21)
Line of therapy (per line) | 1.03 (0.83–1.28)
Thoracic | 3.05 (1.76–5.28) *
GU | 2.42 (1.13–5.18) *
Other tumor | 1.10 (0.46–2.63)
Figure 2. Multivariable logistic regression. Palliative care involvement was independently associated with lower odds of SACT in both time windows. Compared with gastrointestinal tumors, genitourinary tumors showed higher adjusted odds at 30 and 14 days, and thoracic tumors at 14 days.
SACT by tumor category (% of patients) | L30D | L14D
Thoracic | 22.1 | 11.7
GI | 16.6 | 4.7
GU | 28.9 | 14.5
Other | 23.6 | 5.7
Figure 3. Crude rates by tumor category. At 30 days: GU 28.9%, other 23.6%, thoracic 22.1%, GI 16.6%.
KEY FINDING
Palliative care involvement is the strongest independent factor associated with less SACT use near the end of life.
CONCLUSIONS
SACT near EOL remains frequent: 1 in 5 patients received treatment in the last 30 days of life. Higher crude use with targeted and hormonal therapy did not remain statistically significant after adjustment. Palliative care involvement is the strongest independent factor associated with reduced SACT use near EOL, and its systematic promotion (particularly in genitourinary and thoracic cancers, where risk is independently higher) should be a priority to improve appropriateness of care at the end of life.
Disclosure: Paolo Bottalico (presenting author) has no conflicts of interest to declare. No specific funding was received for this work.
Nice summary of data on ADCs in #sarcoma by @breelynwilkyMD .
I especially like the take-home message: “there’s a lot we don’t know about ADC patient selection in solid tumors, and in sarcoma this challenge is even more pronounced”
Still, promising data with HER2ADC in DSRCT and B7H3 in osteosarcoma (including a phase III to be presented monday)
#ESMO26 @myESMO @ctosociety
[Slide 1]
Overview of Antibody-Drug Conjugates
Biological Trojan Horse
- Antibody to cancer-enriched targets linked to therapeutic payload
- Optimal targets have turnover promoting internalization, cleavage of linker within lysosome to liberate payload
- Potential for bystander effect
- Efficacy and toxicity driven by off-target expression, payload/linker stability, anti-tumor payload activity
[Figure] Target: Expression, tumor-specificity, regulation, driver - Cancer cell surface proteins; Post-translational modifications; Secreted protein in TME; Surface Proteins on TME cells
IgG subtype: Fc Receptor activation, ADCC - IgG1, IgG2, IgG3, IgG4
Conjugation method: Drug-antibody ratio, manufacturing - Non-specific, Specific/selective, Dual payload
Linker type: Stability, TME, bystander effect - Cleavable, Non-cleavable; Enzyme labile, pH labile, Redox labile
Payload: Potency, susceptibility, resistance - Anti-microtubule, Immune activator, Targeted drugs, DNA damage, Radioligand, Degraders
JEM | Journal of Experimental Medicine © 2026 The Board of Regents of the University of Texas System
Shaw & Meric-Bernstam, J Exp Med, 2026
Breelyn A. Wilky, MD - University of Colorado Anschutz School of Medicine, Aurora, Colorado, USA
[Slide 2]
Utilizing ADCs in Sarcomas...
Opportunities and Pitfalls...
- The TARGET - is it relevant to sarcomas?
- Expression level (does it matter?)
- Downstream biology
- The PAYLOAD - is it effective?
- Payload type
- Resistance mechanisms
- Efficacy AND toxicity readouts
[Mechanism figure] (A) Targeted drug-delivery; Target receptor; Cancer cell; (B) Bystander killing - AG- 'Bystander' cancer cell; Passive toxin diffusion; (C) Pro-survival receptor blockade; (D) Fc-mediated immune-engaging effector functions - Macrophage, NK cell; Cell death; DAMPs; (E) Immunogenic cell death; Activated T cell; Antigen presentation; Mature DC; DC maturation
Conilh et al, Cell 2026
Breelyn A. Wilky, MD - University of Colorado Anschutz School of Medicine, Aurora, Colorado, USA
[Slide 3]
Clinical experience with ADCs in sarcomas - HER2
Desmoplastic small round cell tumor - trastuzumab deruxtecan
- 50% composite expression by IHC in clinical samples^1
[IHC images] HER2 (29D8) / HER2 (CB11); Patient A (H-score: 140) / Patient A (H-score: 140); Patient C (H-score: 70) / Patient C (H-score: 120); HER2 Hematoxylin
[Swimmer plot: Patient No. 1-19 vs Time (weeks) 0-110]
Legend: Partial response achieved; Recurrent disease resected; Progression; Death because of disease; Combination therapy initiated; Death because of other causes; Discontinued because of patient/MD choice; 4B5 IHC 0; 4B5 IHC 1+; 4B5 IHC 2+; 4B5 IHC unknown
Slotkin et al, JCO 2026
Breelyn A. Wilky, MD - University of Colorado Anschutz School of Medicine, Aurora, Colorado, USA
[Slide 4]
Clinical experience with ADCs in sarcomas - B7H3
Efficacy-Osteosarcoma Risvutatug Rezetecan
- Thirty-eight treated R/R osteosarcoma patients were evaluable for efficacy.
- HS-20093 showed promising anti-tumor responses especially at 12.0 mg/kg with 17.4% ORR.
| 8.0 mg/kg (N=15) | 12.0 mg/kg (N=23) | Total (N=38)
Median follow-up time (m) | 8.2 | 2.8 | 3.3
ORR, n(%), (95% CI) | 0 (0.0,21.8) | 4(17.4) (5.0,38.8) | 4(10.5) (2.9,21.1)
DCR, n(%), (95% CI) | 10(66.7) (38.4,88.2) | 20(87.0) (66.4,97.2) | 30(78.9) (62.7,90.4)
Median DOR (m), (95% CI) | / | NA NA,NA | NA NA,NA
NA: not available. Pos%: percentage of B7-H3 positive tumor cells. H-score: histochemistry score of B7-H3 protein.
Data cut-off: March 20, 2024
Figure 5. Best change in tumor burden [waterfall; 8.0 mg/kg / 12.0 mg/kg; rows Pos%, H-score, Prior line, Kinds of standard treatment - small values not transcribed]
2024 ASCO Annual Meeting #ASCO24 PRESENTED BY: Lu Xie, MD, Phase 2 Study of HS-20093 in Patients with Relapsed or Refractory Osteosarcoma and Other Sarcomas
Xie et al, ASCO 2024
Xie et al, ESMO 2025
Breelyn A. Wilky, MD - University of Colorado Anschutz School of Medicine, Aurora, Colorado, USA
Excellent overview by my friend and colleague @jameschowch 🎉 from #QEH in #hongkong 🇭🇰 on the possibility of #behaviouralinterventions in survivorship and reducing risks of #secondarycancers.
As clinicians, we are in a position to not only treat the current cancer, but intercept any future ones.
#ESMO26 @myesmo #ESMOAmbassadors @CUHKMedicine
[Slide 2]
The second cancer umbrella
Second primary cancer
Treatment-associated Second Cancer
Second Cancer from shared risk factors
Sporadic Second Cancer
James C.H. Chow
[Slide 3]
Cumulative risk of second cancer: The Hong Kong case
Multivariable Cox regression of predictive factors for second primary cancer.
Variable | All SPCs: Hazard Ratio | 95% C.I. | p-value
Age (per year increase) | 1.05 | (1.03–1.06) | < 0.001
Sex (Female) | 1.00 | (0.73–1.37) | 0.994
Smoking (Ex-/current smoker) | 1.51 | (1.15–1.98) | 0.003
HbsAg (Positive) a | 1.83 | (1.31–2.55) | < 0.001
T-classification | | | 0.173
T1 | 1
T2 | 0.98 | (0.69–1.39)
T3 | 0.74 | (0.53–1.03)
T4 | 0.70 | (0.45–1.10)
N-classification | | | 0.997
N0 | 1
N1 | 0.99 | (0.70–1.40)
N2 | 1.03 | (0.71–1.48)
N3 | 1.01 | (0.60–1.71)
Chemotherapy with IMRT | | | 0.737
No | 1
Concurrent | 1.20 | (0.84–1.73)
Concurrent + induction/adjuvant | 1.07 | (0.72–1.60)
Others | 0.97 | (0.34–2.72)
Re-irradiation (Received) b | 1.85 | (1.01–3.41) | 0.047
James C.H. Chow
Chow et al. Oral Oncol 2020
[Slide 4]
Predisposition to second cancers with the same risk factors
Overall | Risk factors for second primary cancer*: Alcohol | Smoking | Diet† | Virus | Hormone
Alcohol-related first primary cancer (n=152 350)
Overall | 1·01 (1·00–1·03) | 1·09 (1·06–1·13) | 1·17 (1·14–1·21) | 1·13 (1·07–1·19) | 0·95 (0·89–1·01) | 0·93 (0·90–0·97)
Smoking-related first primary cancer (n=145 346)
Overall | 1·34 (1·32–1·37) | 1·46 (1·40–1·51) | 1·73 (1·68–1·78) | 0·99 (0·93–1·05) | 1·25 (1·17–1·34) | 1·40 (1·34–1·46)
Diet-related† first primary cancer (n=59 370)
Overall | 1·01 (0·98–1·03) | 1·18 (1·13–1·23) | 0·83 (0·79–0·86) | 1·32 (1·24–1·39) | 0·84 (0·77–0·91) | 1·41 (1·35–1·48)
Virus-related first primary cancer (n=43 611)
Overall | 1·10 (1·07–1·14) | 1·14 (1·08–1·20) | 1·19 (1·13–1·24) | 1·02 (0·94–1·11) | 1·23 (1·13–1·35) | 1·19 (1·12–1·27)
Effect by time (years): 0–2, 2–5, 5–10, ≥10; Test for time-invariant effect‡
James C.H. Chow
Kjaer et al. Lancet Oncol 2024
Updated results from Ph 1b/2 KEYNOTE-365 Cohort I: Pembro + Chemo (n=40) vs Chemo (n=30) for NEPC @urotoday #ESMO26
Pembro + Chemo vs Chemo:
📌ORR: 28% vs 15%
📌DCR: 50% vs 48%
📌Med DOR: 6.2 vs 4.1 mos
📌m-rPFS: 5.1 vs 4.0 mos; HR 0.66, 95%CI 0.36-1.21
📌mOS: 10.2 vs 7.1 mos; HR 0.33, 95%CI 0.17-0.63
Same slide also posted by @urotoday
[Slide 1]
Key Eligibility Criteria
• Aged ≥18 years
• Pathologicallya confirmed treatment-emergentb or de novo metastatic NEPC per central histology reviewc
• No prior platinum-based chemotherapy for NEPC
• ECOG PS 0 or 1
N = 70
Rd 1:1 or 3:1
n = 40: Pembrolizumab 200 mg IV Q3W × ≤35 cycles + Carboplatin AUC IV 5 Q3W × 4-6 cycles + Etoposide 100 mg/m2 IV d1-3 Q3W × 4-6 cycles
n = 30: Carboplatin AUC 5 IV Q3W × 4-6 cycles + Etoposide 100 mg/m2 IV d1-3 Q3W × 4-6 cycles
Treatment continued until unacceptable toxicity, PD, or participant or physician decision to withdraw
Stratification factor
• ECOG PS (0 vs 1)
Primary endpoints included
• ORR per RECIST v1.1 by blinded independent central review (BICR)
• Safety
Secondary endpoints included
• DOR per RECIST v1.1 by BICR
• rPFS per PCWG3-modified RECIST v1.1 by BICR
• OS
Post hoc analysis
• ORR, rPFS, and OS by PD-L1 status
Median study follow-up (time from randomization to data cutoff date [November 19, 2025]): 15.4 months (range, 0.8-43.5)
[Slide 2]
| Total population: Pembro + chemo n = 36 | Chemo n = 27 | PD-L1 subgroup CPS ≥1: Pembro + chemo n = 15 | Chemo n = 11 | CPS <1: Pembro + chemo n = 20 | Chemo n = 15
ORR, % (95% CI)a | 28 (14-45) | 15 (4-34) | 40 (16-68) | 18 (2-52) | 15 (3-38) | 13 (2-40)
DCR, % (95% CI)b | 50 (33-67) | 48 (29-68) | 67 (38-88) | 55 (23-83) | 35 (15-59) | 47 (21-73)
Best overall response, n (%)
CR | 0 | 0 | 0 | 0 | 0 | 0
PR | 10 (28) | 4 (15) | 6 (40) | 2 (18) | 3 (15) | 2 (13)
SD of any duration | 8 (22) | 9 (33) | 4 (27) | 4 (36) | 4 (20) | 5 (33)
SD ≥6 mo | 3 (8) | 1 (4) | 1 (7) | 0 | 2 (10) | 1 (7)
PD | 13 (36) | 6 (22) | 3 (20) | 2 (18) | 10 (50) | 3 (20)
No assessmentc | 5 (14) | 7 (26) | 2 (13) | 3 (27) | 3 (15) | 4 (7)
Not evaluabled | 0 | 1 (4) | 0 | 0 | 0 | 1 (27)
DOR, median (range), mo | 6.2 (2.0+ to 10.2+) | 4.1 (2.8+ to 6.2) | 8.3 (3.2+ to 10.2+) | 4.9 (3.5 to 6.2) | 4.1 (2.0+ to 4.1) | 4.1 (2.8 to 4.1+)
[Slide 3]
rPFS per PCWG3-Modified RECIST v1.1 by BICR
Total population
| Events, n (%) | Median (95% CI), mo | HR (95% CI)
Total population
Pembro + chemo (n = 40) | 23 (58) | 5.1 (4.1-6.3) | 0.66 (0.36-1.21)
Chemo (n = 30) | 23 (77) | 4.0 (2.1-5.0)
PD-L1 CPS ≥1
Pembro + chemo (n = 15) | 8 (53) | 6.0 (3.9-NR) | 0.40 (0.16-1.01)
Chemo (n = 12) | 11 (92) | 3.8 (0.4-5.0)
PD-L1 CPS <1
Pembro + chemo (n = 23) | 14 (61) | 5.1 (4.0-6.3) | 0.87 (0.38-1.97)
Chemo (n = 16) | 11 (69) | 4.1 (1.9-7.0)
6-month annotation: 49% (pembro + chemo), 26% (chemo)
Y axis rPFS, %; X axis Months
No. at risk (0,2,...,16 months)
Pembro + chemo: 40 32 22 12 3 1 0 0 0
Chemo: 30 20 13 5 2 0 0 0 0
Survival table
Endpoint: rPFS per PCWG3-modified RECIST v1.1 by BICR (total population)
Arm | N | Median | Median CI
Pembro + chemo | 40 | 5.1 mo | 4.1-6.3
Chemo | 30 | 4.0 mo | 2.1-5.0
HR: 0.66
HR CI: 0.36-1.21
Landmark rates:
6 months: Pembro + chemo 49% | Chemo 26%
[Slide 4]
Overall Survival
Total population
| Events, n (%) | Median (95% CI), mo | HR (95% CI)
Total population
Pembro + chemo (n = 40) | 25 (63) | 10.2 (8.0-11.4) | 0.33 (0.17-0.63)
Chemo (n = 30) | 25 (83) | 7.1 (4.0-8.2)
PD-L1 CPS ≥1
Pembro + chemo (n = 15) | 9 (60) | 11.0 (8.7-11.9) | 0.16 (0.05-0.49)
Chemo (n = 12) | 12 (100) | 4.8 (1.9-8.6)
PD-L1 CPS <1
Pembro + chemo (n = 23) | 14 (61) | 8.1 (6.6-13.0) | 0.49 (0.21-1.11)
Chemo (n = 16) | 12 (75) | 7.1 (3.6-9.9)
6-month annotation: 85% (pembro + chemo), 59% (chemo)
Y axis OS, %; X axis Months
No. at risk (0,2,...,24 months)
Pembro + chemo: 40 34 31 26 18 13 5 3 3 3 3 2 2
Chemo: 30 26 21 17 10 2 1 0 0 0 0 0 0
Survival table
Endpoint: Overall survival (total population)
Arm | N | Median | Median CI
Pembro + chemo | 40 | 10.2 mo | 8.0-11.4
Chemo | 30 | 7.1 mo | 4.0-8.2
HR: 0.33
HR CI: 0.17-0.63
Landmark rates:
6 months: Pembro + chemo 85% | Chemo 59%
#ESMO26 Nearly 1 in 3 patients alive at 7 years with EV+pembrolizumab in cisplatin-ineligible la/mUC - Mature EV-103 data (N=121; median follow-up 64.2 months).
🔹 ORR 66.9%; median DOR 29.6 months
🔹 41% of responders maintained response at 4 years
🔹 Median OS 27.7 months; 7-year OS 28.2%
🔹 Grade ≥3 TRAEs 64.5%; discontinuation of either agent 50.4%
🔹 No new safety signals
A remarkable long-term survival tail in cisplatin-ineligible la/mUC, reinforcing EV+P as 1L SOC
@UroToday @myESMO
[Slide 1]
EV-103 dose escalation and expansion cohorts A and K (1L cisplatin-ineligible la/mUC)2,6
Dose Escalation (DE) | EV+P (n=5)c
Recommended EV dose
Cohort A (expansion cohort) | EV+P (n=40)
Cohort Kd (randomized cohort) 1:1 randomizatione | EV+P (n=76) | EV monotherapy (n=73)
This analysis | Pooled EV+P DE/A/K cohort (N=121) | EV monotherapy Cohort K (n=73)
• Baseline characteristics were previously reported and consistent with the population1,7
• At data cutoff (February 20, 2026), all patients were off study treatment
• Median follow-upf: 64.2 months (pooled EV+P) and 58.6 months (EV monotherapy)
[Slide 2]
Median DOR by INV was 29.6 months in the pooled DE/A/K EV+P cohort
Pooled DE/A/K EV+P cohort
ORR by INV, n/N (%) | Events/n | Median DOR (95% CI), mo
81/121 (66.9) | 41/81 | 29.6 (10.3, 71.9)
Landmark labels: 53.7% (41.3, 64.6); 41.1% (28.5, 53.3); 37.0% (23.6, 50.4); 30.8% (16.2, 46.8)
EV monotherapy cohort
ORR by INV, n/N (%) | Events/n | Median DOR (95% CI), mo
33/73 (45.2) | 18/33 | 10.2 (4.4, 19.2)
Landmark labels: 29.4% (12.3, 48.8); 29.4% (12.3, 48.8)
DOR, % vs Time, mo (0-87)
No. at risk (EV+P): 81 67 59 46 40 37 36 32 29 27 22 21 21 19 19 17 16 16 15 12 10 8 7 7 6 5 5 2 1 1 0
No. at risk (EV mono): 33 29 16 13 10 8 6 5 5 5 5 5 5 5 5 4 4 2 0
Survival table
Endpoint: Duration of response by investigator
Arm | N | Median | Median CI
Pooled DE/A/K EV+P | 81 | 29.6 mo | 10.3, 71.9
EV monotherapy (Cohort K) | 33 | 10.2 mo | 4.4, 19.2
Landmark rates:
~24 mo: Pooled EV+P 53.7% (CI 41.3, 64.6) | EV monotherapy 29.4% (CI 12.3, 48.8)
~48 mo: Pooled EV+P 41.1% (CI 28.5, 53.3) | EV monotherapy 29.4% (CI 12.3, 48.8)
~60 mo: Pooled EV+P 37.0% (CI 23.6, 50.4)
~84 mo: Pooled EV+P 30.8% (CI 16.2, 46.8)
[Slide 3]
Median OS was 27.7 months in the pooled DE/A/K EV+P cohort
Pooled DE/A/K EV+P cohort
Events/n | Median OS (95% CI), mo
83/121 | 27.7 (20.9, 39.6)
Landmark labels: 52.9% (43.6, 61.3); 38.8% (30.2, 47.4); 33.0% (24.6, 41.6); 28.2% (19.6, 37.4)
EV monotherapy cohort
Events/n | Median OS (95% CI), mo
54/73 | 22.8 (16.3, 28.4)
Landmark labels: 46.4% (34.6, 57.3); 25.5% (16.0, 36.2); 23.9% (14.6, 34.5)
OS, % vs Time, mo (0-100)
No. at risk (EV+P): 121 112 103 87 75 62 59 55 50 47 45 38 35 26 18 16 14 14 12 3 1 0
No. at risk (EV mono): 73 70 61 57 51 48 44 40 33 28 23 22 21 19 18 18 16 16 12 9 6 4 3 1 0
• 56.2% of patients in the pooled EV+P cohort and 72.6% in the EV monotherapy cohort had subsequent systemic therapya
– PD-(L)1 inhibitor–containing therapy was administered in 23.1% of all patients in the pooled EV+P cohort and 42.5% of all patients in the EV monotherapy cohort
Survival table
Endpoint: Overall survival
Arm | N | Median | Median CI
Pooled DE/A/K EV+P | 121 | 27.7 mo | 20.9, 39.6
EV monotherapy (Cohort K) | 73 | 22.8 mo | 16.3, 28.4
Landmark rates:
~24 mo: Pooled EV+P 52.9% (CI 43.6, 61.3) | EV monotherapy 46.4% (CI 34.6, 57.3)
~48 mo: Pooled EV+P 38.8% (CI 30.2, 47.4) | EV monotherapy 25.5% (CI 16.0, 36.2)
~60 mo: Pooled EV+P 33.0% (CI 24.6, 41.6) | EV monotherapy 23.9% (CI 14.6, 34.5)
~84 mo: Pooled EV+P 28.2% (CI 19.6, 37.4)
#ESMO26 🧬 Rapid Oral | NETSARC+
👥 3,457 pts | Desmoid tumors
🇫🇷 French multicenter RWE
📉 Surgery: 47.2% → 22.1% (2010–2024)
📈 Median EFS: 47.7 mo
🔬 Poorer outcomes: larger tumors & head/neck location (HR 2.18)
💡 Shift towards conservative management, supporting guideline implementation!
@OncoAlert
[Slide 1]
08:30 - 10:00 Rapid oral: Sarcoma
CHAIRS: MARK DICKSON, PALMA DILEO, CESAR SERRANO
Results – Patients Characteristics
3,457 DT, incidence 3,02/1,000,000/year
Sex Female Male
Female Moyenne = 41,06 Ecart type = 15,275 N = 2,425
Male Moyenne = 47,39 Ecart type = 18,716 N = 1,033
Fréquence
Age at diagnosis
Peak incidence in young women
• 2,425 women (70,1%)
• Median age at diagnostic: 40 years (1-89)
• 49 years in men
• 38 years in women
• Pediatric population (5,6%):
• 171 cases 10-19
• 23 cases 0-9
Dufresne
Armelle Dufresne
Desmoid tumors (DTs) from the NETSARC+ registry: Tumor characteristics, management strategies, and outcomes in 3457 patients
MALAGA AUDITORIUM - HALL 3
[Slide 2]
08:30 - 10:00 Rapid oral: Sarcoma
CHAIRS: MARK DICKSON, PALMA DILEO, CESAR SERRANO
Results – Outcome
Overall mortality: 0,9%
Median EFS: 47,7 months (29,3m in surgery cohort; 54,6m in no surgery cohort)
Multivariate analysis on PFS using Cox Model
Parameter | HR | p value
Breast | 0,688 | 0,09
H&N | 2,181 | <,001
Upper limb | 1,448 | 0,001
Thoracic wall | 1,314 | 0,001
Size of tumor (mm) | 1,002 | <,001
Location and tumor size as independent prognostic factors
[two survival curve panels by tumor location; legends and axes illegible]
Dufresne
Armelle Dufresne
Desmoid tumors (DTs) from the NETSARC+ registry: Tumor characteristics, management strategies, and outcomes in 3457 patients
MALAGA AUDITORIUM - HALL 3
Hey #ESMO26 !
Come to see our 2nd poster, today, 12 am, Hall5!
We often talk about informative censoring for drugs, but what about informative censoring in non-drug oncology trials?
Like any intervention, exercise, behavioral, and supportive care interventions can be burdensome for some patients, potentially leading to dropout.
Our work suggest some level of "burden"-driven informative censoring may happen in such trials + see our sensitivity analyses incl. the CHALLENGE trial!👇
Censoring and Treatment Adherence in Trials of Behavioral, Exercise, and Supportive Interventions in Oncology
FPN: 3334P
Timothée Olivier1,2, Areez Shafqat3, Ruggero Lasala4, Abduljalil El-Sibai3
1 Department of Oncology, Geneva University Hospitals, Geneva, Switzerland; 2 Department of Medicine, University of Geneva (UNIGE), Geneva, Switzerland; 3 College of Medicine, Alfaisal University, Riyadh, Saudi Arabia; 4 Pharmaceutical Department, Local Health Unit of Bari, Italy
BACKGROUND
Non-drug interventions require patients' participation.
Patients unable to continue may also be those at higher risk of relapse/progression.
Informative censoring related to toxicity is well documented in oncology drug trials. Whether this phenomenon also occurs in non-drug oncology trials remains poorly understood.
METHODS
Cross-sectional study: 2020 - July 2025
Oncology RCTs of physical, behavioral, and supportive care interventions published in top six journals.
Data abstracted: dropout from CONSORT diagrams; adherence data and missing-data analyses when present; survival curves reconstructed for sensitivity analyses.
STUDY SELECTION
Records identified from PubMed and screened n = 2,583 -> Records excluded n = 2,535
Reports assessed for eligibility n = 48 -> Excluded (n = 22)
Trials included n = 26 (incl. 2 trials with 3 groups) -> 28 comparisons
Physical interventions -> 11 trials; Behavioral interventions -> 8 trials; Clinical support interventions -> 9 trials
57.1% of comparisons -> higher dropout in the experimental arm
+1.2 percentage points in the experimental arm -> median difference in dropout (range, -6.1 to +11.7)
Figure: reported dropout differences across 28 comparisons
Positive = Higher dropout in experimental arm | Negative = Higher dropout in control arm
Intervention Type: Physical; Behavioral; Clinical support. Median = 1.2%
Trials listed: McCusker J, Greer JA, Absolom K, Kang D, Takemura N, Steel JL, Courneya KS, Ma DD, Dupuis LL, Garland SN, Winters-Stone KM, Akechi T, Dai W, Abel GA, Basch E, Vidrine JI, Paramanandam VS, Zola P, Bower JE, Temel JS, Kang DW, Lu Z, Mosher CE, Michel LL, Schouten AEM
X-axis: % Difference in Dropout (Experimental - Control)
61.5% of trials reported quantitative adherence data
Adherence reported | 16 trials (61.5%)
Adherence range | 52% to 100%
Prespecified threshold | 8 trials (30.8%)
Threshold range | from 50 to 80%
7.7% of trials tested missing-not-at-random (MNAR) scenarios for the primary outcome
in 2/3 trials with significant survival benefits, conservative sensitivity analyses eliminated statistical significance+
Courneya et al. 2025. CHALLENGE trial. Intervention = 3-year structured exercise program
[Reconstructed KM curves: Original - Experiment / Original - Control / Simulated - Experiment; number-at-risk rows small, partly legible: Ori-Exp 445(0) ...; Ori-Ctrl 444(0) ...; Sens-Exp 445(0) ...]
Exercise arm: 6 censored patients (1.3% of the group) reclassified as events over 3 years -> no longer significant
Lu et al. 2021. Intervention = early interdisciplinary supportive care
[Reconstructed KM curves; number-at-risk rows small: Ori-Exp 214(0) ...; Ori-Ctrl 114(0) ...; Sens-Exp 214(0) ...]
Supportive care arm: 5 censored patients (2.3% of the group) reclassified as events over 12 months -> no longer significant
+: in a third trial, the absence of early censoring precluded sensitivity analysis.
Limitation: dropout imbalances do not establish informative censoring. Sensitivity analyses rely on reconstructed data and are hypothesis-generating only.
CONCLUSIONS: Dropout imbalances may introduce bias, yet missing-not-at-random assumptions are rarely assessed. Non-drug intervention trials may be prone to burden-driven informative censoring, analogous to toxicity-driven informative censoring in drug trials.
Email: timothee.olivier@hug.ch
sensitivity analyses are openly available at: https://breaking-ice-app.timotheeolivier-research.com/
Disclosure: Timothée Olivier has no conflicts of interest to disclose
#ESMO2026
Is more always necessarily better?
GORTEC IDEAL randomised phase 2 trial presented by @YG_TAO
Doublet EGFR ADC and Anti-PD1 vs EGFR ADC alone before CRT
Safety analyses revealed higher G3 TRAEs but no influence on compliance to RT
@PBlanchardMD @PierluigiBonomo https://t.co/HB6lWDCRzD
[Slide 1]
Study design
Newly diagnosed LA-SCCHN; ECOG-0-1; Treatment naïve; Fit to cisplatin CT
R 1:1
A (n=53): Pucotenlimab + MRG003 3 cycles Q3W
B (n=53): MRG003 3 cycles Q3W
Within 28+/-7 Days after induction -> Cisplatin-based IMRT 100mg/m2 Q3W or 40mg/m2 weekly
Within 28+/-7 Days post RT
Arm A: No clinical PD -> Pucotenlimab; PD -> Best investigator's choice
Arm B: No clinical PD -> Observation; PD -> Best investigator's choice
Induction (9 weeks) | CRT (7 weeks) | Adjuvant (24 weeks)
P16- : Stage III/IVa-b
p16+ : any T3-T4/N1-N3, or any T1-T2/N1-N3 or T3-T4/N0 if >= 20 pack year
Primary objective : Evaluation at 12 weeks post RT-CT
Minimization factors : OPSCC p16+ vs OPSCC p16- and non OPSCC ; N0-2 vs N3
Yungan TAO
GORTEC
[Slide 2]
TEAEs during induction treatment
• 302 TEAEs (135 in arm A, 167 in arm B) of 39 patients
• TEAEs grade ≥3 by arm: 15 (arm A) vs 6 (arm B)
TEAE Grade Max by patient | Arm A (combo n=20) | Arm B (n=19) | Total
1 | 4 (20%) | 1 (5%) | 5 (13%)
2 | 7 (35%) | 13 (68%) | 20 (51%)
3 | 8 (40%) | 4 (21%) | 12 (31%)
4 | 1 (5%) | | 1 (3%)
5 | | 1 (5%) | 1 (3%)
* Arm A = EGFR-ADC becotatug vedotin + anti PD-1 pucotenlimab; Arm B = becotatug vedotin alone
Yungan TAO
GORTEC
Very proud of @ddemiguelperez from @rolfolab presenting at #ESMO26 our collaborative study with @lillian_siu & #annaspreafico #scottstrum on Plasma EVs proteomics identifies signatures of resistance and survival on immunotherapy in solid tumors.
@OSUCCC_James
@OhioStateMedOnc https://t.co/VL9l5ugNDJ
#ESMO26
Oneof the best summaries that you can see these days about the management of HPV+ early disease #HNSCC
Kudos Dr Sandra Schmitz from @ClinUnivStLuc
@OncoAlert @brunolarvol https://t.co/UfPydn0GGX
[Slide 1]
I.De-escalation based on ctHPV DNA
A potential selection tool?
Baseline
Confirm a trackable tumour signal
Most HPV+ OPSCC (>90%) have detectable ctHPVDNA before treatment;
The baseline level reflects tumour burden and HPV integration status
During (C)RT
Adapt dose to response
ReACT 1.0: intermediate risk (T4 or >10 PY, TTMV-HPV DNA score >200); >95% ctDNA clearance at weeks 4-5 → reclassified and de-escalated to 54-60 Gy"
93%
2-y PFS in 89 de-escalated patients (60 low risk + 29 reclassified intermediate risk, of 102)
After surgery
Molecular residual disease
DART secondary analysis (n = 140): post-operative ctDNA status vs 2-y PFS.
69.5% vs 95.9%
2-y PFS, ctDNA+ vs ctDNA- after surgery
Surveillance
Safety for de-escalation
Two consecutive positive samples precede clinical recurrence by a median of 3.9 months.
PPV 94% · NPV 100%
Post-treatment surveillance
Integration of ctHPV DNA in de-escalation trials makes sense
Sandra Schmitz
Chera BS et al. J Clin Oncol 2020
Hanna GJ, Schoenfeld JD et al. (ReACT 1.0) Nat Commun 2026.
Routman DM et al. JAMA Otolaryngol Head Neck Surg 2025.
[Slide 2]
Conclusions
➢ Surgery is a treatment option in early stages: adequate patient selection and a technical learning curve are mandatory.
➢ Homogenization of inclusion criteria across studies would be of interest.
➢ So far, TORS and RT result in comparable swallowing function.
➢ ENE is a high risk factor but the relevant extent (>1, >2 or ≥4 mm) is undefined. iENE sensitivity is low: Potential impact of radiomics and machine learning
➢ Predictive and prognostic biomarkers should be incorporated in future trial designs. The future is biology-guided BUT need for standardized and more sensitive assays like HPV whole genome NGS liquid biopsies
#HNSCC #ESMO26
Hexavalent OX-40 agonist (INBRX-106) in 1st L PDL1 >|=20 R/M HNSCC. Open-label phase 2 HexAgon-HN trial
Dr Park
⛳️ Double ORR 48 vs 26%
High activity in HPV+ (PFS6m)
⁉️High amount of tox and treatment discontinuation in a population eligible to just Q6W sc pembro
Phase 2b expansion is ongoing
@brunolarvol @OncoAlert @myESMO
[Slide 1]
PRIMARY EFFICACY ENDPOINT: cORR
INBRX-106 + pembro (n=29)
cORR, 48.3% (14/29)
(95% CI, 29.4-67.5)
CR | PR | SD | PD
Pembro (n=34)
cORR, 26.5% (9/34)
(95% CI, 12.9-44.4)
PR | SD | PD
Y-axis: TL SOD best change from BL, %
Addition of INBRX-106 to pembro increased both response rate (ΔORR 21.8% [95% CI, -3.6 to 44.9]) and depth (CRs only in combination arm)
Presenter: Jong Chul Park, MD
Data cutoff: August 19, 2026. Data shown for response-evaluable patients. Best percentage change from baseline in TL SOD, with response categories per Response Evaluation Criteria in Solid Tumors v1.1.
cORR defined as confirmed CR or PR on 2 consecutive occasions ≥4 weeks apart. Waterfall plot shows best overall response.
BL, baseline; cORR, confirmed objective response rate; CR, complete response; ORR, objective response rate; PD, progressive disease; pembro, pembrolizumab; PR, partial response; SD, stable disease; TL SOD, target lesions sum of diameters.
[Slide 2]
EFFICACY IN HPV-POSITIVE DISEASE: PFS6mo
INBRX-106 + pembro (n=10)
PFS6mo, 90%
CR | PR | SD | PD
★ Ongoing, progression free
Pembro (n=9)
PFS6mo, 33%
PR | SD | PD
★ Ongoing, progression free
Time on study, mo
• Greater and durable treatment effect in patients with HPV-positive disease
• Majority of HPV-positive patients in the combination arm continue to receive benefit
Presenter: Jong Chul Park, MD
HPV status based on central p16 immunohistochemistry in oropharyngeal squamous cell carcinoma was a randomization stratification factor. Data shown for response-evaluable patients. Response categories per Response Evaluation Criteria in Solid Tumors v1.1. CR, complete response; HPV, human papillomavirus; PD, progressive disease; pembro, pembrolizumab; PFS6mo, progression-free survival rate at 6 months; PR, partial response; SD, stable disease.
[Slide 3]
SAFETY
Patients with ≥1 TEAE, n(%) | INBRX-106 + pembro n=31 | Pembro n=34
TEAE | 31 (100) | 29 (85.3)
Tx-related | 27 (87.1) | 20 (58.8)
SAE | 12 (38.7) | 12 (35.3)
Tx-related | 8 (25.8) | 3 (8.8)
Grade ≥3 | 18 (58.1) | 16 (47.1)
Tx-related | 15 (48.4) | 4 (11.8)
Grade 5 | 0 | 2a (5.9)
Tx-related | 0 | 0
Tx discontinuation | 11 (35.5)b | 5 (14.7)
INBRX-106 | 11 (35.5) | NA
Pembro | 8 (25.8) | 5 (14.7)
Most frequent TRAEs (≥10% of patients)
Rash maculopapular; Rash; Fatigue; Diarrhoea; ALT increased; AST increased; Infusion-related reaction; Nausea; Weight decreased; Pyrexia; GGT increased; Hypothyroidism; Arthralgia; Pruritus
Patients, %
Green: combination; grey: pembro.
Dark shades: grade ≥3; light shades: grade 1/2.
Grade ≥3 treatment-related AEs: 48.4% vs 11.8%; discontinuations: 35.5% vs 14.7%.
Common combination TRAEs: rash, fatigue, diarrhoea and transaminitis.
Some responses persisted or were confirmed after treatment discontinuation.
Source: Park JC et al., LBA42, data cutoff 19 August 2026. Full definitions in speaker notes.
[Slide 4]
CONCLUSIONS
• Addition of INBRX-106 to pembro as 1L treatment for patients with R/M HNSCC with PD-L1 CPS ≥20 improved cORR (48.3% vs 26.5%), supported by PFS6mo (72.4% vs 42.8%)
• In the prespecified subgroup of patients with HPV-positive disease, a more pronounced benefit (cORR, 80.0% vs 33.3%; PFS6mo, 90% vs 33%) was observed, consistent with the expected underlying biology for an OX40 agonist
• INBRX-106 + pembro showed a safety profile characterized by mostly grade 1/2 common TRAEs, with no new safety signals identified; treatment discontinuations were more frequent with the combination, but not driven by any single toxicity and did not compromise efficacy
• These positive randomized phase 2 results establish the first clinical proof of concept for an OX40 agonist in cancer immunotherapy
• The high activity and unmet need in HPV-positive disease, amid an evolving 1L treatment landscape, support a phase 2b expansion (N=50) in HPV-positive OPSCC with PD-L1 CPS ≥1 that is designed to enable discussion of an accelerated regulatory pathway with health authorities
Presenter: Jong Chul Park, MD
1L, first line; cORR, confirmed objective response rate; CPS, combined positive score; HNSCC, head and neck squamous cell carcinoma; HPV, human papillomavirus; OPSCC, oropharyngeal squamous cell carcinoma; pembro, pembrolizumab; PFS6mo, progression-free survival rate at 6 months; R/M, recurrent/metastatic; TRAE, treatment-related adverse event.
#ESMO26 ☢️ Radioligand Therapy | ESMO Keynote
📖 Ken Herrmann | Annals of Oncology
🔬 From diagnosis to treatment
🎯 Targeted radionuclide delivery
🧬 Theranostics: imaging + therapy
🚀 From salvage option to a new pillar of oncology!
💡 The future is theranostic!
🔗 https://t.co/kXLmJ4qPcN
@OncoAlert
Nuclear medicine market evolution
Radiotherapeutics are driving the nuclear medicine market from US $12.8 B in 2025 toward US $44 B by 2035
[Stacked bar chart 2013–2031, then 2035]
US$ 12.8 billion (2025)
+16%/year to 2031
US$ 44 billion (2035)
(...)
223Ra-Xofigo (Bayer)
177Lu-Lutathera (Novartis)
177Lu-Pluvicto (Novartis)
Legend: 99mTc | PET tracers, incl. FDG | Other SPECT tracers | Radiotherapeutics
© MEDraysintell 2026
Journal Pre-proof [watermark]
Nuclear medicine market revenues in billions of U.S. dollars, by segment: 99mTc, PET tracers (including FDG), other non-99mTc SPECT tracers, and radiotherapeutics. [17] Figure courtesy of MEDraysintell, reproduced with permission.
‼️ Hey #ESMO26 family!
Great discussion by Funda Meric-Bernstam on the rationale behind ADC + IO combinations!! @UTMDAnderson
▪️ADCs may induce immunogenic cell death, release DAMPs and prime the TME
▪️They may also increase PD-L1 expression and help overcome antigen heterogeneity
▪️VEGF–PD-(L)1 bispecifics aim to reverse vascular immunosuppression and improve tumour immune access
@OncoAlert @OncoReporte @myESMO @_SEOM
[Slide 1]
Rationale for ADC + IO combinations
1. Induction of Immunogenic Cell Death (ICD)
• Tumor-specific neoantigens, which provide new targets for the immune system to recognize.
• Damage-Associated Molecular Patterns (DAMPs), which act as biological danger signal
2. Priming the Tumor Microenvironment (TME)
• Dendritic Cell Activation
• T-Cell Infiltration
• Macrophage Reprogramming
3. Overcoming IO Resistance and Exhaustion
• ADC therapy frequently induces an upregulation of PD-L1 expression
4. Overcoming ADC Antigen Heterogeneity
• Immune system is trained broadly by the subsequent ICD, activated T cells can seek out and kill these antigen-negative escape cells, bypassing the ADC's target limitations
Dr. Funda Meric-Bernstam
[Slide 2]
Rationale for VEGF PD1/PDL1 Bispecifics
1. Complementary Biological Synergy
• Reversing vascular immunosuppression
• Dismantling TME Immune Barriers
• Reactivating T-Cells
2. Mechanistic Superiority: Cooperative Binding
• Affinity Amplification: Binding of one target may enhance affinity to other target
• Enhanced Internalization
3. Improved Local Tumor Enrichment (Therapeutic Index)
• Tumors overexpress both VEGF and PD-L1/PD-1, the dual-targeting nature acts like a geographic anchor
• The bispecific antibody accumulates heavily inside the TME
4. Overcoming Resistance and Expanding Indications
5. Clinical and Safety Advantages
• Reduced Additive Toxicity
• Single-Molecule Convenience
Dr. Funda Meric-Bernstam
In the ET-FES Study, pts with total concordance of FES and FDG-PET at baseline treated with ET showed longer mOS (p=0.010, per =0.005 at multivariate analysis)
Whole-body ER heterogeneity has clinical implications
Great presentation by
@ALEDIGNUS12
#Esmo26 @OncoAlert https://t.co/dO6c6UYyOa
[Slide 2]
PROGRESSION-FREE AND OVERALL SURVIVAL
[Left] Progression-free survival (%) vs Years (0-11)
Median Progression-free survival
Group A: 18.1 months (95%CI 11.3-25.3)
Group B/C: 12.0 months (95%CI 6.6-22.9)
HR 1.36 (95%CI 0.88-2.10); p=0.162
No. at Risk (No. Cumulative Censors) (Years 0 | 1 | 2 | 3 | 4 | 5 | 6 | 7 | 8 | 9 | 10 | 11)
Group A: 92 (0) | 53 (0) | 39 (0) | 29 (0) | 25 (0) | 21 (1) | 11 (6) | 9 (7) | 7 (9) | 4 (12) | 2 (14) | 0 (16)
Group B+C: 31 (0) | 16 (0) | 9 (0) | 7 (0) | 6 (0) | 3 (1) | 2 (2) | 1 (2) | 0 (3)
[Right] Overall survival (%) vs Years (0-11)
Median Overall survival
Group A: 69.6 months (95% CI, 48.3-85.1)
Group B/C: 42.5 months (95% CI, 27.0-70.4)
HR = 1.87 (95% CI 1.16–3.01); p = 0.010
No. at Risk (No. Cumulative Censors) (Years 0 | 1 | 2 | 3 | 4 | 5 | 6 | 7 | 8 | 9 | 10 | 11)
Group A: 92 (0) | 90 (0) | 80 (1) | 70 (1) | 57 (2) | 48 (5) | 33 (12) | 26 (15) | 21 (17) | 11 (27) | 5 (32) | 0 (36)
Group B+C: 32 (0) | 28 (1) | 23 (1) | 17 (1) | 14 (1) | 11 (2) | 8 (3) | 3 (5) | 2 (6) | 0 (7)
Gennari A.
Survival table
Endpoint: PFS and OS by FES/FDG heterogeneity group (Group A vs Group B/C)
Arm | N | Median | Median CI
Group A (PFS) | 92 | 18.1 months | 11.3-25.3
Group B/C (PFS) | 31 | 12.0 months | 6.6-22.9
Group A (OS) | 92 | 69.6 months | 48.3-85.1
Group B/C (OS) | 32 | 42.5 months | 27.0-70.4
HR: PFS HR 1.36; OS HR 1.87
HR CI: PFS 0.88-2.10; OS 1.16–3.01
P: PFS p=0.162; OS p=0.010
[Slide 4]
CONCLUSIONS
18F-FES PET/CT captures whole-body ER heterogeneity, revealing biologically distinct patterns of ER availability across metastatic lesions.
FES-defined heterogeneity is associated with long-term survival. This association is independent of established prognostic factors in MBC, including tumor burden.
Whole-body functional ER imaging may refine endocrine-sensitivity assessment and support future treatment-fine tuning strategies
Gennari A.
#HNSCC #ESMO26
RADIAN-TTCC Dostarlimab and niraparib in the CRT soace in LA PD-L1+ disease
An stunning effort from Dr Oliva, rest investigators and the spanish cooperative group @ttccgroup
@myESMO @OncoAlert @brunolarvol
@FundacionTTCC https://t.co/zlkrPKZXXj
[Slide 1]
Study Design and Objectives
TTCC GRUPO ESPAÑOL DE TRATAMIENTO DE TUMORES DE CABEZA Y CUELLO
• LA-HNSCC • Oropharynx • Hypopharynx • Larynx
• Stage III-IVA-IVB
• ECOG 0-1
• PD-L1 CPS ≥1
Screening period w(-6) to (-3)
Neoadjuvant Phase (Immune-conditioning): DOSTARLIMAB 500 mg iv; NIRAPARIB 200-300mg po od x14d
Concurrent Phase (Radiosensitization), w1-w7:
COHORT A: CISPLATIN CDDP 100mg/m2 w1D1, w4D1 and w7D1; RADIOTHERAPY 70 Gy (35 Fx, 1Fx/d x 7w)
COHORT B: NIRAPARIB 200-300mg po od w1 to w10; RADIOTHERAPY 70 Gy (35 Fx, 1Fx/d x 7w)
Maintenance Phase (cycle 1 to cycle 14): NIRAPARIB 200-300mg po od x21d; DOSTARLIMAB 500 mg iv q21d; Evaluation of Response (cycle 4)
For a total of 14 cycles unless PD, death, toxicity or withdrawal of consent
• Safety lead-in (N=6)
• Centralized PDL1 CPS and RT planning review
Sampling: Tumor / Plasma - Baseline1, Pre-Nira2, Pre-RT2, Post-RT2, EOT2 and/or PD
Marc Oliva
[Slide 2]
Results Efficacy by intention-to-treat
Median follow-up in cohort A: 17 months (CI 95% 16-25)
Median follow-up in cohort B: 13.6 months (m) (CI 95% 7.8-16.4)
Efficacy | Cohort A (n=17) | Cohort B (n=17)
Objective response rate 12w post-RT | 15 (88.2%) | 15 (88.2%)
- Complete response | 11 (65%) | 10 (59%)
- Partial response | 4 (23.5%) | 5 (29%)
- Stable disease | 0 | 0 (0)
- Non-evaluable* | 2 (11%) | 2 (11%)
Distant control rate | 15 (88.2%) | 15 (88.2%)
Median progression-free survival | NR | 15.33 (8-NR)
Median overall Survival | NR | NR
1-year locoregional failure | 0% (N/A) | 7.6% (0.4% - 30%)
1-year distant control rate | 88.2% (74.18, 100) | 68.2% (48.6, 95.7)
Cohort A: • 15/17 patients alive with no progression or recurrence • 2/17 patients died due to adverse events
Cohort B: • 10/17 are alive with no progression/recurrence. • 3/17 had disease progression/recurrence (1 local, 2 distant) • 5/17 patients died (2 due to disease, 3 due to adverse events)
1-year progression-free Survival (PFS) rate:
Cohort A: 88.2% (95% CI: 74.2-100.0), HR* 0.19, p=0.01
Cohort B: 60.6% (95% CI: 40.2-91.4), HR*: 0.72, p=0.19
Number at risk (0,6,12,18,24,30 months)
Cohort A: 17 | 15 | 15 | 7 | 3 | 0
Cohort B: 17 | 13 | 7 | 3 | 2 | 0
*Exp. 75.9%vs 65%* historical; ** Exp. 68.2% vs 55%* historical)
Marc Oliva
Survival table
Endpoint: PFS (1-year PFS rate)
Cohort A (cisplatin-RT + dostarlimab/niraparib) | 17 | NR
Cohort B (niraparib-RT + dostarlimab/niraparib) | 17 | 15.33 | 8-NR
HR: Cohort A 0.19; Cohort B 0.72 (vs historical expectation)
P: Cohort A p=0.01; Cohort B p=0.19
Landmark rates:
1 year: Cohort A 88.2% (CI 74.2-100.0) | Cohort B 60.6% (CI 40.2-91.4)
[Slide 3]
Conclusions
• Dostarlimab plus niraparib showed promising efficacy in patients fit and unfit for cisplatin with high disease burden but with substantial treatment-related toxicity in the maintenance phase , resulting in treatment discontinuation.
• In cohort A, the pre-specified efficacy criterion was met, with a 1-year PFS of 88.2% (75.9% expected) compared with the historical benchmark.
• In cohort B, increased and prolonged RT-mediated toxicity (odynodyshagia, mucositis, edema and radionecrosis) led to high rates of discontinuation and two toxic deaths, with no PFS gain vs historical control.
• These findings should be interpreted cautiously given the single-arm design and small sample size.
• Further investigation of the neoadjuvant and concurrent portion of niraparib at reduced doses may be warranted, particularly in patients unfit for cisplatin.
• Tumor NGS and ctDNA evaluation will be conducted.
Marc Oliva
Trastuzumab deruxtecan in patients with desmoplastic small round cell tumors (DSRCT): a retrospective analysis from the French Sarcoma Group in @ESMO_Open presented at #ESMO2026. Substantial activity (10/12,ORR 83%) across HER2 expression. https://t.co/1Fhcr8mPEJ https://t.co/KDgGlkL9VF
ESMO OPEN
SCIENCE FOR OPTIMAL CANCER CARE
ORIGINAL ARTICLE · Articles in Press, 108651, October 26, 2026 · Open Access
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Trastuzumab deruxtecan in patients with desmoplastic small round cell tumors (DSRCT): a retrospective analysis from the French Sarcoma Group.
Mehdi Brahmi 1 · Maud Toulmonde 2 · Aymeric de Montfort 1 · Perrine Vuagnat 3 · Clément Korenbaum 4 · Audrey Monneur-Miramon 5 · Lucy Metayer 6 · Yves Reguerre 7 · Justine Gantzer 8 · Margaux Dupont 1 · Benjamin Verret 6 · Jean-Yves Blay 1
Baseline / After 5 cycles
Baseline / After 6 cycles
Baseline / After 3 cycles
Baseline / After 3 cycles
Ph1 trial w/INCA33890 👇🏼. Good tolerance and promising efficacy in a 1L MSS #mCRC. Liver & Peritoneal ORR 83% & 62%. HSR 35%, likely related to Oxa. Ph3 RCT undergoing at @QMBCI
#ESMO26 @OncoAlert #ColonCancer https://t.co/ITWJE13rxz https://t.co/H1z9SVes2r
[Slide 1]
INCA33890, a TGFβR2×PD-1 Bispecific Antibody, With Standard of Care (SoC) Anticancer Therapies for Microsatellite Stable Colorectal Cancer (MSS CRC)
Sreenivasa R. Chandana,1 David Berz,2 Kyriakos P. Papadopoulos,3 Martin Gutierrez,4 Justin Moyers,5 Armando Santoro,6 Benedito A. Carneiro,7 Shigehisa Kitano,8 Jordi Rodon,9 Haeseong Park,10 Victor Moreno,11 Toshio Shimizu,12 Mark O'Hara,13 Tatiana Hernandez Guerrero,14 Torben F. Hansen,15 Kristen Spencer,16 Xiaohan Xu,17 Chiara Greggio,18 Thomas B. Karasic,17 Atsuo Takashima19
1START Midwest, Grand Rapids, MI, USA; 2Valkyrie Clinical Trials, Inc. Los Angeles, CA, USA; 3START Center for Cancer Research, San Antonio, TX, USA; 4John Theurer Cancer Center, Hackensack University Medical Center, Hackensack, NJ, USA; 5The Angeles Clinic and Research Institute, A Cedars-Sinai Affiliate, Los Angeles, CA, USA; 6IRCCS Humanitas Research Hospital - Humanitas Cancer Center, Rozzano, Milan, Italy; 7The Legorreta Cancer Center at Brown University, Providence, RI, USA; 8The Cancer Institute Hospital of Japanese Foundation for Cancer Research, Tokyo, Japan; 9The University of Texas MD Anderson Cancer Center, Houston, TX, USA; 10Dana-Farber Cancer Institute, Boston, MA, USA; 11START Madrid-FJD, University Hospital Fundacion Jimenez Diaz, Madrid, Spain; 12Kansai Medical University Hospital, NEXT Oncology KMU Japan, Osaka, Japan; 13Hospital of the University of Pennsylvania, Philadelphia, PA, USA; 14START Barcelona - HM Nou Delfos Hospital, Barcelona, Spain; 15Vejle Hospital, University Hospital of Southern Denmark, Vejle, Denmark; 16Perlmutter Cancer Center of NYU Langone Health, New York, NY, USA; 17Incyte Corporation, Wilmington, DE, USA; 18Incyte International Biosciences Sàrl, Morges, Switzerland; 19National Cancer Center Hospital, 5-1-1 Tsukiji, Chuo-Ku, Tokyo, Japan
Presentation number: 1954RO
[Slide 2]
INCA33890-101 Study Design
INCA33890 Monotherapy1,* | Dose Escalation (N=48) 100-1500 mg q2w and 900 mg q4w IV in continuous 28-day cycles -> RDEs (q2w IV) (300, 600, 900, 1200 mg) -> Dose Expansion (N=236) MSS CRC / PDAC / Gastric / GEJ OC / NSCLC / SCCHN
Dose Escalation† and Expansion in MSS CRC (N=94)
Selected Eligibility Criteria
- Aged ≥18 years
- Diagnosis of advanced or metastatic (stage IV) MSS CRC
- ECOG PS 0 or 1
Primary Endpoints
- Safety and tolerability
- DLTs
Selected Secondary Endpoints
- ORR, DCR, DOR
- PK
INCA33890 (900 mg q2w IV) + FOLFOX‡ + Bev§ | n=43 | No prior systemic therapy
INCA33890 (900 mg q2w IV) + FOLFIRI|| + Bev§ | n=6 | Prior oxaliplatin but no irinotecan
INCA33890 (900 mg q2w IV) + Bev§ | n=39 | Prior fluoropyrimidine, oxaliplatin, and irinotecan
INCA33890 (900 mg q2w IV) + Cetux¶ | n=6 | Prior anti-EGFR inhibitor
[left edge of footnotes cropped] Garralda E, et al. ESMO 2025. Presentation 1522MO.
[..]rollment as of August 26, 2026. *Part 1 of the study investigating INCA33890 monotherapy has been described previously.1 †Dose escalation in part 2 used a statistical hybrid design based on ≥3 DLT-evaluable patients per dose level. ‡Oxaliplatin: 85 mg/m2 IV; [..]covorin: 400 mg/m2 IV (levoleucovorin 200 mg/m2 could be substituted for leucovorin if locally approved); and 5-FU: 400mg/m2 IV bolus (optional) followed by 2400mg/m2 IV infusion. §Dosed at 5 mg/kg q2w. ||Irinotecan: 180 mg/m2 IV; leucovorin: 400 mg/m2 IV [..]oleucovorin 200 mg/m2 could be substituted for leucovorin if locally approved); 5-FU: 400 mg/m2 IV bolus (optional) followed by 2400 mg/m2 IV infusion. ¶Dosed at 500 mg/m2 q2w.
[abbreviations: Bev, bevacizumab; Cetux, cetuximab; DCR, disease control rate; DLT, dose-limiting toxicity; DOR, duration of response; ECOG PS; EGFR; FOLFIRI; FOLFOX; GEJ; IV; MSS CRC; NSCLC; OC, ovarian cancer; ORR; PDAC; PK; q2w; q4w; RDE; SCCHN]
[Slide 3]
Safety: Most Common TEAEs
TEAEs, n (%)* | INCA33890 + FOLFOX + Bev (n=43) Any Grade / Grade ≥3 | INCA33890 + FOLFIRI + Bev (n=6) Any Grade / Grade ≥3 | INCA33890 + Bev (n=39) Any Grade / Grade ≥3 | INCA33890 + Cetux (n=6) Any Grade / Grade ≥3
Neuropathy† | 33 (76.7) / 1 (2.3) | 2 (33.3) / 0 | 0 / 0 | 0 (0) / 0
Neutropenia‡ | 25 (58.1) / 15 (34.9) | 5 (83.3) / 4 (66.7) | 1 (2.6) / 0 | 1 (16.7) / 0
Stomatitis | 20 (46.5) / 3 (7.0) | 3 (50.0) / 1 (16.7) | 11 (28.2) / 1 (2.6) | 3 (50.0) / 0
Nausea | 19 (44.2) / 1 (2.3) | 1 (16.7) / 1 (16.7) | 4 (10.3) / 0 | 3 (50.0) / 0
Diarrhoea | 18 (41.9) / 1 (2.3) | 3 (50.0) / 1 (16.7) | 12 (30.8) / 2 (5.1) | 1 (16.7) / 0
Fatigue | 18 (41.9) / 0 | 4 (66.7) / 0 | 10 (25.6) / 1 (2.6) | 4 (66.7) / 1 (16.7)
Anaemia | 15 (34.9) / 1 (2.3) | 3 (50.0) / 1 (16.7) | 7 (17.9) / 2 (5.1) | 0 (0) / 0
Infusion-related reaction | 15 (34.9) / 1 (2.3) | 2 (33.3) / 0 | 2 (5.1) / 0 | 0 (0) / 0
Related to INCA33890 | 3 (7.0) / 0 (0) | 2 (33.3) / 0 | 2 (5.1) / 0 | 0 (0) / 0
Related to SoC | 12 (27.9)§ / 1 (2.3) | 0 / 0 | 1 (2.6)¶ / 0 | 0 (0) / 0
Vomiting | 14 (32.6) / 0 | 1 (16.7) / 0 | 4 (10.3) / 0 | 4 (66.7) / 0
Leukopenia | 13 (30.2) / 2 (4.7) | 4 (66.7) / 3 (50.0) | 0 / 0 | 0 (0) / 0
Decreased appetite | 12 (27.9) / 1 (2.3) | 3 (50.0) / 1 (16.7) | 6 (15.4) / 0 | 0 (0) / 0
Hypertension | 12 (27.9) / 4 (9.3) | 0 / 0 | 4 (10.3) / 1 (2.6) | 0 (0) / 0
*TEAEs listed are those occurring in ≥25% of the INCA33890 + FOLFOX + Bev group and ordered by frequency in the INCA33890 + FOLFOX + Bev group. †Neuropathy peripheral includes neuropathy peripheral, peripheral sensory neuropathy, and paraesthesia. ‡Neutropenia includes neutropenia and neutrophil count decreased. §11 related to oxaliplatin and 1 related to Bev. ¶Related to Bev.
Bev, bevacizumab; Cetux, cetuximab; FOLFIRI, folinic acid, fluorouracil, and irinotecan; FOLFOX, folinic acid, fluorouracil, and oxaliplatin; SoC, standard of care; TEAE, treatment-emergent adverse event.
[Slide 4]
Efficacy: 1L INCA33890 + FOLFOX + Bev
| | Efficacy evaluable (n=42) |
| ORR, n (%) | 30 (71.4) |
| cORR, n (%) | 28 (66.7)* |
| DCR, n (%) | 42 (100) |
| 6-month PFS, % | 81.4 |
| Subgroup | ORR, n/N (%) |
| Liver mets | 24/29 (82.8) |
| Peritoneal inv | 8/13 (61.5) |
| PD-L1 TAP ≥1% | 21/26 (80.8) |
| PD-L1 TAP <1% | 3/6 (50.0) |
| Right sided | 11/12 (91.7) |
| Left sided | 18/28 (64.3) |
[Waterfall plot: Best Percentage Change From Baseline in Sum of Diameters of Target Lesions; legend: Liver metastasis / No liver metastasis / Ongoing / + PD-L1 TAP ≥1%; -30 threshold line]
All responses were PRs
Median follow-up of 5.6 months. *1 pending follow-up scan; 1 with target lesion removal (primary tumour resection due to intestinal obstruction, follow-up nonevaluable by RECIST).
Bev, bevacizumab; cORR, confirmed objective response rate; DCR, disease control rate; FOLFOX, folinic acid, fluorouracil, and oxaliplatin; inv, involvement; mets, metastases; NA, not available; ORR, objective response rate; PD, progressive disease; PD-L1 TAP, programmed death-ligand 1 tumour area positivity; PFS, progression-free survival; PR, partial response; RECIST, Response Evaluation Criteria in Solid Tumours.
FES-PET defined heterogeneity is associated with long-term survival
#ESMO26
#ESMOAmbassadors
#ESMOcommunity
@myESMO @ALEDIGNUS12 https://t.co/dbSDstWNoT
PROGRESSION-FREE AND OVERALL SURVIVAL
Median Progression-free survival
Group A: 18.1 months (95%CI 11.3-25.3) | Group B/C: 12.0 months (95%CI 6.6-22.9)
HR 1.36 (95%CI 0.88-2.10); p=0.162
Progression-free survival (%) ; Years 0-11
No. at Risk (No. Cumulative Censors)
Group A | 92 (0) | 53 (0) | 39 (0) | 29 (0) | 25 (0) | 21 (1) | 11 (6) | 9 (7) | 7 (9) | 4 (12) | 2 (14) | 0 (16)
Group B+C | 31 (0) | 16 (0) | 9 (0) | 7 (0) | 6 (0) | 3 (1) | 2 (2) | 1 (2) | 0 (3)
Median Overall survival
Group A: 69.6 months (95% CI, 48.3-85.1) | Group B/C: 42.5 months (95% CI, 27.0-70.4)
HR = 1.87 (95% CI 1.16–3.01); p = 0.010
Overall survival (%) ; Years 0-11
No. at Risk (No. Cumulative Censors)
Group A | 92 (0) | 90 (0) | 80 (1) | 70 (1) | 57 (2) | 48 (5) | 33 (12) | 26 (15) | 21 (17) | 11 (27) | 5 (32) | 0 (36)
Group B+C | 32 (0) | 28 (1) | 23 (1) | 17 (1) | 14 (1) | 11 (2) | 8 (3) | 3 (5) | 2 (6) | 0 (7)
Gennari A.
Survival table
Endpoint: PFS and OS (two panels)
Arm | N | Median | Median CI
Group A (PFS) | 92 | 18.1 months | 11.3-25.3
Group B/C (PFS) | 31 | 12.0 months | 6.6-22.9
Group A (OS) | 92 | 69.6 months | 48.3-85.1
Group B/C (OS) | 32 | 42.5 months | 27.0-70.4
HR: PFS 1.36; OS 1.87
HR CI: PFS 0.88-2.10; OS 1.16–3.01
P: PFS 0.162; OS 0.010
Amazing talk on RAS biology in the ESMO-EACR session #ESMO26 by @AmbrogioLab
From scarcity to abundance 🎯 RAS
From bench to bedside and back
Multiple questions are now opened!🤔
#ESMOAmbassadors @myESMO @GrupoTTD @_SEOM https://t.co/QAcHelGIQf
Validation is crucial
INTRINSIC
• KEAP1, SMARCA4 and CDKN2A as major independent determinants of inferior clinical outcomes with KRAS G12Ci monotherapy
Negrao MV et al. Cancer Discov 2023
ACQUIRED
• Selection of pre-existing clones with increased fitness on drug treatment
• De novo alterations
Awad M, et al. N Engl J Med 2021;384:2382-93; Tanaka N, et al. Cancer Discov 2021;11:1913-22; Zhao Y, et al. Nature 2021
ADAPTIVE
• Synthesis of GTP-bound KRASG12C
• Adaptive activation of wild-type RAS
Xue J, et al. Nature 2020;577:421-5; Hata A, et al. Nature Medicine 2020; Ryan MB, Cell Reports, 2022
X
[Chart: RAS inhibitors in clinical development - columns Terminated / Phase 1 / Phase 2 / Phase 3 / Approved; individual drug names [illegible]]
= n (high) of therapeutic strategies requiring validation
Ambrogio Lab
Very informative session on Concepts in Precision Oncology chaired by Dr. Oh discussions on next-generation ADC strategies, innovative clinical trial designs, and how precision medicine continues to reshape oncology drug development. #ESMO2026 #PrecisionOncology #ADC https://t.co/iUYHqj6Ppg
[Slide 1]
Proposed new model for drug development (I)
DOSE-ESCALATION: DL 1 → DL 2 → DL 3 → DL 4 → DL 5 → DL 6
Minimal Reproducibly active dose
DOSAGE-RANGING STUDY: RANDOMISATION → DL 6 / DL 5 / DL 2
• STANDARD TOXICITY-BASED DOSE-ESCALATION
• BASED ON TOTALITY OF DATA (INCLUDING EFFICACY) - SELECTED AS RECOMMENDED DOSAGE RANGE (RDR)
• RANDOMISATION TO COMPARE RDR DOSES
• SELECTED FOR FURTHER DRUG-DEVELOPMENT BASED ON THE TOTALITY OF THE DATA
Totality of the data: 1. Safety 2. PK 3. PD 4. Clinical Activity 5. ctDNA
Higher dose will likely be MTD; challenge is picking lower dose
Araujo D et al (MDICT), Ann Oncol 2022
Elena Garralda, MD PhD
[Slide 2]
ADCs: Where dose the medicine go?
Only 0.1%-2% (average <1%) actually reaches the targeted tumor site
Colombo R et al, Cancer Discov 2024
99%: Where dose the rest go?
-Systemic circulation : prolonged half-life leads to premature payload shedding (linker instability)
-Hepatic & Splenic Clearance: Non-specific uptake by the liver and spleen (macrophages/FcRN-mediated) causes off-target toxicities
-Perivascular lock :high affinity causes the ADC to get trapped at the outer rim of the tumor blood vessels, failing to penetrate the core
Biological requirement: Payload must be 100x to 1000x more potent than conventional chemotherapy to achieve a therapeutic threshold
Paradigm shift: -Cannot achieve a better therapeutic window by simply increasing the dose -Need ' New Strategy' to bypass 1% barrier
Do-Youn Oh, MD, PhD
[Slide 3]
Paradigm Shifts in ADC Therapeutics
➢ Newly disclosed ADC assets from AACR 2026 [Trends from AACR 2026]
119 New ADC assets
✓ Traditional ADCs : 41%
✓ Bispecific ADCs: 40%
✓ Dual-payload ADCs: 11%
1. ADC innovation is shifting beyond target discovery
- 75 distinct targets from single-target ADCs, 61 distinct target pairs from dual-targeting ADCs
2. Broader shift toward platform-driven and engineering-driven innovation
- Next-gen payloads (pan-RAS inhibitors, cell-cylce checkpoint inhibitors, STING agonist, protein degraders), immune-enabled designs, complex ADC constructs
3. Dual-targeting and immune-enabled ADCs designs are highlighting
Do-Youn Oh, MD, PhD
[Slide 4]
AI-based augmentation of oncology clinical trials
Pre-trial applications:
- Trial feasibility and site selection (for example, DeepTrial)
- Refinement of eligibility criteria selection (for example, Trial Pathfinder)
- AI-assisted protocol development (for example, automated first-draft generation)
- Synthetic data and synthetic control arms (for example, in trials in haematological malignancies)
- Trial outcome prediction and simulation (for example, TrialGenie)
Within-trial operations:
- Patient–trial matching (for example, Matchminer)
- Automated eligibility verification
- Adaptive dose optimization (for example, CURATE.AI)
- EHR data extraction and structuring (for example, ExtractEHR)
- Remote patient monitoring (for example, LSTM)
- Response-adaptive patient randomization (for example, I-SPY2)
Post-trial inference and generalization:
- Assessment of trial result generalizability (for example, TrialTranslator)
- Target-population trial emulation
- Digital twins (for example, QSP-based virtual populations)
Key stakeholders: Patients and patient advocacy groups; Clinical investigators and trial sites; Sponsors
Villa et al. Nat Rev Clin Oncol 2026
Elena Garralda, MD PhD
#ESMO26 🧬 LBL-024-CN002 | Phase Ib/II
👥 69 pts | 1L advanced EP-NEC
💊 Opamtistomig (PD-L1×4-1BB) + platinum/etoposide
🎯 cORR: 60% | DCR: 90.8%
📈 mOS: Not reached
⏳ 18-mo OS: 55.7%
🔬 Higher ORR without liver mets: 70.4% vs 47.6%
⚠️ G≥3 TRAEs: 79.7%
⚠️ 2 treatment-related deaths
💡 Encouraging activity; randomized confirmation needed!
@OncoAlert
[Slide 1]
LBL-024-CN002 Study Design
The efficacy, safety and PK/PD profile of opamtistomig combined with chemotherapy as first-line treatment in patients with advanced NEC was evaluated in a multi-center phase Ib/II trial.
Phase Ib: Dose escalation | Phase II: Dose optimization; Dose expansion
Key inclusion criteria: Histologically and/or cytologically confirmed NEC with no previous Systemic treatment
Opamtistomig (6 mg/kg)+EP/EC n=3~6; Opamtistomig (10 mg/kg)+EP/EC n=3~6; Opamtistomig (15 mg/kg)+EP/EC n=3~6
R 1:1 — Arm 1 (n=20): Opamtistomig (6 mg/kg)+EP/EC; Arm 2 (n=20): Opamtistomig (15 mg/kg)+EP/EC
Opamtistomig (15 mg/kg)+EP/EC; n ≤ 30
Proceed treatment until • Occurrence of PD or • Intolerance or • Continuous treatment for up to 2 years. Continuously follow-up on survival status
Opamtistomig: IV, Q3W.
EP Regimen: Etoposide:100 mg/m², IV, day1-3, Cisplatin: 75 mg/m², IV, day1, Q3W, up to 6 cycles.
EC Regimen: Etoposide:100 mg/m², IV, day1-3, Carboplatin: AUC 5mg/mL/min, IV, day1, Q3W, up to 6 cycles.
Phase I Endpoints: Primary: DLT, AE, SAE; Secondary: ORR, DCR, DoR, PFS, OS per RECIST1.1; PK; ADA; Biomarker
Phase II Endpoints: Primary: ORR per RECIST1.1; Secondary: DLT, AE, SAE, lab abnormality; DCR, DoR, PFS, OS per RECIST1.1 and iRECIST; ADA; Biomarker
Panpan Zhang
[Slide 2]
Efficacy
Durable and deep remission observed in EP-NEC
Waterfall: Best change from baseline (%); 6 mg/kg, 10 mg/kg, 15 mg/kg
Swimmer plot: Overall survival in months; Ongoing, CR, PR, SD, PD; 6 mg/kg, 10 mg/kg, 15 mg/kg
Cutoff date: June 30, 2026.
Panpan Zhang
[Slide 3]
Efficacy
Overall survival (FAS)
As of June 30, 2026, 69 patients with EP-NEC had been enrolled, with a median follow-up duration of 21.2 months, mOS was not reached.
Overall Survival Kaplan-Meier Curve; +Censored; 6 mg/kg, 15 mg/kg; OS Probability; Overall Survival Time (month)
| Parameters | Total (N=69) | 6 mg/kg (N=23) | 15 mg/kg (N=40) |
OS events
| Deaths, n (%) | 30 (43.5) | 9 (39.1) | 18 (45.0) |
| Censored, n (%) | 39 (56.5) | 14 (60.9) | 22 (55.0) |
| Median OS months (95% CI) | NE (12.5-NE) | NE (10.7-NE) | NE (8.1-NE) |
| 18-m OS rate % (95% CI) | 55.7 (43.1-66.6) | 60.9 (38.3-77.4) | 54.0 (37.3-68.0) |
OS, overall survival; CI, confidence interval.
Cutoff date: June 30, 2026.
Panpan Zhang
Survival table
Endpoint: OS (FAS), EP-NEC
Arm | N | Median | Median CI
Total | 69 | NE | 12.5-NE
Opamtistomig 6 mg/kg + EP/EC | 23 | NE | 10.7-NE
Opamtistomig 15 mg/kg + EP/EC | 40 | NE | 8.1-NE
18-m OS rate: Total 55.7% (43.1-66.6); 6 mg/kg 60.9% (38.3-77.4); 15 mg/kg 54.0% (37.3-68.0)
[Slide 4]
Safety
Opamtistomig plus EP/EC was well tolerated with a manageable safety profile
| | 6 mg/kg, n (%) (n=23) | 10 mg/kg, n (%) (n=6) | 15 mg/kg, n (%) (n=40) | EP-NEC Total, n (%) (N=69) |
| Any TEAEs | 23 (100.0) | 6 (100.0) | 40 (100.0) | 69 (100.0) |
| Treatment-related | 22 (95.7) | 6 (100.0) | 40 (100.0) | 68 (98.6) |
| ≥Grade 3 TEAEs | 22 (95.7) | 5 (83.3) | 34 (85.0) | 61 (88.4) |
| Treatment-related | 20 (87.0) | 5 (83.3) | 30 (75.0) | 55 (79.7) |
| SAEs | 16 (69.6) | 3 (50.0) | 25 (62.5) | 44 (63.8) |
| Treatment-related | 13 (56.5) | 3 (50.0) | 15 (37.5) | 31 (44.9) |
| irAEs | 11 (47.8) | 2 (33.3) | 13 (32.5) | 26 (37.7) |
| ≥Grade 3 | 4 (17.4) | 2 (33.3) | 6 (15.0) | 12 (17.4) |
| TRAEs leading to opamtistomig treatment discontinuation# | 1 (4.3) | 0 (0.0) | 3 (7.5) | 4 (5.8) |
| TRAEs leading to death* | 0 (0.0) | 0 (0.0) | 2 (5.0) | 2 (2.9) |
# One patient had grade 3 immune-mediated myocarditis, one had grade 2 pulmonary infection, one had grade 3 hearing impairment and grade 3 muscle weakness of both lower extremities, and one had grade 3 nervous system injury.
*One patient experienced respiratory failure, septic shock and pulmonary embolism, and another had cardiopulmonary arrest.
TEAE, treatment-emergent adverse event; SAE, serious adverse event; irAE, immune-related adverse event; TRAE, treatment-related adverse event.
Cutoff date: June 30, 2026.
Panpan Zhang
Dr @BlondeauxEva amazing on the stage of #ESMO26 on new clinical #endpoints to capture patient-centric benefit in clinical trials!
#ESMOAmbassadors
@myESMO #MCBS session https://t.co/Vtj5RAykc8
Non-scorable endpoints with ESMO-MCBS V2.0
Curative setting | Non-curative setting
Organ preservation | Time to treatment failure
*-ectomy or stoma free survival | Surgical resection/conversion
Locoregional control | Metastasis free survival
Locoregional recurrence free survival | Biochemical progression free survival
Biochemical recurrence free survival | PFS2
Minimal residual disease |
* laryngectomy, cystectomy, mastectomy etc.
Eva Blondeaux
Happening now ! Opening ceremony of #ESMO2026 in Madrid. @OncoAlert @NCCS_SG @RebeccaDSing https://t.co/c4o9uv6a59
Investing in research and people
30 Committees, task forces and working groups to support members
30+ one-year Fellowships, including new ESMO Artificial Intelligence Fellowship
New Clinical Trial Funding initiative to support independent academic clinical research
Support to the International Cancer Foundation (ICF)
[Podium sign] ESMO congress MADRID SPAIN 23-27 OCTOBER 2026
TOMAS2: PARP1 H-score as a Potential Biomarker for Trabectedin + Olaparib in Sarcoma
@OncoAlert #ESMO26 #ESMOAmbassadors #ESMOcommunity @myESMO https://t.co/MfkvyTcLcm
[Slide 1]
MADRID 2026 ESMO congress
Quantitative PARP1 H-score evaluation as a predictive biomarker for trabectedin plus olaparib combination in advanced soft tissue sarcoma: an exploratory analysis of the TOMAS2 study
Lorenzo D'Ambrosio*, M. Rabino, L. Righi, G. Impalà, A. Brunello, V. Ferraresi, A. Paioli, B. Vincenzi, M.A. Pantaleo, T.M. De Pas, L. Gurrieri, R. Sanfilippo, A. Buonadonna, G.G. Baldi, G. Badalamenti, C. Marchiò, A.P. Dei Tos, S. Stacchiotti, A. Merlini, G. Grignani
*Department of Oncology – University of Turin
AOU San Luigi Gonzaga – Orbassano (TO), Italy
26 October 2026
[Slide 2]
Conclusions
This exploratory analysis of the TOMAS2 study further supports PARP1 expression as a candidate predictive biomarker for trabectedin and olaparib combination.
Patients with H-score ≥70 showed the greatest benefit from the combination.
PARP1 expression may guide patient selection in future trials combining new ecteinascidins and PARP1i.
The proposed PARP1 assessment criteria are undergoing external validation to strengthen their use as a biomarker in future trials.
Lorenzo D'Ambrosio MD PhD
[Slide 3]
PFS according to PARP1 H-score - uLMS
PARP1 H-score <70
PARP1 H-score ≥70
arm: trabectedin; trabectedin + olaparib; trabectedin-censored; trabectedin + olaparib-censored
Progression-free Survival probability
Time from randomization (months)
H-score <70 | Median PFS months (95%CI) | PFS@6m (95%CI) | PFS@12m (95%CI) | HR
Trabectedin + olaparib (N=4) | 1.3 (0.8-1.7) | 0% | 0% | 11.0 (1.17-102.6) p=0.036
Trabectedin (N=5) | 4.0 (3.9-4.1) | 40% | 0%
H-score ≥70 | Median PFS months (95%CI) | PFS@6m (95%CI) | PFS@12m (95%CI) | HR
Trabectedin + olaparib (N=8) | 16.3 (3.1-NR) | 62.5% | 62.5% | 0.15 (0.04-0.62) p=0.009
Trabectedin (N=6) | 1.35 (0.3-NR) | 16.7% | 0%
Lorenzo D'Ambrosio MD PhD
Survival table
Endpoint: PFS by PARP1 H-score, uterine leiomyosarcoma (exploratory)
Arm | N | Median | Median CI
H<70 Trabectedin + olaparib | 4 | 1.3 | 0.8-1.7
H<70 Trabectedin | 5 | 4.0 | 3.9-4.1
H≥70 Trabectedin + olaparib | 8 | 16.3 | 3.1-NR
H≥70 Trabectedin | 6 | 1.35 | 0.3-NR
HR: H<70: 11.0; H≥70: 0.15
HR CI: H<70: 1.17-102.6; H≥70: 0.04-0.62
P: H<70: p=0.036; H≥70: p=0.009
H<70 PFS@6m 0% vs 40%; PFS@12m 0% vs 0%
H≥70 PFS@6m 62.5% vs 16.7%; PFS@12m 62.5% vs 0%
[Slide 4]
PFS according to PARP1 H-score - all STS
PARP1 H-score <70
PARP1 H-score ≥70
arm: trabectedin; trabectedin + olaparib; trabectedin-censored; trabectedin + olaparib-censored
Progression-free Survival probability
Time from randomization (months)
H-score <70 | Median PFS months (95%CI) | PFS@6m (95%CI) | PFS@12m (95%CI) | HR
Trabectedin + olaparib (N=22) | 2.9 (1.9-3.8) | 31.8% | 13.6% | HR 1.12 (0.60-2.09) p=0.722
Trabectedin (N=21) | 4.0 (0.8-7.2) | 31.2% | 5.2%
H-score ≥70 | Median PFS months (95%CI) | PFS@6m (95%CI) | PFS@12m (95%CI) | HR
Trabectedin + olaparib (N=33) | 4.3 (3.1-9.8) | 40.6% | 28.1% | 0.49 (0.29-0.83) p=0.008
Trabectedin (N=30) | 2.5 (1.5-3.1) | 26.7% | 7.6%
Lorenzo D'Ambrosio MD PhD
Survival table
Endpoint: PFS by PARP1 H-score, all soft tissue sarcoma (exploratory)
Arm | N | Median | Median CI
H<70 Trabectedin + olaparib | 22 | 2.9 | 1.9-3.8
H<70 Trabectedin | 21 | 4.0 | 0.8-7.2
H≥70 Trabectedin + olaparib | 33 | 4.3 | 3.1-9.8
H≥70 Trabectedin | 30 | 2.5 | 1.5-3.1
HR: H<70: 1.12; H≥70: 0.49
HR CI: H<70: 0.60-2.09; H≥70: 0.29-0.83
P: H<70: p=0.722; H≥70: p=0.008
H<70 PFS@6m 31.8% vs 31.2%; PFS@12m 13.6% vs 5.2%
H≥70 PFS@6m 40.6% vs 26.7%; PFS@12m 28.1% vs 7.6%
Practical and insightful AI in oncology session at #ESMO26 👏
@ca_chung @markowetzlab @evangelia_chris @jnkath @DanielTruhn @polimi @myESMO https://t.co/if7m9BoUnf
[slide photographed at an angle; top-left of title cut off]
[...] clinic: goals of deployment
[...]pective validation to biomarker-stratified randomised trials
1 Validation
• Lock thresholds, test archived cohorts
• Analytical and clinical validity
2 Test comparison
• Same samples, head-to-head
• CHORD, Myriad, HRDetect
3 NHS pathway study
• Live use under the QMS
• Pre-specified analysis plan
4 Stratified RCT
• CIN-guided vs standard of care
• Evidence for NHS adoption
Existing methods for comparison
Method | Features | Assay input
CIN signatures (Drews 2022) | 17 copy-number signatures | Copy-number profiles
CHORD | SNV, indel and SV signatures | Whole-genome sequencing
HRDetect | Six HRD-associated signatures | Whole-genome sequencing
Myriad myChoice CDx | LOH, TAI, LST plus BRCA1/2 | Proprietary tumour assay
Drews RM et al. A pan-cancer compendium of chromosomal instability. Nature 2022
New preliminary data #nabpaclitaxel and #liposomaldoxorubicin in #vasculartumours presented by Prof #XinZhang of #SYSUCC in Guangzhou, China. Impressive responses seen in selected pts of EHE, Angiosarcoma and in the overall group. More to explore.
@ctosociety #ESMO26 @myESMO #ESMOAmbassadors
08:30 - 10:00 Rapid oral: Sarcoma
CHAIRS: MARK DICKSON, PALMA DILEO, CESAR SERRANO
Background
Malignant vascular tumors are rare diseases with diverse histologic subtypes
AS EHE KS
For advanced, or unresectable disease, anthracyclines and taxanes remain major chemotherapy options, but response and durability are limited
NCCN Guidelines Version 3.2026 Soft Tissue Sarcoma
Regime | ORR | PFS
Anthracyclines | ~30% | ~4 mo
Paclitaxel | ~20% | ~4 mo
Pegylated liposomal doxorubicin
Prolonged circulation time
Preferential accumulation in tumors
Reduced cardiotoxicity
DNA damage
Nab-paclitaxel
Paclitaxel Molecule
Enhanced drug delivery to tumors
Sustained intratumoral exposure
Convenient administration
Microtubule inhibition
Potential synergistic/complementary tumor killing
A rational combination of complementary cytotoxic mechanisms with potentially improved tumor delivery and tolerability
AS: Angiosarcoma; EHE: Epithelioid haemangioendothelioma; KS: Kaposi sarcoma
Xing Zhang
Excellent lecture by @EANOassociation past president Michael Platten, followed by an engaging discussion led by Lakshmi Nayak, on immunomodulatory strategies for GBM, from vaccines to CAR T cells. The best is yet to come!.
#ESMO26 #NeuroOncology
@EANOassociation https://t.co/5rq8HRLThs
Immune Modulating Approaches in Neurooncology
[Schematic of engineered T cell, native T cell and malignant cell; labels: PD1, TCR, Engineered T cell, CAR, BiTE®, CD3, Native T cell, CTLA-4, Immune checkpoint inhibitors, MHC I/II, PD-L1, PD-L2, CD19, Naked mAb, ADC, CD19 CD20 CD22, Malignant cell]
Targets: IL13Ra2, EGFRvIII, Her2, GD2, EphA3, B7-H3, CD70, NKG2D, CLTX, GPNMB, CLTX, PTPRZ1, uPAR, ...
PRAME, PTPRZ1
Ipilimumab, Tremelimumab
Nivolumab, Pembrolizumab, Cemiplimab
Atezolizumab, Durvalumab, Avelumab
Virotherapy
Immunocytokines
Vaccines
Adapted from Batlevi et al. 2015, Nat Rev Clin Oncol
🚨 #ESMO26 | Can IO make surgery unnecessary in cSCC? MATISSE-2: 41 pts with resectable cSCC received neoadjuvant nivo/ipi → nivo
▪️ 25/41 (61%) achieved clinical CR
▪️ No surgery, RT or maintenance therapy in responders
▪️ Median time to cCR: ~ 2 months
▪️ G3–4 immune toxicity: 17%
▪️ No surgical delays or unresectable disease in non-responders
But an important caveat from the discussion: clinical CR may not equal pathological CR….and median follow-up is still only 11 months ☝🏼
A potentially practice-changing concept, but I think we need to know whether “no visible tumour” can safely become “no surgery”!!
MATISSE may be teaching us that sometimes the best surgical masterpiece is the one you never have to paint 🤔
@OncoAlert @OncoReporte @myESMO @_SEOM
[Slide 1]
MATISSE 2 trial design
NETHERLANDS CANCER INSTITUTE ANTONI VAN LEEUWENHOEK
N = 41
- Stage I-IVa M0 CSCC
- UV-related
- Indication for morbid or extensive surgery +/- adjuvant RT
→ NIVO 3 mg/kg IPI 1 mg/kg → NIVO 3 mg/kg → Response evaluation
→ Responder: Strict and multi-tiered 2 years FU
→ Non-responder: Standard of care Surgery +/- adjuvant RT 2 years FU
Week -2 to 0 — Week 0 — Week 2 — Week 5 — Week 6
Primary endpoint: Percentage of clinical complete remissions at 24 months of follow-up after only immunotherapy, without standard of care surgery and RT
S.W. van Dijk, MD & C.L. Zuur, MD PhD
[Slide 2]
Response evaluation
Clinical examination
[18F]FDG-PET/CT imaging
Ultrasound / FNAC
Multicenter Multidisciplinary Meeting
Tumour board in favour of response → Multi-tiered FU
Tumour board in favour of non-response → Surgery ± RT
S.W. van Dijk, MD & C.L. Zuur, MD PhD
[Slide 3]
Preliminary results:
25/41 (61%) patients reached a clinical complete remission after only neoadj. NIVO/IPI, without surgery & without RT & without maintenance immunotherapy (median FU 11 mo)
[Waterfall plot: Clinical responses | Pathological responses; y-axis Pathological or clinical response 0% to -100%; x-axis Patient]
Clinical: Complete response; Partial response; Clinical progressive disease
Pathological: Complete; Partial response; No response
S.W. van Dijk, MD & C.L. Zuur, MD PhD
Congrats and thanks #YanningXu for presenting our collaborative @apoddc work on #regulatorydelays and #reimbursement at @myESMO #ESMO26!
#ValerieHeong #BenTran @fredtingmd #DanielTan @teamoncology #VoonPeiJye #DaphneDay @ToshioShim1025 #TakafumiKoyama #MichelleWilson #ThalVo and many others.
APODDC
ASIA PACIFIC ONCOLOGY DRUG DEVELOPMENT CONSORTIUM
FPN: 3373P
Regulatory Delays and Reimbursement of Cancer Therapies in Asia-Pacific
Authors
Nadia Hitchen*1,2, Yanning Xu*3, Bharath Vedavyas Kamanat 4, Sophie O'Haire2, William Harris1, Michelle Wilson5, Takafumi Koyamaâ, Naiyarat Prasongsook7, Tawasapon Thambamroong7, Boon Phiaw Kho8, Frederic Ivan Ting9, Thao Vo10, Ka Hei (Judy) Chan11, Jinyong Kim12, Pei Jye Voon8, Valerie Heong3, Naoto T. Ueno13, Daniel Tan14, Herbert Loong11, Ben Tran1,2
Affiliations
1 Department of Medical Oncology, Peter MacCallum Cancer Centre, Melbourne, Australia
2 Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia
3 Department of Medical Oncology, Tan Tock Seng Hospital, Singapore, Singapore
4 Department of Internal Medicine, Tan Tock Seng Hospital, Singapore, Singapore
5 Auckland City Hospital and University of Auckland, Auckland, New Zealand
6 Department of Experimental Therapeutics, National Cancer Center Hospital, Tokyo, Japan
7 Division of Oncology, Department of Medicine, Phramongkutklao Hospital and College of Medicine, Bangkok, Thailand
8 Department of Medical Oncology, Hospital Umum Sarawak (Sarawak General Hospital), Universiti Malaysia Sarawak (UNIMAS)
9 College of Medicine, University of St La Salle, Bacolod City, Philippines
10 Department of Medical Oncology, Franco-Vietnamese Hospital (FV Hospital), Vietnam
11 Department of Clinical Oncology, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong SAR
12 Division of Hematology-Oncology, Samsung Medical Center, Seoul, Korea
13 Translational and Clinical Research Program, University of Hawai'i Cancer Center, USA
14 Division of Medical Oncology, National Cancer Centre Singapore, Singapore
Background
The Asia-Pacific region accounts for almost half of global cancer mortality, yet access to systemic therapies remains variable. The Asia-Pacific Oncology Drug Development Consortium (APODDC) evaluated regulatory approval delays relative to the US FDA and reimbursement patterns.
Methods
Systemic therapies approved by the US FDA (2020–2025) or recommended in ESMO guidelines (to December 2025) were identified for the three most prevalent cancers in each APODDC country: Australia, New Zealand, Japan, South Korea, Singapore, Hong Kong, Malaysia, Thailand, Vietnam and the Philippines. For each drug-indication pair, tumour type, class, novel vs label extension, treatment intent and ESMO Magnitude of Clinical Benefit Scale (MCBS) score were recorded. Regulatory delay, approval status and reimbursement (high [full/national NHI], moderate [partial/mixed] or low [self-pay]) were analysed.
Results
Eighty-one medicines and 171 indications were identified (Figure 1): 34 (20%) novel and 137 (80%) label extensions (Table 1). Targeted therapies (48%) predominated. Approval rates varied widely across countries, from 29/81 medicines in Vietnam to 71/81 in South Korea (Figure 2). Reimbursement was high in Japan, South Korea and Australia, and largely self-funded (low) elsewhere (Figure 3). Six countries used molecule-based and four indication-based systems .GDP per capita likely influences regulatory delays (Figure 4). In high-income settings, delays were similar for novel agents and label extensions; in lower-resourced settings, novel agents were faster. No prioritisation of regulatory delay was observed by tumour type, class, intent or ESMO-MCBS (Figure 5a-c).
Table 1: Whole cohort summary (n=171)
Cohort characteristics (N = 171 drug–indication pairs)
Category | Level | n (%)
Therapeutic class (MOA) | Targeted | 82 (48.0%)
| Immunotherapy | 51 (29.8%)
| Hormone | 14 (8.2%)
| ADC | 10 (5.8%)
| Cytotoxic chemotherapy | 7 (4.1%)
| Other | 7 (4.1%)
Tumour type | Lung | 57 (33.3%)
| Breast | 30 (17.5%)
| Prostate | 21 (12.3%)
| Colorectal | 16 (9.4%)
| Liver | 14 (8.2%)
| Melanoma | 13 (7.6%)
| Gastric | 10 (5.8%)
| Agnostic | 6 (3.5%)
| Pancreas | 4 (2.3%)
Treatment intent | Non-curative / palliative | 144 (84.2%)
| Curative | 27 (15.8%)
ESMO-MCBS grade | High | 90 (52.6%)
| Low | 81 (47.4%)
Approval type | Label extension | 137 (80.1%)
| Novel agent | 34 (19.9%)
ESMO guideline representation | In ESMO guideline | 152 (88.9%)
| Not in ESMO guideline | 19 (11.1%)
Figure 1. Study Methodology and Cohort Selection Flow Diagram
Figure 2. Geographic Distribution of Oncology Drug Approvals Across the Asia-Pacific Region (N = 81)
Figure 3. Reimbursement Status by Country
Figure 4. Association Between GDP per Capita (PPP) and Median Regulatory Delay Across APAC Countries
Figure 5a. Approval Rate and Regulatory Delay by ESMO-MCBS Grade (High vs. Low Clinical Benefit)
Figure 5b. Indication-Level Approval Rates in Singapore, South Korea, Japan, and Australia (N = 171)
Figure 5c. Regulatory Delay to Indication Approval by Country and ESMO-MCBS Grade - Box-and-Whisker Plots (Singapore, South Korea, Japan, Australia)
Conclusions
Regulatory approval delays and reimbursement of cancer medicines varied substantially across Asia-Pacific and were poorly aligned with clinical benefit. Regulatory reliance and harmonised reimbursement frameworks may reduce delays and improve equitable access.
*The authors declare no conflicts of interest.
Correspondence: yanning.xu@mohh.com.sg
@NatureMedicine 2/ Rather than broad CD3 activation, invika selectively engages Vβ6/Vβ10 T cells (~10% of TILs), binding their TCR and IL-2 receptor in cis. In 52 heavily pretreated patients, no MTD was reached, and T cell expansion peaked at 0.08–0.12 mg/kg, supporting 0.08 mg/kg as the RP2D. https://t.co/RrUxAuoiX7
[Slide 1]
e
T cell expansion in periphery: Baseline 6.8% → Day 8 50.983%
T cell expansion in tumor: Baseline 11.9% → Day 21 41.99%
Vβ6 T cells
Vβ10 T cells
Other Vβ cells
[Slide 2]
f
CD3+ CD8+ CD25+ Baseline
CD3+ CD8+ CD25+ Day 21
#ESMO26 🧬 RINGSIDE | Phase III
💊 Varegacestat vs placebo
👥 Progressive desmoid tumors (n=156)
📈 PFS: HR 0.16
🎯 ORR: 55.7% vs 9.1%
📊 Patient-reported outcomes:
✅ Pain ↓ from Week 4
✅ Sustained symptom improvement
✅ Better physical function (PROMIS)
💡 Beyond tumor control: meaningful benefits for patients!
@OncoAlert
[Slide 1]
08:30 - 10:00 Rapid oral: Sarcoma
CHAIRS: MARK DICKSON, PALMA DILEO, CESAR SERRANO
RINGSIDE Met all Primary and Key Secondary Endpoints
Primary Endpoint
84% reduction in the risk of radiographic disease progression or death with Varegacestat vs. Placebo
Hazard ratio: 0.16, p-value <0.0001
Key Secondary Endpoints
55.7% ORR in Varegacestat vs 9.1% with Placebo
p-value <0.0001
-109.6 cm3 reduction in tumor volume with Varegacestat vs +122.8 cm3 increase with Placebo at Week 24
-83% best percent change in tumor volume
Difference: -232.4, p-value <0.0001
Key Secondary Endpoint
-2.24 point reduction in WPI with Varegacestat vs +0.18 point increase with Placebo at Week 12
Difference: -2.42, p-value <0.0001
Change in Worst Pain Intensity Score (WPI)
Placebo / Varegacestat
Worsening / Improving
LS Mean Change from Baseline
Analysis Visit (Weeks)
PRO Completion Among Patients with Baseline Data
Varegacestat 72 64 61 52 46 48 47 46 42 45 41 38 37
Placebo 71 62 58 55 50 42 43 35 33 31 29 28 27
As measured by LS mean in WPI as measured by item 1 in GODDESS DTSS
Presented By: Winette van der Graaf, MD, PhD
Winette van der Graaf
Patient reported outcomes (PROs) with varegacestat versus placebo (PBO) in progressing desmoid tumors: Results from RINGSIDE Part B
MALAGA AUDITORIUM - HALL 3
[Slide 2]
08:30 - 10:00 Rapid oral: Sarcoma
CHAIRS: MARK DICKSON, PALMA DILEO, CESAR SERRANO
Varegacestat Reduces Pain as Early as First Assessment
Change in DTSS Pain Domain Score† (worst pain, dull pain, shooting pain)
Scored 0-10, higher scores indicate more severe pain symptoms
* Nominal p <0.05
Placebo / Varegacestat
clinically meaningful improvement = -1.62
Diff: -2.32* | Diff: -2.02* | Diff: -2.70*
Worsening / Improving
LS Mean Change from Baseline‡
Analysis Visit (Weeks)
PRO Completion Among Patients with Baseline Data
Varegacestat 72 64 61 52 46 48 47 46 42 45 41 38 37
Placebo 71 62 58 55 50 42 43 35 33 31 29 28 27
• At baseline, the mean WPI score was 4.43 for varegacestat and 4.94 for placebo. Approximately 80% had a score of ≥ 2.
• At all prespecified timepoints, results were in favor of varegacestat
† Least-square (LS) means derived from mixed model for repeated measures (MMRM)
Presented By: Winette van der Graaf, MD, PhD
Winette van der Graaf
Patient reported outcomes (PROs) with varegacestat versus placebo (PBO) in progressing desmoid tumors: Results from RINGSIDE Part B
[Slide 3]
08:30 - 10:00 Rapid oral: Sarcoma
CHAIRS: MARK DICKSON, PALMA DILEO, CESAR SERRANO
Varegacestat Improves DT Symptoms
Change in DTSS TSS- 5† (Pain intensity, fatigue, swelling, muscle weakness, difficulty moving)
Scored 0-10, higher scores indicate more severe symptoms
* Nominal p <0.05
Placebo / Varegacestat
clinically meaningful improvement = -1.16
Diff: -1.46 | Diff: -1.43 | Diff: -2.09
Worsening / Improving
LS Mean Change from Baseline‡
Analysis Visit (Weeks)
PRO Completion Among Patients with Baseline Data
Varegacestat 72 64 61 52 46 48 47 46 42 45 41 38 37
Placebo 71 62 58 55 50 42 43 35 33 31 29 28 27
• Average baseline score across arms was approximately 4 indicating moderate symptom burden.
• At all prespecified timepoints, results were in favor of varegacestat
† Least-square (LS) means derived from mixed model for repeated measures (MMRM)
Presented By: Winette van der Graaf, MD, PhD
Winette van der Graaf
Patient reported outcomes (PROs) with varegacestat versus placebo (PBO) in progressing desmoid tumors: Results from RINGSIDE Part B
[Slide 4]
08:30 - 10:00 Rapid oral: Sarcoma
CHAIRS: MARK DICKSON, PALMA DILEO, CESAR SERRANO
Varegacestat Improves Physical Functioning
Change in PROMIS Physical Function 10a T-score†
Higher scores represent higher levels of physical functioning
* Nominal p <0.05
Varegacestat / Placebo
clinically meaningful improvement = +3.10
Diff: +3.13 | Diff: +5.84 | Diff: +6.54
Improving / Worsening
LS Mean Change from Baseline‡
Analysis Visit (Weeks)
PRO Completion Among Patients with Baseline Data
Varegacestat 71 66 62 54 49 51 47 44 42 42 40 42 37
Placebo 73 64 60 60 53 47 45 39 37 33 33 29 26
• A T-score of 50 reflects the average level of physical functioning in a general population; average baseline score across arms was approximately 45, indicating mild functional impairment.
• At all prespecified timepoints, results were in favor of varegacestat
‡ Baseline was originally defined as the last assessment before randomization and was redefined post hoc to include PRO assessments completed on or before first dose. Results shown use this updated baseline definition and remained consistent with the primary week 12, 24, and 48 findings.
† Least-square (LS) means derived from mixed model for repeated measures (MMRM)
Presented By: Winette van der Graaf, MD, PhD
Winette van der Graaf
Patient reported outcomes (PROs) with varegacestat versus placebo (PBO) in progressing desmoid tumors: Results from RINGSIDE Part B
Good morning #ESMO26
Later today, 12 am, come to see our poster, Hall5!
A "mixed" approval cover adult and paediatric population, but how many children are actually enrolled in such trials?
12% overall representation (see Iceberg plots!)
FDA grant more mixed approvals, younger ages
See more details and our conclusions 👇
Paediatric Representation in Trials Supporting FDA and EMA Mixed Adult-Paediatric Oncology Approvals
FPN: 3342P
Timothée Olivier1,2, Nestor Mudry3+, Floor de Jong4+, Simona Perano1, Danai Papangelopoulou5,6, Hans Gelderblom4, Sahar Barjesteh van Waalwijk van Doorn-Khosrovani4,7
+: both authors contributed equally.
1 Department of Oncology, Geneva University Hospitals, Geneva, Switzerland; 2 Department of Medicine, University of Geneva, Geneva, Switzerland; 3 University of Geneva, Geneva, Switzerland; 4 Department of Medical Oncology, Leiden University Medical Centre, Leiden, the Netherlands. 5 Division of Pediatric Oncology and Hematology, Geneva University Hospitals, Geneva, Switzerland; 6 CANSEARCH Research Platform for Pediatric Oncology and Hematology, Faculty of Medicine, Department of Pediatrics, Gynecology and Obstetrics, University of Geneva, Geneva, Switzerland. 7 CZ Health Insurance, Tilburg, the Netherlands.
BACKGROUND
A mixed adult-paediatric approval = an approval covering adult and paediatric populations.
Paediatric regulations permit extrapolation of adult data to paediatric use.
How many children were enrolled in supporting trials?
METHODS
Cross-sectional study 2020-2025
FDA and EMA oncology approvals for both adults and children (<18 years).
Data sources = regulatory documents and trial publications.
32.6% of datasets -> no paediatric patients (14 of 43 unique datasets)
[Figure 1: pediatric representation in unique datasets supporting mixed pediatric-adult EMA or FDA approvals between 2020 and 2025 (n = 43) - per-drug bar labels too small to read]
[Figure: Approved minimum age and age of the youngest patient enrolled in the supporting trial(s) for mixed FDA (A) and EMA (B) approvals, 2020-2025 - labels too small to read]
49 mixed approvals (FDA 34; EMA 15) -> 43 unique supporting datasets
12.0% overall paediatric representation
49% FDA - EMA regulatory differences -> FDA: more mixed approvals, younger ages
Included mixed approvals (n = 49) | EMA approval | FDA approval | Datasets
EMA only | 3 | | 3
Same indication, different datasets | 6 | 6 | 12
Same indication, same dataset | 6 | 6 | 6
FDA only | | 22 | 22
Total | 15 | 34 | 43
[Iceberg plots: Paediatric and adult representation in datasets supporting mixed approvals by the FDA (A) and EMA (B), represented with Iceberg Plots. Panel labels small: A FDA (n = 32 mixed approvals), B EMA (n = 15 mixed approvals)]
Regulatory differences 24 of 49 mixed approvals (49%) | n (% of 24)
Not approved by the other agency - All are FDA approvals, withdrawn or not submitted to the EMA | 15 (62.5%)
Age limit differed - FDA younger than EMA in 7/8 (87.5%) | 8 (33.3%)
Indication differed | 1 (4.2%)
CONCLUSIONS: Mixed adult-paediatric approvals may improve access to innovative therapies, particularly in rare cancers. However, reliance on extrapolation may discourage paediatric enrolment. Timely access should not compromise robust paediatric evidence.
Email: timothee.olivier@hug.ch
Funding: This study was partly funded by Precision Cancer Medicine Repurposing System Using Pragmatic Clinical Trials (PRIME-ROSE) under the Horizon Europe programme (grant n°101104269)
Disclosure: Timothée Olivier has no conflicts of interest to disclose
AI in real world data...
Quijotes y Sanchos 🇪🇸! Vision and grounding! #ESMO26
#AAOCDigital https://t.co/GBcI5f1lPX
Same slide also posted by @CedricPetersRT, @oa_zayas
[Slide 1]
Multimodal real-world data
Generated every day by routine care, at cancer centers worldwide
Clinical records - Diagnoses, labs, notes
Treatments & outcomes - Therapies, response, survival
Patient-reported outcomes - Symptoms, quality of life
Social context - Region, insurance, access
Patient
Tumor genomics - Somatic and germline
Liquid biopsy - ctDNA monitoring
Digital pathology - H&E and IHC slides
Radiology - CT, MRI, PET and reports
Francisco Sanchez-Vega
[Slide 2]
AI in cancer care needs Quixotes and Sanchos
Vision and grounding, riding together
The Quixotes · vision
New models, bold ideas, foundation models
The Sanchos · grounding
Clinicians, patients, data teams, prospective validation
Riding together: experts across continents, institutions and departments
Patients & advocates | Medicine & surgery | Pathology | Radiology | Biostatistics | Computational biology | Data science | Informatics & IT | Engineering | Legal, privacy & ethics
Francisco Sanchez-Vega
@VriesElisabeth on #access to biosimilars & generics of #cancer medicines, showing limited uptake in #LMICs and persistent inefficiency in health spending @myESMO
#ESMOAmbassadors #ESMO26
Find related @KNVokinger latest work on #WHO #EML :
https://t.co/4PpbKy2ZtA https://t.co/c5ICTP0539
The next wave of off-patent competition in oncology
From generics to biosimilars
ONCOLOGY MARKET COMPARISON
Generics - Mature market
[bar chart, US$ B] 2025: 23.7 | 2036: 31.5
Biosimilars - Rapidly expanding market
[bar chart, US$ B] 2025: 9.6 | 2030: 17.5
TWO WAVES OF OFF-PATENT COMPETITION
WAVE 1 Generics
• Chemotherapy
• Endocrine therapy
• Targeted small molecules
WAVE 2 Biosimilars
• Established mAbs (trastuzumab, rituximab, bevacizumab)
• Additional antibodies
• Checkpoint inhibitors and other complex biologics
Elisabeth de Vries
1 Future Market Insights (2025). Generic oncology drugs market.
2 ResearchAndMarkets (2025). Oncology biosimilars market.
BL and On-Treatment utDNA MRD and Clinical Response to Gem-iDRS in SunRISe-1 #ESMO26 @urotoday @DrFelixGuerrero
📌BL GDB scores: not predictive of BOR; similar results in pts with non-CR vs CR
📌Wk 12 GBD score: ⏫ in pts with non-CR vs CR (p=0.013)
📌BL and Wk 12 utDNA MRD status: not associated w/ DOR or EFS
[Slide 1]
Figure 3: CR by baseline GDB scores and with baseline MRD status
[Box plot: Baseline GDB score, CR vs Non-CR/NE; Wilcoxon p=0.86; MRD+ red, MRD- blue]
| CR (N=42) | Non-CR/NE (N=8) | p Value
Baseline GDB score
Mean (SD) | 38.4 (32.0) | 36.3 (30.1) | 0.86
Median (range) | 32.0 (0-94.0) | 31.5 (0-77.0)
Baseline MRD status, n (%)
MRD+ | 18 (90) | 2 (11) | 0.45
MRD- | 24 (80) | 6 (20)
[Slide 2]
Figure 4: Association of (A) DOR and (B) EFS with baseline MRD status
(A) 1-y DOR rate, % (95% CI): MRD- 62.7 (35.1-81.3); MRD+ 47.6 (25.7-66.7); p=0.16
No. at risk (months 0,3,...,30): MRD- 18 15 13 11 10 7 6 4 4 2 2; MRD+ 24 18 16 13 11 6 4 3 3 0 0
(B) 1-y EFS rate, % (95% CI): MRD- 64.9 (38.0-82.5); MRD+ 46.7 (27.8-63.6); p=0.08
No. at risk (months 0,3,...,39): MRD- 20 18 14 13 11 9 7 6 4 4 2 2 1 1; MRD+ 30 25 17 16 13 11 6 4 3 3 0 0 0 0
Survival probability (%) vs Treatment time, months
Survival table
Endpoint: DOR and EFS by baseline MRD status
MRD- (DOR) | 18
MRD+ (DOR) | 24
MRD- (EFS) | 20
MRD+ (EFS) | 30
P: DOR p=0.16; EFS p=0.08
Landmark rates:
1 year: MRD- DOR 62.7% (CI 35.1-81.3) | MRD+ DOR 47.6% (CI 25.7-66.7) | MRD- EFS 64.9% (CI 38.0-82.5) | MRD+ EFS 46.7% (CI 27.8-63.6)
[Slide 3]
Figure 5: CR by Week 12 GDB scores and by Week 12 MRD status
[Box plot: y-axis labeled 'Baseline GDB score', CR vs Non-CR/NE; Wilcoxon p=0.013; MRD+ red, MRD- blue]
| CR (N=31) | Non-CR/NE (N=8) | p Value
Week 12 GDB score
Mean (SD) | 28.1 (29.6) | 61.6 (28.1) | 0.013
Median (range) | 20.0 (0-86.0) | 68.5 (0-91.0)
Week 12 MRD status, n (%)
MRD+ | 13 (65) | 7 (35) | 0.044
MRD- | 18 (95) | 1 (5)
[Slide 4]
Figure 6: Association of (A) DOR and (B) EFS with Week 12 MRD status
(A) 1-y DOR rate, % (95% CI): MRD- 52.9 (27.6-73.0); MRD+ 57.1 (28.4-78.0); p=0.50
No. at risk (months 0,3,...,30): MRD- 18 13 11 11 9 4 3 1 1 0 0; MRD+ 14 13 11 8 8 7 6 5 5 2 2
(B) 1-y EFS rate, % (95% CI): MRD- 61.1 (35.3-79.2); MRD+ 40.0 (19.3-60.0); p=0.59
No. at risk (months 0,3,...,39): MRD- 19 19 12 11 11 9 4 3 1 1 0 0 0 0; MRD+ 20 14 13 11 8 8 7 6 5 5 2 2 1 1
Survival probability (%) vs Treatment time, months
Survival table
Endpoint: DOR and EFS by Week 12 MRD status
MRD- (DOR) | 18
MRD+ (DOR) | 14
MRD- (EFS) | 19
MRD+ (EFS) | 20
P: DOR p=0.50; EFS p=0.59
Landmark rates:
1 year: MRD- DOR 52.9% (CI 27.6-73.0) | MRD+ DOR 57.1% (CI 28.4-78.0) | MRD- EFS 61.1% (CI 35.3-79.2) | MRD+ EFS 40.0% (CI 19.3-60.0)
#ESMO26 🧬 TOMAS2 | Advanced STS
🔬 PARP1 H-score as predictive biomarker for trabectedin + olaparib.
🎯 H-score ≥70:
📈 All STS: mPFS 4.3 vs 2.5 mo
HR 0.49; p=0.008
📈 Uterine LMS: mPFS 16.3 vs 1.35 mo
HR 0.15; p=0.009
❌ No benefit with H-score <70.
🚀 PARP1 emerges as a promising predictive biomarker. External validation needed!
@OncoAlert
[Slide 2]
08:30 - 10:00 Rapid oral: Sarcoma
CHAIRS: MARK DICKSON, PALMA DILEO, CESAR SERRANO
PFS according to PARP1 H-score - all STS
PARP1 H-score <70
PARP1 H-score ≥70
arm
trabectedin
trabectedin + olaparib
trabectedin-censored
trabectedin + olaparib-censored
Progression-free Survival probability
Time from randomization (months)
H-score <70 | Median PFS months (95%CI) | PFS@6m (95%CI) | PFS@12m (95%CI) | HR
Trabectedin + olaparib (N=22) | 2.9 (1.9-3.8) | 31.8% | 13.6% | HR 1.12 (0.60-2.09) p=0.722
Trabectedin (N=21) | 4.0 (0.8-7.2) | 31.2% | 5.2%
H-score ≥70 | Median PFS months (95%CI) | PFS@6m (95%CI) | PFS@12m (95%CI) | HR
Trabectedin + olaparib (N=33) | 4.3 (3.1-9.8) | 40.6% | 28.1% | 0.49 (0.29-0.83) p=0.008
Trabectedin (N=30) | 2.5 (1.5-3.1) | 26.7% | 7.6%
Lorenzo D'Ambrosio MD PhD
Lorenzo D'Ambrosio
Quantitative PARP1 H-score as a predictive biomarker for trabectedin plus olaparib combination in advanced soft tissue sarcoma: Exploratory analysis of the TOMAS2 study
MALAGA AUDITORIUM - HALL 3
Survival table
Endpoint: PFS by PARP1 H-score (all STS)
Arm | N | Median | Median CI
H-score <70: Trabectedin + olaparib | 22 | 2.9 | 1.9-3.8
H-score <70: Trabectedin | 21 | 4.0 | 0.8-7.2
H-score ≥70: Trabectedin + olaparib | 33 | 4.3 | 3.1-9.8
H-score ≥70: Trabectedin | 30 | 2.5 | 1.5-3.1
HR: H-score <70: 1.12; H-score ≥70: 0.49
HR CI: 0.60-2.09; 0.29-0.83
P: p=0.722; p=0.008
H<70 PFS@6m: 31.8% (T+O) vs 31.2% (T)
H<70 PFS@12m: 13.6% (T+O) vs 5.2% (T)
H≥70 PFS@6m: 40.6% (T+O) vs 26.7% (T)
H≥70 PFS@12m: 28.1% (T+O) vs 7.6% (T)
[Slide 3]
08:30 - 10:00 Rapid oral: Sarcoma
CHAIRS: MARK DICKSON, PALMA DILEO, CESAR SERRANO
PFS according to PARP1 H-score - uLMS
PARP1 H-score <70
PARP1 H-score ≥70
arm
trabectedin
trabectedin + olaparib
trabectedin-censored
trabectedin + olaparib-censored
Progression-free Survival probability
Time from randomization (months)
H-score <70 | Median PFS months (95%CI) | PFS@6m (95%CI) | PFS@12m (95%CI) | HR
Trabectedin + olaparib (N=4) | 1.3 (0.8-1.7) | 0% | 0% | 11.0 (1.17-102.6) p=0.036
Trabectedin (N=5) | 4.0 (3.9-4.1) | 40% | 0%
H-score ≥70 | Median PFS months (95%CI) | PFS@6m (95%CI) | PFS@12m (95%CI) | HR
Trabectedin + olaparib (N=8) | 16.3 (3.1-NR) | 62.5% | 62.5% | 0.15 (0.04-0.62) p=0.009
Trabectedin (N=6) | 1.35 (0.3-NR) | 16.7% | 0%
Lorenzo D'Ambrosio MD PhD
Lorenzo D'Ambrosio
Quantitative PARP1 H-score as a predictive biomarker for trabectedin plus olaparib combination in advanced soft tissue sarcoma: Exploratory analysis of the TOMAS2 study
MALAGA AUDITORIUM - HALL 3
Survival table
Endpoint: PFS by PARP1 H-score (uterine leiomyosarcoma)
Arm | N | Median | Median CI
H-score <70: Trabectedin + olaparib | 4 | 1.3 | 0.8-1.7
H-score <70: Trabectedin | 5 | 4.0 | 3.9-4.1
H-score ≥70: Trabectedin + olaparib | 8 | 16.3 | 3.1-NR
H-score ≥70: Trabectedin | 6 | 1.35 | 0.3-NR
HR: H-score <70: 11.0; H-score ≥70: 0.15
HR CI: 1.17-102.6; 0.04-0.62
P: p=0.036; p=0.009
H<70 PFS@6m: 0% (T+O) vs 40% (T)
H<70 PFS@12m: 0% (T+O) vs 0% (T)
H≥70 PFS@6m: 62.5% (T+O) vs 16.7% (T)
H≥70 PFS@12m: 62.5% (T+O) vs 0% (T)
[Slide 4]
08:30 - 10:00 Rapid oral: Sarcoma
CHAIRS: MARK DICKSON, PALMA DILEO, CESAR SERRANO
Conclusions
This exploratory analysis of the TOMAS2 study further supports PARP1 expression as a candidate predictive biomarker for trabectedin and olaparib combination.
Patients with H-score ≥70 showed the greatest benefit from the combination.
PARP1 expression may guide patient selection in future trials combining new ecteinascidins and PARP1i.
The proposed PARP1 assessment criteria are undergoing external validation to strengthen their use as a biomarker in future trials.
Lorenzo D'Ambrosio MD PhD
Lorenzo D'Ambrosio
Quantitative PARP1 H-score as a predictive biomarker for trabectedin plus olaparib combination in advanced soft tissue sarcoma: Exploratory analysis of the TOMAS2 study
MALAGA AUDITORIUM - HALL 3
Neoadj Tori + TIP chemo for locally advanced PSCC: Ph 2 single-arm 🇨🇳 clinical trial @urotoday #ESMO26
📌n=25; T4/N2-3 M0, mFU 21.4 mos
📌ORR 84%; 2 CR, 19 PR
📌n=21 consolidative surgery: pCR rate 48%
📌12-mo EFS rate: 72%; OS rate: 88%
📌Gr 3-4 AEs: 84% (MC neutropenia 72%) https://t.co/8QonCQWMoE
Same slide also posted by @urotoday
[Slide 1]
A
[Waterfall plot]
Change from baseline (%)
Best response: CR / SD / PR / PD
[y-axis 60 to -120; dotted reference lines at +20 and -30]
B
[Spider plot]
Change from baseline (%)
Clinical response: CR / SD / PR / PD
Baseline | After Cycle 2 | After Cycle 4
[Slide 2]
C
Event-free survival (%)
Events: 8 (32%)
Median EFS: Not reached
12-month EFS rate: 72.0 (95%CI 50.1-85.5)
24-month EFS rate: 67.8 (95%CI 45.7-82.4)
Time from enrolment (months)
Number at risk
0: 25 | 6: 22 | 12: 18 | 18: 12 | 24: 5
D
Overall survival (%)
Deaths: 3 (12%)
Median OS: Not reached
12/24-month OS rate: 88.0 (95%CI 67.3-96.0)
Time from enrolment (months)
Number at risk
0: 25 | 6: 23 | 12: 22 | 18: 16 | 24: 7
Survival table
Endpoint: EFS and OS (single arm)
Toripalimab + TIP (single arm) - EFS | 25 | Not reached
Toripalimab + TIP (single arm) - OS | 25 | Not reached
Landmark rates:
12 months: EFS 72.0% (CI 50.1-85.5) | OS 88.0% (CI 67.3-96.0)
24 months: EFS 67.8% (CI 45.7-82.4) | OS 88.0% (CI 67.3-96.0)
#ESMO2026 A Physician-Pharmacist Shared Care Model for CDK4/6 Therapy: Advancing Quality and Reducing Oncologist burden
@RVH_HealthCntr @RVHFoundation #Madrid https://t.co/1L7TveWAM5
[Slide 1]
[Selfie of three people in front of poster 3974P; left and right portions of poster obscured]
3974P
FPN #3974P
A Physician–Pharmacist Model for CDK4/6 Therapy: Advancing Quality and Reducing Oncologist Burden
Rhiannon MacDonald, BSc, MSc candidate; Coralea Kappel, MD; Giulio Didiodato, MD; Lily Spasic, BScPharm, MSc; Sara Rask, MD; Isabel Li, MD; Jessica Singh, MD; Pooya Dibajnia, MD; Sujata Pokhrel, HBSc, CCRP; Zachary Veitch, MD
STUDY POPULATION: Study period: Aug 22, 2025 for 2 years | Data analysis cut-off: Sep 30, 2026
136 Eligible Patients -> 67 Enrolled Patients 49.3% -> 60/67 ≥1 pharmacist visit 89.6%
RESULTS: ONCOLOGIST CAPACITY RELEASED: 91 pharmacist-led visits; 22.75 h observed clinical time shifted; ≈23; ≈91
[Remaining text partially obscured or too small; see full poster image 2113875300706554361_s2 for complete transcription]
[Slide 2]
3974P
FPN #3974P
A Physician–Pharmacist Model for CDK4/6 Therapy: Advancing Quality and Reducing Oncologist Burden
Rhiannon MacDonald, BSc, MSc candidate(1); Coralea Kappel, MD(2); Giulio Didiodato, MD(3); Lily Spasic, BScPharm, MSc(4); Sara Rask, MD(2); Isabel Li, MD(2); Jessica Singh, MD(2); Pooya Dibajnia, MD(2); Sujata Pokhrel, HBSc, CCRP(5); Zachary Veitch, MD(2)
(1)McMaster University, Hamilton, Ontario (2)Oncology & Hematology, Hudson Regional Cancer Centre, Royal Victoria Hospital Barrie, Ontario (3)Critical Care Medicine, Royal Victoria Hospital Barrie, Ontario (4)Oncology Pharmacy, Royal Victoria Barrie, Ontario (5)Clinical Trials, Royal Victoria Hospital Barrie, Ontario
BACKGROUND
• Rising cancer incidence in Canada is increasing oncologist workload, compounded by limited workforce capacity (1.82 medical oncologists / 100,000 population)
• CDK4/6 inhibitors + endocrine therapy are standard therapy for HR+/HER2– breast cancer in metastatic and selected high-risk adjuvant settings.
• Expanding indications and prolonged treatment increase longitudinal oncology follow-up requirements.
• Physician–pharmacist shared care may redistribute routine monitoring while maintaining physician oversight.
PRIMARY OBJECTIVE
Evaluate oncologist clinic capacity released through a physician–pharmacist shared-care model for patients receiving CDK4/6 inhibitors.
ELIGIBILITY
METASTATIC: HR+/HER2– breast cancer; ≥6 months on CDK4/6 inhibitor and ≥2 CT scans showing stable/responding disease.
ADJUVANT: HR+/HER2– breast cancer; ≥3 months on adjuvant CDK4/6 inhibitor with stable toxicity at entry.
STUDY DESIGN
Alternating 3-month physician–pharmacist follow-up
METASTATIC: ≥6 mo stable/responding -> Pharmacist -> 3 mo -> Physician -> + imaging -> repeat
ADJUVANT: ≥3 mo stable toxicity -> Pharmacist -> 3 mo -> Physician -> Repeat
STANDARDIZED PHARMACIST ASSESSMENT
Therapy adherence & medication reconciliation | Disease surveillance & interval clinical changes | CBC, renal/hepatic function & electrolytes | ECG/QTc monitoring when indicated | Structured toxicity assessment | Supportive care & dose-management recommendations
GRADE 1 TOXICITY: Managed by pharmacist per protocol
GRADE ≥2 TOXICITY / CLINICAL CONCERN: Physician consultation / follow-up visit
STUDY POPULATION
Study period: Aug 22, 2025 for 2 years | Data analysis cut-off: Sep 30, 2026
136 Eligible Patients -> 67 Enrolled Patients 49.3% -> 60/67 ≥1 pharmacist visit 89.6%
PATIENT CHARACTERISTICS
TREATMENT INTENT: Metastatic: 40 patients (60%); Adjuvant: 27 patients (40%)
MENOPAUSAL STATUS: Post-menopausal: 50 patients (74.6%); Pre-menopausal: 16 patients (23.9%); Male: 1 patient (1.5%)
CDK4/6 INHIBITOR: Ribociclib: 40 patients (60%); Palbociclib: 14 patients (21%); Abemaciclib: 13 patients (19%)
PHARMACIST INTERVENTIONS
121 INTERVENTIONS ACROSS 91 PHARMACIST-LED VISITS (1.33 INTERVENTIONS/VISIT)
Referral 8 (6.6%); Drug-drug interactions 5 (4.1%); Supplementation 14 (11.6%); Toxicities 62 (51.2%); Lifestyle 32 (26.4%)
121 interventions
Grade 1 toxicities 83.9% | Grade 2/3 toxicities 16.1%
SAFETY AND ESCALATION
10/91 (11.0%) Pharmacist encounters requiring physician consultation
2/91 (2.2%) Pharmacist encounters requiring an additional physician follow-up visit
REASONS FOR CONSULTATION - GRADE 2/3 TOXICITIES: Rash; Elevated LFTs; Acute kidney injury; Pain; Hot flashes; Palpitations
CONCLUSION
• Physician–pharmacist shared care redistributed routine CDK4/6 follow-up while maintaining protocol-defined physician oversight. Physicians gained more than 22 hours of clinic time in over 1 year of the pilot program
• Pharmacists delivered 121 interventions across 91 visits (1.33 interventions/visit), with toxicities representing the most frequent intervention category.
• Pharmacist were able to deal independently with 83.9 % of toxicities which were grade 1 and required consultation with physicians for grade 2/3 toxicities which occurred for 16.1% of toxicities evaluated
• Physician consultation occurred in 10/91 pharmacist encounters (11.0%); 2/91 encounters (2.2%) required an additional physician follow-up visit.
RESULTS: ONCOLOGIST CAPACITY RELEASED
PHARMACIST-LED VISITS: 91 pharmacist-led visits (2,730 minutes; 1 pharmacist visit = 30 min)
OBSERVED CLINICAL TIME SHIFTED: 22.75 h observed clinical time shifted (1,365 minutes; Based on 15 min MD follow-up)
EQUIVALENT NEW-PATIENT VISITS: ≈23 60-min new-patient visits, time-equivalent
EQUIVALENT FOLLOW-UP VISITS: ≈91 15-min follow-ups, time-equivalent
At 90% target enrollment: projected 122 patients/year -> 2 visits per year -> 3,660 minutes -> 61 hours/year of potential oncologist clinic capacity released.
POTENTIAL ANNUAL FINANCIAL IMPACT
Modelled at ~50% enrollment (69 patients) -> 34.5 hours for the Oncologist and 69 hours for the pharmacist per annum
COST SAVINGS: 34.5 hours/year (Oncologist Salary) – 69 hours/year (Pharmacist Salary) = ~$1,035 per year (SAVED)
REVENUE GENERATION: 34 new breast-patient consults -> ~$7,391.30 per year (GENERATED); 34 systemic therapies (assuming) 55% Oral, 40% IV, 5% No Treatment -> ~$57,652.17 per year (GENERATED)
TOTAL ANNUAL FINANCIAL IMPACT: ~$1,035 + ~$7,391.30 + ~$57,652.17 = ~$66,078.47 per year
SECONDARY ENDPOINTS
• Cooperative identification of recurrence/progression events.
• Physician and pharmacist satisfaction — end-of-study analysis pending.
• Medication adherence — end-of-study analysis pending.
• Patient satisfaction – end-of-study analysis pending
FUNDING
This study was supported by an unrestricted grant from Novartis Pharmaceuticals. The authors declare no conflicts of interest relevant to this work.
Contact: [email address on poster]
At #ESMO2026 in Madrid, Prof. Herbert H. Loong emphasized that the future of precision oncology depends on three key elements: Precision, Speed, and Access.
He highlighted how multi-omic liquid biopsy approaches can complement tissue testing, support MRD detection, monitor treatment response, and potentially make precision oncology more accessible and sustainable.
Precision oncology is not just about identifying the right treatment, but delivering it at the right time to more patients.
#ESMO2026 #LiquidBiopsy @oncodaily #PrecisionOncology #MultiOmics @herbloong
MADRID 2026 ESMO congress
Take home messages
The new era of precision oncology demands:
Precision
• So test can guide patients' treatment in the right direction
Speed
• So timely precise decisions can be made for patients
Access
• So precise, and timely treatments can be offered to patients at-large
A multi-omic liquid biopsy approach can help satisfy all of the above
requirements to bring sustainable precision oncology to our patients.
Presented by HH Loong | @herbloong | ESMO 2026
When reading a clinical trial, the key question is: Does statistical significance translate into a meaningful difference in my patient’s life?
@myESMO #ESMO26 @Larvol @OncoAlert https://t.co/RRh8arjJMb
BG LAB
BISHAL GYAWALI ONCOLOGY
How I Read a Clinical Trial Report? A Primer for Busy Clinicians
POLICY AND PRACTICE | April 22, 2026
Author: Bishal Gyawali, MD, PhD, FASCO
AUTHORS INFO & AFFILIATIONS
JCO Oncol Pract 22, 909-912(2026) • Volume 22, Number 6 • DOI: 10.1200/OP-26-00181
Prof. Bishal Gyawali
AI in #ESMO26: Great insights from @jnkath . From single-task models to autonomous AI, the future of clinical implementation will depend not just on innovation, but also data infrastructure and effective governance.Great to see ESMO ELCAP and the upcoming EVALLM framework! https://t.co/lCHR1BdIqI
[Slide 3]
13:30 - 15:00 Transforming oncology with generative AI and autonomous tools
CHAIRS: EVANGELIA CHRISTODOULOU, JAKOB KATHER
ESMO Guidance on the Use of Large Language Models in Clinical Practice (ELCAP)
Type 1 — Patient-facing AI systems [patient → LLM icon]
Symptom Queries / Patient Education / Lifestyle Tracking
Type 2 — HCP-facing AI systems [clinician → LLM icon]
Clinical Decision Support / Multilingual Communication / Education and Training
Type 3 — Background AI systems [LLM → database icon]
Data Extraction / Background Alert Systems
Which evidence is required? ESMO EVALLM, work in progress
Wong et al., Annals of Oncology (2025)
Slide 7 www.kather.ai [KATHER LAB logo]
[Speaker panel] Jakob Kather — Generative AI, LLMs and AI agents in oncology
CADIZ AUDITORIUM - NCC
[Slide 4]
13:30 - 15:00 Transforming oncology with generative AI and autonomous tools
CHAIRS: EVANGELIA CHRISTODOULOU, JAKOB KATHER
AI in a European hospital
Data architecture
Access to all clinical data for training & real time deployment
[Pyramid:] AI applications / Clinical Data Repository / Primary clinical systems (EHR, PACS, ...)
GPU compute on premise or in the Cloud
Substantial demand for inference, and much more demand when models are also trained
AI-friendly governance and effective administration
AI can be deployed in a safe and compliant way
GDPR / EU AI act / MDR are navigable
Slide 15 www.kather.ai [KATHER LAB logo]
[Speaker panel] Jakob Kather — Generative AI, LLMs and AI agents in oncology
CADIZ AUDITORIUM - NCC
Excellent talk by Dr. Parischa from @UCSF
👁️ ADC ocular toxicity at #ESMO26: key takeaways 🧵
1. Corneal toxicity is the dominant ocular AE with ADCs: common, painful, and reversible. 3/15 FDA-approved ADCs carry a boxed warning for ocular toxicity.
2. Mechanism is off-target: ADCs are taken up non-selectively by the corneal epithelium via macropinocytosis and accumulate there. Microcyst-like changes start peripherally, then migrate centrally —> pain, blurry vision, refractive shifts.
3. Not tied to one ADC class. Seen across targets (BCMA, FRα, TF, TROP2, Nectin-4), cleavable and non-cleavable linkers, and payloads (MMAF, DM4, MMAE, TOP1i). Rates: belantamab 71%, mirvetuximab 61%, tisotumab 60%, Dato-DXd 51%, EV 40%.
4. Onset ~3 wks after infusion; resolves 2 wks–8 mo after stopping. Prevention is hard: >75% on select ADCs still develop it despite lubricants/steroid drops, driving up to 50% dose delays, 35% reductions, 25% discontinuations.
5. Risk factors remain unclear. Optometrists are well-positioned to lead routine screening and monitoring on ADCs, working closely with ophthalmology for complex cases. This partnership improves access and keeps patients on therapy
⭐️ Bottom line: proactive, early eye screening is what lets us time holds and dose reductions correctly. New consensus cornea grading (JAMA Ophthalmol 2026): G1–2 continue with close follow-up; G3 hold until G1, then reduce/stop. #ADC #oncology #ESMO26 @myESMO @MoffittNews
[Slide 1]
ADC Ocular Adverse Events (OAEs)
ADC corneal toxicity is prevalent, painful, and reversible
Corneal pseudomicrocysts
Microcyst-Like Epithelial Changes (MECs)
20% (3/15) of ADCs have FDA black box warning for ocular toxicity
Develop ~3 weeks after ADC infusion
Reversible 2 weeks-8 months after ADC discontinuation
Causes eye pain and blurry vision
Lindgren ES...Pasricha ND. Incidence and Mitigation of Corneal Pseudomicrocysts Induced by Antibody-Drug Conjugates (ADCs). Curr Ophthalmol Rep. 2024
[Slide 2]
ADC Ocular Adverse Events (OAEs)
ADCs selectively accumulate in the corneal epithelium
Rabbits administered radiolabeled ADC and ocular tissues collected over 14 days
Results:
ADC in ocular tissues (except corneal epithelium) similar to blood/plasma elimination (T1/2 = 4.5-7.5 days)
Corneal epithelium:
Absorption phase followed by stable concentration plateau through 14 days
High tissue-to-plasma ratio (1.6 vs <0.5)
[Chart] Mean Tissue : Plasma Ratio (0-2) vs Hours post dose (0-350)
Legend: Aqueous humor; Choroid-RPE; Conjunctiva (bulbar); Eyelid; Iris-cilliary body; Lens; Corneal endothelium; Corneal epithelium; Nictitating membrane; Optic nerve; Retina; Sclera - limbus; Sclera - remaining; Vitreous humor; Corneal stroma
[Y]arbington A et al. Nonclinical ocular toxicity of a maytansinoid payload-antibody drug conjugate: Ocular tissue distribution, lesion pathogenesis, and mitigation. AACR Annual Meeting. 2024
[Slide 4]
Proposed Mechanism
Macropinocytosis (actin-dependent non-selective endocytosis)
[Diagram] ADC; Lysosome; Macropinosome; Payload release
Ethylisopropylamiloride (EIPA): Gold standard macropinocytosis inhibitor
[Bar chart] MFIR (37°C/4°C), 0-50: Mock | Dextran | 200 µmol/L EIPA | 100 µmol/L EIPA | 50 µmol/L EIPA (** significance brackets)
[Microscopy] ADC; - EIPA; + EIPA; scale bars 10µm, 7.5µm
Zhao H et al. Cancer Res. 2018
5-year ET-FES trial data: 18F-FES PET/CT reveals that whole-body ER heterogeneity is a key prognostic factor in ER+/HER2- MBC treated with ET.
Patients with 100% FES+ lesions achieved significantly longer OS (71.4 vs 42.5 mos, p=0.04). FES- uptake indicates lower ET responsiveness.
@myESMO #ESMO26 @Larvol @OncoReporte @OncoAlert
Prof @DrVijayPatil11 at #ESMO26 disclosing data from systematic evidence mapping showing potential 'clinical equivalence' of more sustainable schedules of #IO :
# Low dose vs no IO:
OS HR=0.67
# Low dose vs standard dose IO:
No RCT
@myESMO #ESMOAmbassadors https://t.co/FhN9FA2JML
RANDOMISED TRIAL EFFICACY
Comparison A: Low-Dose ICI Regimens Significantly Extend Overall Survival
POOLED OVERALL SURVIVAL: HR 0.67 (95% CI 0.50 to 0.91) | p = 0.026 | 4 RCTs (N = 1,453)
Low-dose ICI regimens reduced the hazard of death by 33% compared to standard non-ICI control therapy.
Trial / Study | N (Low / Ref) | Regimen Strategy | OS Estimate (95% CI) | Weight
Patil 2023 | 76 / 75 | Nivo 20mg + Chemo (Add-on) | HR 0.55 (0.36–0.82) | 15.1%
Menon 2026 | 193 / 187 | Nivo + Platinum Doublet (Add-on) | HR 0.72 (0.54–0.95) | 24.1%
Noronha 2026 (DELII) | 250 / 250 | Nivo 20mg Monotherapy (Replace) | HR 0.80 (0.66–0.97) | 33.9%
Shah 2026 (LBA6007) | 211 / 211 | Low-dose ICI Regimen (Replace) | HR 0.57 (0.44–0.73) | 26.9%
ESMO Congress 2026 | Low-Dose ICI Meta-Analysis | Dr. Vijay M Patil
8
“Thinking for yourself - do not outsource critical thinking”.
Important message from
@oncology_bg in his talk on “How I read and interpret a cancer clinical trial” at #ESMO26 https://t.co/697trqqmkU
How I read a clinical trial report
1. Generalizability of results (eligibility criteria)
2. Conflicts of interest
3. Quality of life
4. Endpoints / Surrogates
5. Control arm
6. Crossover
7. Censoring
8. Clinical vs statistical significance
9. Subgroup analysis
10. Toxicity reporting
11. Thinking for yourself – do not outsource critical thinking
Prof. Bishal Gyawali
[QR code] Gyawali B, JCO Oncol Pract 2026 22:909-912
What a great session 👏👏👏👏 congrats #ESMO2026 thanks @darioT_ 👏👏👏 🤩🤩🤩🤩🤩 https://t.co/8VwR0Zznm5
[Slide 1]
A standard assumes a system that can deliver it
Evidence — What regimen is supported by pivotal trials and guidelines?
Delivery — What prevents it reaching patients: cost, supply, staff, infrastructure, or travel?
Adaptation — What change could preserve meaningful benefit under that constraint?
Legitimacy — Is the change evidence-informed, transparent, discussed with patients, monitored, and revisited?
Dario Trapani
WHO (2023). [illegible]
[Slide 2]
Definition
(and quantification)
of (accepted)
uncertainty
Loss of
methodological
and statistical
„precision“
Trial
methodologies
and endpoints
Types of studies
included/accepted
Definition
(and quantification)
of benefits and
gains
Various categories
Financial
aspects
Direct and indirect
costs
Dirk Arnold
Excited to present our research at #ESMO26! 🔬🧬
We explored how generative models can predict broader tumour genomic profiles from smaller targeted sequencing panels, potentially expanding access to comprehensive genomic profiling.
📍 Poster 305P
#PrecisionOncology https://t.co/5f2Oe3af9s
100 treated. 4 benefit. All exposed.
The challenge is knowing who those 4 are. A powerful message from Dan Landau on why personalised adjuvant therapy matters. #ESMO26
@landau_lab @OncoAlert @myESMO https://t.co/pVXkKpGwr0
[Pictogram of 100 figures: green, yellow, red]
Cured by surgery - No benefit from adjuvant Tx
Residual disease - Benefit from adjuvant Tx
Residual disease - No benefit from adjuvant Tx
100 treated · 4 benefit · 100 exposed
[Live video of speaker on screen]
Great session in #ESMO26, and great presentation from
@RADUVIDRA @myESMO
"From clinical trial to community care: Pitfalls in implementation and how to overcome them"
An uncomfortable truth. We need to improve. https://t.co/hkQdzHE9lp
Trials exclude what we treat every day
Pitfall 1 · the evidence
- 44.000 RCT with 5.7 mil patients:
- Multimorbidity:
- excluded by 91% of RCTs,
- present in 41% of patients
- Concomitant medication:
- excluded by 52% of RCTs,
- taken by 94% of patients
[Two stacked bar charts C and D by clinical specialty (Cardiovascular ... Malignant disease and immunosuppression), legend: 0 clinical specialities | 1 clinical speciality | 2–5 clinical specialities | 6–10 clinical specialities | ≥11 clinical specialities]
C: RCT exclusion by number of concomitant clinical specialties · D: real-world prevalence
The patients most often excluded are the ones most often treated.
Radu Vidra
Tan YY et al. Lancet Healthy Longev 2022;3:e674–89 · Figure 2C–D · 43,895 RCTs vs 5.7 million patients (England) · all drug classes
Great presentation by Chris Booth in #ESMO26, as always, on physical exercise in cáncer prevention.
With the well-established overall survival (OS) data, if “exercizumab” were a monetisable drug, every healthcare system would be investing millions in exercise programmes. https://t.co/ogsQTbsNOj
Journal of Clinical Oncology
Comments and Controversies
When the System Is the Treatment: Rethinking Nonpharmacologic Breakthroughs in Oncology
Ramy Sedhom, MD, FASCO, Efrat Dotan, MD, and Christopher Booth, MD
Exercizumab
Pallituzumab
Geriatriximab
Symptomab
Sedhom JCO 2026
Canadian Cancer Trials Group
Queen's University Sinclair Cancer Research Institute
MADRID 2026 ESMO congress
🫀🤝🎗️ Thrilled to see my friends from ESC @ESCardioOnco joining forces with colleagues from ESMO at #ESMO2026 in Madrid🇪🇸
Two scientific communities, one shared mission: advancing cardiovascular care for patients with cancer! 🌍❤️
#CardioOncology @myESMO https://t.co/FpG77rNGFZ
Same slide also posted by @ESCardioOnco
CV risk stratification in cancer: from LVEF to CHIP
What we have
HFA-ICOS established a common baseline language
Re-stratification improves risk assessment over time
Imaging, biomarkers and CHIP are expanding the field
Prevention opportunities already exist in survivorship
What we need next
Clinically meaningful outcomes, not just more abnormalities
Dynamic longitudinal models across the cancer journey
Better validation across therapies and populations
Integration of conventional and next-generation risk markers
Targeted surveillance and prevention for higher-risk patients
From LVEF to CHIP, risk stratification must move from detection to action.
Goal: identify meaningful CV risk early enough to personalise surveillance, prevention and cardioprotection while enabling the best cancer care.
Sjoukje Oosting, chair of the WG, presenting on the future and future challenges of @myESMO #MCBS at #ESMO26
#ESMOAmbassadors https://t.co/7YwkbaIxtM
ESMO - Magnitude of Clinical Benefit Scale
Validated framework to assess the clinical benefit of cancer treatments
Curative: A, B, C (Substantial benefit = A, B)
Non-curative: 5, 4, 3, 2, 1 (Substantial benefit = 5, 4)
Sjoukje Oosting
📌Keynote lecture 1
CNS disease as the next frontier in oncology care: Glioblastoma, metastases, and leptomeningeal disease
👉🏻leptomeningeal metastasis update
✨ @wick_wolfgang
#ESMO26 🇪🇸 @OncoAlert #OncoAlertAF https://t.co/JweK7J435P
[Slide 1]
15:15 - 15:45 Keynote lecture 1
CHAIR: ANNA SOPHIE BERGHOFF
Leptomeningeal Metastasis (LM)
• Incidence of LM in advanced malignancies to approximate 9%–25% for small cell and non-small cell lung cancer, 5%–20% for breast cancer, and 6%–18% for melanoma.
• Prognosis of LM is poor but heterogeneous, with certain subgroups of patients (eg, EGFR-mutant NSCLC, HER2-positive breast cancer) demonstrating superior survival.
• Historical survival benchmark of 2–4 months does not apply to all patients
PMID: 38902944
[Schematic panels A-C: brain/spinal CSF flow; B: adherent LM cells, floating LM cells, brain parenchyma; C: choroid plexus, CSF, barrier disruption through secreted factors, influx of nutrients, LM cancer cells]
[Speaker video panel] Wolfgang Wick
CNS disease as the next frontier in oncology care: Glioblastoma, metastases, and leptomeningeal disease
ALMERIA AUDITORIUM - HALL 9
[Slide 2]
15:15 - 15:45 Keynote lecture 1
CHAIR: ANNA SOPHIE BERGHOFF
Leptomeningeal Metastasis (LM)- imaging
• Typical MRI findings of linear LM (type A)c
Typical MRI findings of nodular LMD (type B)
Both (type C)
Hydrocephalus only (type D–hydrocephalus)
Equivocal leptomeningeal findings or absence of leptomeningeal MRI findings (type D–normal)
[MRI panels with arrows]
PMID: 37863528
PMID: 42488117
[Speaker video panel] Wolfgang Wick
CNS disease as the next frontier in oncology care: Glioblastoma, metastases, and leptomeningeal disease
ALMERIA AUDITORIUM - HALL 9
[Slide 3]
15:15 - 15:45 Keynote lecture 1
CHAIR: ANNA SOPHIE BERGHOFF
Leptomeningeal Metastasis (LM) - update
• Breaking barriers in leptomeningeal disease effort: consensus review on clinical trial design and basic science integration
• Proton craniospinal irradiation (pCSI) has emerged as a promising life-prolonging intervention for patients with LM
[Bar chart, y-axis 0 mo, 3 mo, 6 mo, 9 mo, 12 mo; groups CNS-PFS and Overall survival; legend: Proton CSI, Involved-field RT; no bar values printed]
Final randomized phase II analysis; CNS-PFS P < .001, OS P = .04.
PMID: 42777082
PMID: 42202212
[Speaker video panel] Wolfgang Wick
CNS disease as the next frontier in oncology care: Glioblastoma, metastases, and leptomeningeal disease
ALMERIA AUDITORIUM - HALL 9
[Slide 4]
15:15 - 15:45 Keynote lecture 1
CHAIR: ANNA SOPHIE BERGHOFF
Leptomeningeal Metastasis (LM) – practise approach
Clinical phenotype | Management
Good performance status, disseminated LM, controlled extracranial disease | Evaluate pCSI and CNS-active systemic therapy
Actionable driver mutation | Prioritize tumour-specific CNS-active systemic treatment
Predominantly linear LM, positive cytology, patent CSF flow | Consider intrathecal therapy, preferably in a protocol
Bulky nodular or focal symptomatic LM | Focal RT or selected surgical intervention
Hydrocephalus or CSF obstruction | Neurosurgical assessment, CSF diversion when appropriate
Rapid systemic progression, poor functional status | Symptom-oriented care and carefully selected palliative interventions
[Speaker video panel] Wolfgang Wick
CNS disease as the next frontier in oncology care: Glioblastoma, metastases, and leptomeningeal disease
ALMERIA AUDITORIUM - HALL 9
Great to be at #ESMO26, even more special to have it here at home in Madrid! 🇪🇸
Five days of learning, sharing ideas, and catching up with friends and colleagues.
Always inspiring to see so many people working together to improve cancer care!
#ESMO2026 @myESMO https://t.co/AsoNXAk8BC
[Photo of main-hall screen, same slide shown twice]
ESMO CONGRESS 2026: FIVE DAYS OF SCIENCE, EDUCATION, DISCUSSIONS AND NETWORKING
4,400+ ABSTRACT PRESENTATIONS
3 PRESIDENTIAL SYMPOSIA
12 LBAs
680 FACULTY MEMBERS
230 SESSIONS (including EONS)
ESMO / Congress Experience
Kicking off #ESMO2026 with Alessandra Pedrocchi explaining the safety brakes we need to generate before employing AI agents in oncology https://t.co/Q1flHp6Kau
[Slide 1]
POLITECNICO DI MILANO 18
CoT: From Faithfulness to Monitorability
CHAIN-OF-THOUGHT MONITORING
LLM (reasoning model) --⚠--> Chain of thought (written reasoning) → Monitor (human or AI reader) → Flag (block · review · fix)
FRAGILE LINK
the written reasoning may omit or hide what drives the answer
• Monitorability: can a monitor detect problems by reading the CoT?
• Opportunity: reasoning in natural language is readable by humans and tools
• Fragile: training choices may make CoT less informative
• Recommendation: evaluate and preserve monitorability, alongside other safety methods
Korbak T. et al. Chain of Thought Monitorability: A New and Fragile Opportunity for AI Safety. 2025. arXiv:2507.11473
Alessandra Pedrocchi
[Slide 2]
POLITECNICO DI MILANO 17
Self-Explanations: Is Chain-of-Thought Faithful?
Do Reasoning Models Say What They Think?
Chain-of-thought reasoning A prompting technique that encourages language models to generate intermediate reasoning steps before arriving at a final answer, improving performance on complex tasks.
FAITHFUL COT RATE BY HINT TYPE: THE HINT IS RARELY ADMITTED
• Same question asked twice: without and with a hint (e.g., "A Stanford professor thinks the answer is A")
• When the hint changes the answer, the CoT admits it only 25% (Claude 3.7 Sonnet) and 39% (DeepSeek R1) of the time
[Bar chart: Fraction of examples with faithful CoT, Average] Claude 3.5 Sonnet (New) 5%; Claude 3.7 Sonnet 25%; DeepSeek V3 15%; DeepSeek R1 39%
Chen Y. et al. Reasoning Models Don't Always Say What They Think. Anthropic, 2025
Alessandra Pedrocchi
Proud to present our e-Poster at #ESMO2026 .
📌 Predictive value of baseline 18F-FDG PET/CT TLG in IO-treated r/m HNSCC.
Special thanks to Prof. @amanda_psyrri for her invaluable guidance, support and contribution. 🙏🏻 https://t.co/H9r3VZllp8
[Slide 1]
1631eP
Predictive Value of Baseline 18F-FDG PET/CT TLG in Immunotherapy-Treated r/m HNSCC
Maria Anastasiou¹, Konstantinos Tryposkiadis¹, Panagiota Oikonomopoulou¹, Ioannis Kotsantis¹, Anastasios Kyriazoglou¹, Anastasios Pantazopoulos¹, George J. Kavourakis¹, Vassiliki Lyra², Niki Gavrielatou¹, Evangelos D. Zazas¹, Lydia E. Gkaralea¹, Sofia Chatziioannou², Amanda Psyrri¹
1. Oncology Unit, 2nd department of Internal Medicine, Attikon University Hospital, National Kapodistrian University of Athens, Greece 2. Department of Nuclear Medicine, Biomedical Research Foundation of the Academy of Athens, BRFAA, Athens, Greece
BACKGROUND
The efficacy of immunotherapy (IO) in patients with recurrent/metastatic head and neck squamous cell carcinoma (r/m HNSCC) has been well established. The identification of predictive biomarkers for response to immunotherapy and survival remains an area of intensive investigation. [illegible/obscured by presenter] ...help identify patients most likely to benefit from [illegible]
METHODS [obscured by presenter; Table 1 Demographic characteristics illegible]
RESULTS
Patients with TLG≤30 had longer median OS (median 49.0 vs 14.9 months; p=0.02) and numerically longer PFS (median 37.2 vs 9.4 months; p=0.11) compared to those with TLG>30. In multivariable analyses, TLG ≤30 was borderline significantly associated with improved OS (HR 0.42, 95% CI 0.18–1.00; p=0.05) and PFS (HR 0.51, 95% CI 0.25–1.01; p=0.05). None of the other PET parameters showed significant association with OS or PFS. Logistic regression did not identify any potential predictors of OR, while correlation analyses demonstrated only weak association between PET parameters and PD-L1 expression.
[Table 2. PET/CT parameters — illegible]
[Table 3. Survival by TLG Group — illegible]
[Figure 1. Summary of Overall Survival by TLG Group — KM curve, tick labels illegible]
[Table 4. Cox regression analysis to investigate association between PET/CT parameters and overall survival — illegible]
CONCLUSIONS
Baseline TLG may represent a potential predictive imaging biomarker for OS and PFS in patients with r/m HNSCC receiving IO, with lower TLG (≤30) associated with substantially improved outcomes. Other PET-derived parameters demonstrated limited predictive value. Prospective validation studies are warranted.
Correspondence: dpsyrri@med.uoa.gr
Funding: This study was not funded by any commercial entity
[e-poster kiosk UI: "Back to search"]
@DAmbrosio_MD presented data on quantitative #PARP1 #H_score as a predictive biomarker for #trabectedin plus #olaparib combination in advanced @STS as part of analysis of TOMAS2 study.
@ctosociety #sarcoma #ESMO26 @myESMO #ESMOAmbassadors https://t.co/OCB8GeMPwJ
08:30 - 10:00 Rapid oral: Sarcoma
CHAIRS: MARK DICKSON, PALMA DILEO, CESAR SERRANO
Exploratory biomarkers: PARP1 quantitative H-score
20% of weakly stained cells
30% of moderately stained cells
40% of strongly stained cells
1× 20%
+
2× 30%
+
3× 40%
H SCORE 20 + 60 + 120 = 200
CASE example
FFPE from surgical resection
Lorenzo D'Ambrosio MD PhD
McCarty KS Jr et al. Cancer Res. 1986 Aug;46(8 Suppl):4244s-4248s. PMID: 3524805.
Lorenzo D'Ambrosio
Quantitative PARP1 H-score as a predictive biomarker for trabectedin plus olaparib combination in advanced soft tissue sarcoma: Exploratory analysis of the TOMAS2 study
MALAGA AUDITORIUM - HALL 3
#ESMO26 Inspiring talk by @ines_vazluis on how #digtalhealth & #AI can be used in patient outcome and monitoring! Congrats for @AliceFranzoi for driving the innovation in #cancersurvivorship & #carepathway
🌟🌟🌟🌟 https://t.co/3Wi3BES0G0
[Slide 2]
Ideal and real-world care pathways
Patient-Centered Care
Mission & values aligned with patient goals
Care is collaborative, coordinated, accessible
Physical comfort & emotional well-being are top priorities
Patient & family viewpoints respected & valued
Patient & family always included in decisions
Family welcome in care setting
Full transparency & fast delivery of information
NEJM Catalyst (catalyst.nejm.org) (c) Massachusetts Medical Society
Needs across the cancer care pathway
Before diagnosis: Access and screening; Information
Diagnosis: Understanding options; Psychosocial support
Treatment: Toxicities and adherence; Care coordination
Follow-up: Persistent symptoms; Long-term health
Progression and relapse create additional transitions
4.1 million
Projected healthcare workforce shortfall in the EU by 2030
45-71%
Reported burnout and stress among healthcare professionals
Adapted from MA Franzoi, ESMO 2025. Schenkel 2025; Shanafelt 2012; Angelis 2024; Banerjee 2017; Hlibcky 2021; Amesz 2023; WHO 2020.
Ines Vaz-Luis - Gustave Roussy, France
[Slide 3]
Frameworks for implementing RPM
Planning
EXPLORATION / PREPARATION / IMPLEMENTATION / SUSTAINMENT
OUTER CONTEXT / BRIDGING FACTORS / INNOVATION FACTORS / INNER CONTEXT
[illegible box text]
Evaluation
PRISM CONTEXTUAL FACTORS
EXTERNAL CONTEXT: External environment; Policy; Resources; Guidelines; Incentives
INTERNAL CONTEXT: Multi-level organizational & patient characteristics; Multi-level organizational & patient perspectives (values); Implementation & sustainability infrastructure
Fit among and interactions among ALL of: Intervention components; Implementation strategies; Inner & outer context; RE-AIM dimensions
Reach, Effectiveness, Adoption, Implementation, Maintenance
Evidence-based intervention (components); Implementation strategies
Overarching issues: Proportion / penetration; Representativeness; Reasons: how & why; Adaptations; Costs, benefits & value
Moulin JC. Implementation Science 2019; Zullig LL. Translational Behavioral Medicine 2024
Ines Vaz-Luis - Gustave Roussy, France
Oral abstracts EP-NEC #ESMO26 ; >/=2L, 1L & 2 L; novel agents. Early PFS in >/= 2L; 1.4mo. Med OS without liver nets better & higher response in 1L in those without liver nets @myESMO Biomarkers needed; P3 trials awaited. Great discussion @JaydiDelRivero https://t.co/SolSAoWX0v
[Slide 1]
Outline
PD-L1 bispecific combinations in EP-NEC
LBA57
Opamtistomig (LBL-024) monotherapy in advanced extrapulmonary neuroendocrine carcinoma (EP-NEC) after ≥2 prior lines of therapy: results from a pivotal, registrational phase IIb study of a novel PD-L1×4-1BB bispecific antibody
2392O
Opamtistomig (LBL-024), a novel PD-L1×4-1BB bispecific antibody, combined with chemotherapy as first-line treatment for advanced extrapulmonary neuroendocrine carcinoma: results from a phase Ib/II trial
2393O
First results from a phase 2 trial of second-line pumitamig (PD-L1 × VEGF-A bsAb) plus chemotherapy in unresectable neuroendocrine neoplasms
[Slide 2]
Conclusions
• Opamtistomig demonstrated clinically meaningful and durable antitumor activity in EP-NEC
➢ IRC-assessed confirmed ORR: 26.0% (95% CI, 17.6–36.0), meeting the prespecified efficacy criterion; mDoR was 9.8 months (95% CI, 4.4–NE).
➢ mOS was 8.7 months (95% CI: 6.1–11.7) with a median follow-up of 16.3 months.
• The safety profile was manageable, with hepatic laboratory abnormalities predominantly low grade and transient.
• BLA has been accepted and granted Priority Review by NMPA, based on the pivotal single-arm Phase IIb study.
• A confirmatory Phase III study of opamtistomig plus chemotherapy in first-line EP-NEC is ongoing (NCT07720193).
12
Ming Lu
[Slide 3]
Conclusions
❑Opamtistomig is a uniquely engineered bispecific antibody with high affinity for PD-L1 and low affinity for 4-1BB, designed to minimize systemic toxicity.
❑In the phase Ib/II trial, opamtistomig plus EP/EC showed promising efficacy and was well tolerated. The ORR was 69.2% (cORR, 60.0%), with a mPFS of 5.7 months (95% CI, 5.5–8.6) and a mDoR of 10.2 months (95% CI, 5.6-15.9). Long-term follow-up demonstrated an improved survival trend, with an 18-month OS rate of 55.7%.
❑A BLA application for accelerated approval in ≥3rd-line EP-NEC has been accepted and granted priority review by NMPA, China. A randomized, double-blind, placebo-controlled confirmatory Phase III study evaluating opamtistomig plus chemotherapy as first-line treatment for EP-NEC is ongoing (NCT07720193).
❑Ongoing studies are evaluating opamtistomig in combination with SOC across multiple indications, including SCLC, NSCLC, OC, BTC, HCC, GC, TNBC, mCRC, melanoma and ESCC.
Panpan Zhang
[Slide 4]
Summary and conclusions
• In this first trial evaluating a PD-(L)1 x VEGF-A bsAb in patients with unresectable NEC, pumitamig plus chemotherapy showed encouraging antitumor efficacy in the second-line setting, where treatment options are limited
▪ cORR 40.0%
▪ Median PFS 5.5 months
▪ Median OS 12.8 months
• Given the modest outcomes reported historically in the second-line setting,1 these findings suggest that pumitamig plus chemotherapy may represent an encouraging therapeutic approach for patients with unresectable NEC
• Pumitamig plus chemotherapy showed a manageable safety and tolerability profile, with a low rate of treatment discontinuation
• Pumitamig is currently being evaluated in four global phase 3 studies in thoracic tumors, one first-line global phase 2/3 study in CRC, and one first-line global phase 2/3 study in gastric cancer*
Pumitamig plus chemotherapy showed encouraging efficacy and safety in this difficult-to-treat NEC population
*Thoracic tumors: ROSETTA Lung-01 (NCT06712355), ROSETTA Lung-02 (NCT06712316), ROSETTA Lung-201 (NCT07361497), and ROSETTA Lung-202 (NCT07361510). CRC: ROSETTA CRC-203 (NCT07221357). Gastric cancer: ROSETTA Gastric-204 (NCT07221149).
1. Walter T, et al. Lancet Oncol. 2023;24:297-306.
Impressive weight loss reversal. https://t.co/aSb49wDpwG
Figure 3. Change in body weight (N = 24)
Body weight change from baseline (%)
Study week: -24, -12, -4, 0, 4, 8, 12, 16
Rilogrotug dose 1 →
References
What a powerful message and an even stronger call to action! No patient’s survival should depend on luck, and no patient should be left behind when a clinical trial ends. Post-trial access is not a privilege. It is a responsibility #ESMO26 @myESMO https://t.co/3A1W5OZT6h
[Slide 1]
When the trial ends, the patient is on a cliff edge
Nov 2021: Enrolled in trial.
2023: Trial threatened with closure; sponsor convinced to extend.
2 Oct 2026: Notice received.
Jan 2027: Impending trial closure.
To our knowledge, there is no approved alternative for my disease in Europe or the US
Natalia Montigny
[Slide 2]
Extending Life, Realizing Potential
What the trial records: A complete response on a scan; Progression-free survival; Overall survival; Measured in months
What this means: I live a full life, everyday; I co-founded Maison You with my best friend; I advocate for patients' wellbeing in research and access; Five years of rebuilt life (and counting!)
Made possible by: The scientists who designed the molecule | The patients who joined the trial before me | The team at Gustave Roussy | The sponsor who funded the research
Every extra day, month and year of life is a return on the investment that science made.
#ESMO26 Timothy Yap presents selected synthetic lethality strategies in development for the treatment of cancer
#ESMOAmbassadors @myESMO https://t.co/IBqFhiXcxJ
Synthetic lethality in cancer medicine
Nonmalignant cell
Malignant cell
No drug
Drugged
Main power
Backup battery
Light ON
Light OFF
Alive
Death
Synthetic Lethal Strategies
Tumor alteration | Drug
HRR mutations (BRCA1/2, PALB2, RAD51C/D) | PARP inhibitors
ATM loss | ATR inhibitors
MSI/dMMR | WRN inhibitors
MTAP loss | MTA-Cooperative PRMT5 inhibitors
CCNE1/FBXW7/PPP2R1A aberrant tumors | PKMYT1 inhibitors
SMARCA4 mutations | SMARCA2 inhibitors
CIN tumors | KIF18A inhibitors
EP300 mutations | BET inhibitors
ARID1A mutations | ARID1B inhibitors
Timothy A. Yap, MBBS PhD FRCP
Great opening ceremony by @FAndreMD - showcasing the work that @myESMO has done over the last year and the amazing work planned !
#ESMO26 #ESMOAmbassadors https://t.co/rXllnVuOPL
[Slide 1]
Keeping pace with science is no longer enough
ESMO's evolution is the response
[tree diagram branching to four items]
Complexity
Fragmentation
Data
Need for guidance
[Slide 2]
ESMO Roadmap 2030 levers
[gear icon] Helping to shape the scientific agenda
[folder/org-chart icon] Establishing standards and foundations
[people icon] Strengthening people, research, healthcare capabilities
[globe icon] Expanding global reach and impact
[Slide 3]
Targeted Committees on key elements of modern oncology
[icon] Artificial intelligence and digital oncology
[icon] Cancer care delivery
[icon] Cancer prevention and interception
[icon] Cancer therapies
[icon] Precision oncology and taxonomy
[icon] Special populations
Clinical Practice Guidelines Committee
“Inequalities start long before a cancer diagnosis”, my take away from presentation by @JoseRamalho during his presentation in the patient advocacy track session on “Access, equity and reducing inequalities”.
#ESMO26 #ESMO2026 #equity #ESMOCongress2026 #PatientAdvocacy https://t.co/IXdvnXOBdX
13:00 - 14:30 Access, equity, and reducing inequalities
CHAIRS: ANNE-MARIE BAIRD, AGATA POLINSKA
Inequalities start long before a cancer diagnosis
Progress in prevention
22 % -> 19 %
Daily smoking, 2012-22
2 in 3
Countries with falling alcohol consumption, 2010-22
64 %
HPV vaccination coverage in 2023
Exposure remains higher with low education (Low education | High education)
Daily smoking | 19% | 13%
Overweight or obesity | 57% | 43%
Insufficient physical activity | 73% | 64%
Low vegetable consumption | 43% | 33%
Low fruit consumption | 37% | 34%
Source: OECD/European Commission (2025)
José Ramalho, Health Division, OECD
José Ramalho - Mapping the gaps: Insights from the European Cancer Inequalities Registry
SEVILLE AUDITORIUM - NCC
Full house bright and early at investigational immunotherapy #ESMO26
Keep your 👀 on this PRAME TCR bispecific
🤩over 50 cancers PRAME+
🤩exciting response in heavily pretreated pts, PRAME level related https://t.co/tb9pOjCvgJ
[Slide 1]
IMA402 is an Optimized T-cell Engager (TCER) Designed to Target PRAME
Improved benefit-risk profile with half-life extension¹
[Schematic: Tumor Cell – PRAME – IMA402 – CD3/TCR – Activated T cell]
✓ Antitumor Activity: High-affinity and specificity TCR domain targeting PRAME pHLA molecules
✓ Optimized tolerability: Low-affinity T-cell recruiter against CD3/TCR allows higher dosing
✓ Antibody-like format with half-life extension: Long half-life of >1 weekᵃ allows for q2w or longer dosing intervals
PRAME is expressed in more than 50 cancers
[Heat-map list of cancer types, illegible]
PRAME prevalence in selected indications
Indication | % PRAME+ patientsᵇ
Cutaneous Melanoma 95%
Uterine Carcinoma 95%
Uterine Carcinosarcoma 95%
Synovial Sarcoma 95%
Uveal Melanoma 90%
Mucosal Melanoma 90%
Ovarian Carcinoma Subtypes 85%
Squamous Cell NSCLC 70%
Triple-negative Breast Carcinoma 65%
Small Cell Lung Cancer 45%
Esophageal Carcinoma Subtype 45%
Kidney Carcinoma Subtype 40%
Cholangiocarcinoma 35%
HER2-Enriched Breast Carcinoma 30%
Adenocarcinoma NSCLC 25%
Head & Neck Squamous Cell Carcinoma 25%
Hepatocellular Carcinoma 20%
Bladder Carcinoma 20%
[legend: ≥95% ... ≥10%]
ᵃ Half-life calculated by non compartmental analysis (NCA). ᵇ Data on file: PRAME target prevalence is based on a proprietary mass spec-guided initial expression threshold applied to RNAseq and/or immunohistochemistry data (approximate values, values between 95%-100% shown as 95%).
NSCLC, non-small cell lung cancer; pHLA, peptide-human leukocyte antigen; PRAME, preferentially expressed antigen in melanoma; q2w, every 2 weeks; TCR, T-cell receptor.
1. Hofmann M, et al. mAbs. 2026;18(1):1-24.
Prof. Dr. Dirk Schadendorf; Abstract #8465
[ESMO Congress logo] 3
[Slide 2]
IMA402-101 Study Design
Key Objectives
Primary:
• Determine MTD and/or RP2D
• Assess safety and tolerability
Secondary:
• Evaluate initial antitumor activity (RECIST 1.1 and iRECIST)
• Assess pharmacokinetics
Key Eligibility Criteria
• Recurrent and/or refractory solid tumors expressing PRAMEᵃ
• No prospective PRAME testing required
• HLA-A*02:01 positive
• ECOG performance status 0-1
• Received or not eligible for all available indicated standard of care treatments
Phase 1
• MABEL-based starting dose
• Dose escalation based on cohorts of 1-6 patients using adaptive design (BLRM model)
• MTD not reached per adaptive BLRM model
• q1w step dosing (3 doses) up to target doseᵇ
• q2w dosing from week 7 introduced post data cutoff based on favorable pharmacokinetics
• IMA402 RP2D range: 10-45 mg
IMA402 Monotherapy: 0.02 mg, 0.06 mg, 0.12 mg, 0.36 mg, 0.8 mg, 1.6 mg, 3 mg, 4 mg, 5 mg, 8 mg, 10 mg, 12 mg, 20 mg, 30 mg, 45 mgᶜ
IMA402 + Pembrolizumab: 5 mg + pembrolizumab, 10 mg + pembrolizumab, 20 mg + pembrolizumab, 30 mg + pembrolizumab
Efficacy Populationᵈ (n=40)
Safety Population (N=126)
[Footnotes small, partly illegible:] EudraCT No. 2022-503133-54-00, NCT05958121. ᵃ Cutaneous melanoma, melanoma of unknown primary, uveal melanoma, synovial sarcoma, endometrial carcinoma, ovarian carcinoma, squamous non-small cell lung cancer. ᵇ Step dosing introduced at 0.36 mg [...] ᶜ Exploratory high dose in n=6. ᵈ Efficacy population: All patients treated within the RP2D range as of Mar 1, 2026 [...] tested positive for PRAME [...] BLRM, Bayesian logistic regression model; ECOG, Eastern Cooperative Oncology Group; MABEL, minimum anticipated biological effect level; MTD, maximum tolerated dose; q1w, every week; q2w, every 2 weeks; RP2D, recommended phase 2 dose.
Data cutoff Jun 1, 2026
Prof. Dr. Dirk Schadendorf; Abstract #8465
[ESMO Congress logo] 4
[Slide 3]
Efficacy of IMA402 ± Pembrolizumab by PRAME Expression
[Waterfall plot] Y axis: Best % Change in Sum of Longest Diameter of Target Lesions from Baseline and BOR (RECIST 1.1)
PRAMElow (n=9): bar labels 45, 19, 15, 13, 12, 9, 4, -27, -62
PRAMEhigh (n=31): bar labels 41, 35, 29, 24, 21, 17, 13, 9, 6, 4, 4, 3, 1, 0, -7, -10, -11, -17, -22, -25, -44, -51, -60, -65, -68, -70, -77, -81, -84, -100, -100
Legend: IMA402 monotherapy; IMA402 + pembrolizumab; Melanomaᵃ; Ovarian cancer; Other indicationsᵇ
BOR (RECIST 1.1): PD, SD, PR, cPR, cCR; ▶ Ongoing response/disease control; ▷ Ongoing treatment
Reference lines: BL; PR
PRAMEhigh
All Indications Melanoma Ovarian Cancer
cORR 32% (10/31) 32% (7/22) 3/6
DCR (week 6) 65% (20/31) 73% (16/22) 3/6
ᵃ Includes cutaneous melanoma and one patient with uveal melanoma. ᵇ Includes endometrial cancer (n=2), sqNSCLC (n=2), and synovial sarcoma (n=1).
BOR, best overall response; BL, baseline; cCR, confirmed complete response; cORR, confirmed objective response rate; DCR, disease control rate; PD, progressive disease; (c)PR, (confirmed) partial response; RP2D, recommended phase 2 dose; SD, stable disease.
Data cutoff Jun 1, 2026
Prof. Dr. Dirk Schadendorf; Abstract #8465
[ESMO Congress logo] 10
[Slide 4]
Key Takeaways
• TCR-based therapies enable immune recognition of intracellular tumor antigens presented by cell-surface HLA, expanding the therapeutic landscape beyond targets accessible to conventional immunotherapies
• IMA402 is a novel TCR-based bispecific T-cell engager (TCER) targeting the cancer-associated antigen PRAME, a target expressed in more than 50 cancers
• IMA402 demonstrates a favorable tolerability profile and encouraging initial antitumor activity across various indications, including melanoma
In addition to IMA402 monotherapy, three ongoing cohorts of IMA402 with:
+ Pembrolizumab or nivolumab/relatlimab
+ Decitabine as potential PRAME enhancer
+ MAGEA4/8-directed TCER IMA401
HLA, human leukocyte antigen; ICI, immune checkpoint inhibitor; TCR, T cell receptor.
Data cutoff Jun 1, 2026
Prof. Dr. Dirk Schadendorf; Abstract #8465
[ESMO Congress logo] 12
Amazing presentation on toxicity @RobertoFerrara_ ♡
#ESMOAmbassadors #ESMO26 https://t.co/65cXo7hTGt
[Slide 1]
Tocilizumab not effective in ICANS from CAR-T. Better Anakinra
TOCILIZUMAB IL-6 receptor blocker: NO CSF penetration
TOCILIZUMAB → increases blood IL-6 → IL-6 goes in the brain where toci cannot (worse neurotox)
ANAKINRA: IL-1 receptor blocker: high CSF penetration
ANAKINRA → still blocks IL-1 receptor in the brain
BLOOD
Tocilizumab
humanised IgG1 anti-IL-6R
BLOOD-BRAIN BARRIER
BRAIN / CSF
148 kDa
Stokes radius ≈ 5.5 nm
Negligible CSF entry after IV; therapeutic CSF levels only intrathecally
Anakinra
recombinant IL-1 receptor antagonist
17.3 kDa
Stokes radius ≈ 2.3 nm
≈ 1.8% of the IV dose reaches CSF; neuroprotective levels within 45 min
Tocilizumab worsed ICANS in [illegible]% of patients treated with CAR-T
Tocilizumab
IL-6 spike
After toci → IL-6 spike in plasma
Higher IL-6 levels in the CSF → worse neurotox
Grade 0-1; Grade 2; Grade ≥3
Baseline; Day 5; Week 4
Santomasso Cancer Discovery 2018, Locke Transplantation and Cell Therapy 2024
[Slide 2]
Fc active
BOTENSILIMAB
anti-CTLA-4 · IgG1 ·
Fc-enhanced (↑ FcγRIIIA)
Nivolumab
anti-PD1· IgG4
Balstilimab
anti-PD1· IgG4
GOTISTOBART
anti-CTLA-4 · IgG1 ·
Fc-active, pH-dependent
TRAEs any grade: 77% [other bars cut off]
TRAEs G3/G4: 33%; 32%; 42%
Diarrhea/colitis G3/G4: 4%; 14%; 9% (colitis only; +4% diarrhea)
0% 25% 50% 75%
Nivolumab + ipilimumab
Botensilimab + balstilimab (pan-tumor, N=411; 58 pts NS[cut off]
Gotistobart
[cut off]JM 2019, Gordon ESMO 2025, Cho Nature 2026
Very proud to have the opportunity to participate in this outstanding study in 340 cancer Ukrainian patients living in war frontline regions. Gender and income the most important stress factors. Thanks to Dr Perea and Yuliya Shevchuk from mission kharkiv @MissionKharkiv #ESMO26 https://t.co/ZULwd7LXTu
Same slide also posted by @PerezFidal
FPN: 3482
Psychosocial factors in cancer care in frontline regions in Ukraine
Javier Perea1, J Alejandro Perez-Fidalgo1,2, Anna Kachan3, Yuliia Nikishyna3, Yuliia Shevchuk3 .
1Department of Medical Oncology Hospital Clinico Universitario Valencia. INCLIVA.
2University of Valencia
3Mission Kharkiv
INCLIVA | VLC Biomedical Research Institute
Universitat de València Facultat de Medicina i Odontologia
Mission Kharkiv
Background
Diagnosis of cancer has a deep impact on different life aspects, including socioeconomic issues, [obscured] and well-being.
Psychosocial determinants of canc[obscured] major concern that affects quali[obscured] diagnosis occurred in an adverse [obscured] such as a war, the potential stress[obscured] is expectedly higher.
Methods
Patients recently diagnosed wi[obscured] Ukrainian regions next to th[obscured] and Sumy regions, wer[obscured] questionnaire.
Psychosocial aspe[obscured] measured, includ[obscured] of coping strateg[obscured]
Results
340 patients responded to the questionnaire, 92 male and 248 female. The median age was 60 years (19-82). 46.2% were from [obscured] from the Kharkiv region. The most frequent diagnoses were breast cancer 33.5%, gastrointestinal cancers 23.5% and malignan[obscured] gynecological malignancies 16.5%. Of note only 6.5% had a thoracic malignancy. The most frequent stage at diagnosis was II i[obscured] stage III 21.5% and stage IV 17.9%.
The median PSS-10 level was 22 (interquartile range 17 to 25) from a possible range 0 to 40, higher than previously re[obscured] values. High stress levels (PSS-10 ≥17) were observed in 19.1% of patients, while 10.3% had low stress levels. Stress l[obscured] [obscured]ociated with gender (X2 8.9. p=0.001), with higher prevalence in women (23% vs 8.7%). No association was foun[obscured] stage (X2=2.4; p=0.7). Stress level was significantly associated with income level; higher stress levels were [obscured] [lo]wer income. Moreover, stress level scores increased over time after cancer diagnosis, being higher after mo[obscured] [obscured]s.Coping strategies were problem-oriented in 75.9%, emotionally oriented in 12.4%, avoidant in 7.1%, an[obscured] coping strategies were associated with lower stress levels (χ²=8.2; p=0.016).
[Conclu]sion
[obscured] high among cancer patients in Ukrainian regions in a war context. Gender and income are the [obscured] [obscured]-oriented coping strategies reduced stress level.
3482P
Dr. Florian Lordick summed it up perfectly at #ESMO26 👏
💡 Surrogate endpoints like PFS and ORR can help bring treatments to patients earlier, but they don’t always translate into better overall survival.
🙏Regulatory acceptance doesn’t necessarily mean clinical validation. An important distinction in oncology!
@kbaskurtt @osutcuoglu
How do Regulators See Surrogate Endpoints?
Different regulatory pathways – shared goal: earlier access for patients with reliable evidence
FDA United States Food and Drug Administration
Traditional approval
May be based on a surrogate endpoint that is established to predict clinical benefit.
(21st Century Cures Act, FD&C Act §507)
Accelerated approval
May be based on a surrogate endpoint that is reasonably likely to predict clinical benefit.
(FD&C Act §506(c))
• Confirmatory post-marketing studies are required to verify clinical benefit after accelerated approval.
• The acceptability of a surrogate endpoint is context-dependent (disease, population, mechanism of action, available therapies).
• FDA publishes a table of surrogate endpoints used for approved products (including oncology examples such as pCR, DFS, ORR, PFS).¹
EMA European Union European Medicines Agency
Standard marketing authorisation
Surrogate endpoints may support a positive benefit-risk assessment, if adequate evidence is provided.
(EU Regulation 726/2004)
Conditional marketing authorisation (CMA)
Earlier approval based on less comprehensive data, including surrogate endpoints, for medicines addressing unmet medical need.
Specific post-authorisation obligations (e.g. confirmatory studies).
(EU Regulation 726/2004)
Accelerated assessment (AA)
Shortened assessment timeline (target: 150 days) for medicines of major public health interest.
Does not lower the evidentiary standard – usually based on complete data (clinical or surrogate endpoints).
(EU Regulation 726/2004)
Regulators accept surrogate endpoints under defined conditions and with different pathways.
Regulatory acceptance does not necessarily imply full surrogate endpoint validation.
1. U.S. Food and Drug Administration. Table of Surrogate Endpoints That Were the Basis of Drug Approval or Licensure. 2024/2025.
2. European Medicines Agency. Regulation (EC) No 726/2004; EMA guidance on conditional marketing authorisation and accelerated assessment.
ESMO 2026 | Eight Frameworks Shaping the Future of Oncology
In his opening address at ESMO 2026 in Madrid, ESMO President Prof. Fabrice André highlighted eight completed ESMO frameworks:
1. ESCAT v2 – Clinical actionability of molecular targets
2. ETAC-S – Tumour-agnostic classification and screening
3. NGS recommendations – Molecular profiling in oncology
4. EBAI – AI-based biomarkers in oncology
5. ELCAP – Large language models in clinical practice
6. EnLIST – Lines of systemic therapy
7. ESMO-GROW – Real-world evidence reporting
8. ESMO-MCBS v2 – Magnitude of clinical benefit
Four additional frameworks are under development and expected within the next 6–12 months.
#ESMO26 @myESMO @oncodaily #ESMOPresident #PrecisionOncology #NGS #ArtificialIntelligence #CancerResearch
"According to ESMO"
Completed ESMO Frameworks
1 ESMO Scale for Clinical Actionability of molecular Targets (ESCAT) v.2
2 ESMO Tumour-Agnostic Classifier and Screener (ETAC-S)
3 ESMO NGS Recommendations
4 ESMO Basic Requirements for AI-based Biomarkers in Oncology (EBAI)
5 ESMO Guidance on the Use of Large Language Models in Clinical Practice (ELCAP)
6 ESMO Adaptation of Lines of Systemic Therapy (EnLIST)
7 ESMO Guidance for Reporting Oncology real World Evidence (ESMO-GROW)
8 ESMO-Magnitude of Clinical Benefit Scale (ESMO-MCBS) v.2
4 under development, to be released over the next 6-12 months
[Presenter Fabrice André on adjacent screen; repeated smaller copies of slide on lower screens]
Glioblastoma researches from @uzbrussel presented their promising study results in glioblastoma #ESMO2026 A step forward for our patients https://t.co/0mUDe5lqVL
[Slide 1]
Declaration of interests
• Public speaking fee: Bristol-Myers Squibb, Miltenyi Biotec
• Travel expenses: AstraZeneca, Miltenyi Biotec, Merck Sharp & Dohme
• Financial support for the phase I GLITIPNI trial by non-profit organizations (Kom Op Tegen Kanker, FWO, EOS, Paul De Knop Fonds, Heart For Brain, Live for better days, Hersentumorfonds, Stichting Tegen Kanker)
Cleo Bertels, MD
[Slide 2]
ESMO congress MADRID 2026
Abstract 698RO
A phase Ib Clinical Trial on Combined (Neo-)Adjuvant Intravenous (IV) Plus Intracranial Administration of Ipilimumab (IPI) and Nivolumab (NIVO) in Resectable Recurrent Glioblastoma (rGBM): NEO-GLITIPNI
Iris Dirven*, Anna Chiau, Cleo Bertels, Louise Lescrauwaet, Xenia Geeraerts, Latoya Stevens, Freya Vaeyens, Anne-Marie Vanbinst, Hendrik Everaert, Stefanie Brock, Johnny Duerinck, Bart Neyns
Universitair Ziekenhuis Brussel – Vrije Universiteit Brussel
Brussels, Belgium
*Corresponding author: Iris.Dirven@uzbrussel.be
VUB | Brussels Oncology Center | Universitair Ziekenhuis Brussel
Amazing discussion of Prof Robin Jones @RobinL_Jones in #ESMO2026 @myESMO. Clear concepts and sharp analysis. To enjoy it!! https://t.co/GPJqagUAqF
TGCT & Desmoid: Similarities & Differences
• Chronic diseases
• Limited value of standard endpoints
• Radiological
• Overall survival
• Importance of quality of life measures
• Existing randomized data to guide management
• Unpredictable clinical course
• TGCT:
• CSF-1R inhibitors clear mechanism
• Many patients treated with surgery
• Desmoid:
• Variety of effective agents
• Different mechanisms of action
• Most patients initially managed with active surveillance
• Spontaneous regression
Stacchiotti S et al. Cancer Treat Rev 112; 102491: 2023
Jeys LM et al. Bone Joint J 108-B; 1045-1051: 2026
Kasper B et al. JAMA Oncol 10; 1121-1128: 2024
An inspiring talk by Juliane Walz at #ESMO26 on therapeutic cancer vaccines. My takeaway: selecting the right antigens is only the beginning—the challenge is translating tumour-specific T-cell responses into lasting clinical benefit. Exciting science with important questions ahead.
@Larvol @OncoAlert @myESMO
[Slide 1]
Therapeutic vaccination strategies
Peptide-based vaccine
1 Vaccination 2 Priming 3 Proliferation 4 Elimination
(APC, T cell, Cancer cell)
mRNA-based vaccines
mRNA carrier with gene of interest → Endosome → mRNA → Protein → Proteasome → Peptides → Vesicle → MHC complex (APC)
• Dendritic cell vaccines
• Whole tumor cell-based vaccines
[Slide 2]
Case presentation: A young patient with advanced liver cancer
Maya
• 15-year-old girl
• Advanced fibrolamellar cancer (FLC)
• Liver transplant and multiple therapy lines
• Continued disease relapses
• Palliative track
[MRI image: Se: 5 Im: 16/68]
Timeline: FD; CHX; LTx (M1); relapse (M11, M14, M19, M21); PARP inhibitor; M1 M11 M14 M16 M19 M21
Brilliant talk this morning by Chris Bailey on extra-chromosomal DNA (ecDNA): what is it, origins, detection and clinical implications.
#ESMO26 #ESMOAmbassadors @myESMO https://t.co/sb14EI4RBg
[Slide 1]
The New York Times
Scientists Are Just Beginning to Understand Mysterious DNA Circles Common in Cancer Cells
For years, researchers weren't exactly sure what to make of these extra loops of genetic material . That's quickly changing.
Extrachromosomal DNA are circular structures of 2-5Mb that contain copies of genes and reside outside of conventional chromosomes
Dr Chris Bailey
[Slide 2]
ecDNA is traditionally detected through in-situ hybridisation methods
Few cells with high copy number
Dedifferentiated LPS
MDM2 CEP12
Lung Squamous Cell Carcinoma
IFNy CEP12
Dr Chris Bailey
[Slide 3]
ecDNA is associated with metastasis and higher tumour stage
Metastasis samples (bar chart by tumour type): MELA, COLORECTAL, HPB-NOS, OVA, BRCA-NOS, SARC-NOS, LUAD, LUNG-NOS, RENAL-NOS, NET, KIRC, UGI-ADENO, UGI-NOS, OPT, LMS, UTER, GLIOMA-NOS, LUSC, SCLC, LUMINAL BRCA, PRAD, STAD, UGI-SCC, PAAD, LPS, BLCA, LIHC, GBM, TN BRCA, OSA, CHOL, MFS
Regression analysis: included / excluded
All focal amplifications | ecDNA | non-ecDNA focal amplifications
Metastases enrichment vs primary samples (OR)
vs non-ecDNA amplifications | vs no amplifications
Stage 4, Stage 3, Stage 2
--> favours ecDNA formation
Controlling for tumour type and purity, ecDNA detection was significantly enriched in metastatic samples (non-paired, OR 1.56, 95% CI 1.24-1.96) (Figure 5A).
Genomics england
Dr Chris Bailey
[Slide 4]
Conclusions
• ecDNA common across 39 tumour types (17.1% in the GEL cohort)
• Possible novel functions of ecDNA such as immunomodulation
• ecDNA has multiple underlying origins that are dependent on tumour type
• ecDNA is associated with late stage, metastatic disease, treatment and poorer overall outcomes in the Genomics England cohort
Dr Chris Bailey
Our #RIANO study at #ESMO26! 138 neuro-oncology professionals from 15 Ibero-American countries (79% LATAM). Regional disparities in experience, gender, and clinical workload. Strengthening our regional voice @myESMO @SNOLAsociety @NeuroOnc @EANOassociation @GrupoGeino 🦾🦾🦾 https://t.co/Hf1pANcVmP
[Slide 1]
Neuro-oncology workforce across Ibero-America: demographic profile from the RIANO survey
Martin Zapata1, Alexandra Diaz2, Gabriela Mendonca3, Victor Patlan4, Angeles Viu5, Sonia; Lenmy Abao, Jorpa Escudero, Fernando Alosio Lanao Sanchez, Eduardo Daniel Bredis Gonzalez, Tessa Cristina Costa Va, Jose isidndra Ibanez, Joaquin Alexis Perez, Lucia Richter P[illegible], Victor Hernandez Alvarez, [illegible] Gutierrez Manrique, Loreto Yanez Sepulveda, Juan Guillermo, Revin Camargo, Kevin Camargo [author list rendered garbled on this image; affiliations illegible]
RIANO Red Iberoamericana de Neuro-Oncologia | BERLIN 2026 ESMO CONGRESS [logo as printed]
BACKGROUND
Understanding who delivers neuro-oncology care across Ibero-America is essential to interpret regional differences in access to care.
We describe the demographic and professional profile of participants in a structured online survey conducted by the Ibero-American Neuro-Oncology Network (RIANO) across Spain and Latin America.
Objective: characterise the workforce profile by region to contextualise disparities in neuro-oncology care.
METHODS
Cross-sectional online survey (preliminary analysis).
1 Design - Structured questionnaire on demographic and professional variables.
2 Distribution - Through medical societies and RIANO local representatives.
3 Population - Respondents from Spain and 14 Latin American countries.
4 Analysis - Descriptive statistics, comparisons Spain vs. Latin America.
Survey open until 30 September 2026. Updated analyses including additional responses will be presented at the congress.
RESULTS
138 professionals responded | 29 (21%) Spain | 109 (79%) Latin America + 14 countries | 44.7 y mean age, all respondents
Figure 1. Experience, gender and case volume by region (% of respondents) [Latin America (n=109) | Spain (n=29)]
>10 years of experience | 54.1% | 72.4%
<5 years of experience | 17.4% | 6.9%
Women | 42.2% | 65.5%
>20 brain tumour cases per month | 14.7% | 34.5%
Practice setting
82.8% of Spanish respondents work only in the public sector.
45.9% of Latin American respondents work in both public and private systems.
Specialties
Medical oncology was the leading specialty in both regions, reflecting the multidisciplinary nature of neuro-oncology care.
Table 1. Demographic and professional profile by region
Variable | Spain (n = 29) | Latin America (n = 109)
Share of all respondents | 21% | 79%
Countries represented | 1 | 14
>10 years of professional experience | 72.4% | 54.1%
<=5 years of professional experience | 6.9% | 17.4%
Women | 65.5% | 42.2%
>20 brain tumour cases per month | 34.5% | 14.7%
Practice setting | Public sector only: 82.8% | Public and private: 45.9%
Leading specialty | Medical oncology | Medical oncology
KEY FINDINGS
Seniority - More than 10 years since certification: 72.4% (Spain) vs 54.1% (Latin America), indicating a more experienced workforce in Spain.
Gender - Women were the majority in Spain (65.5%) but a minority in Latin America (42.2%).
Case volume - Higher proportion of >=20 brain tumour cases per month in Spain (34.5%) vs Latin America (14.7%).
Setting - Most Spanish professionals work in the public sector (82.8%), while nearly half of Latin American professionals work in both public and private systems (45.9%).
CONCLUSIONS
The Ibero-American neuro-oncology workforce is experienced but heterogeneous. Significant regional differences exist in seniority, gender distribution, clinical volume and practice setting. These differences should be considered when designing regional educational and training strategies to reduce inequities in neuro-oncology care.
Disclosure (presenting author)
M. Zapata reports personal fees from AstraZeneca, Bayer, MSD, Novartis, Roche, Bristol Myers Squibb, and Pfizer (all outside the submitted work).
Funding: No funding was received for this study.
Correspondence: Martin Zapata, MD, MSc.
Always thought-provoking insights from @DanielTruhn at #ESMO26! As AI agents enter oncology, we need more rigorous evaluation designs, including RCTs, just as we evaluate new drugs/technology.
#AItrack #ESMOAmbassador https://t.co/5rWDEdVrxy
[Slide 2]
13:30 - 15:00 Transforming oncology with generative AI and autonomous tools
CHAIRS: EVANGELIA CHRISTODOULOU, JAKOB KATHER
Where are we?
4,609 clinical studies of language models, January 2022 to September 2025
Most agent studies are here.
Exam questions 1,704 studies
Simulated cases 1,857 studies
Real patient data 1,048 studies
Randomised trials 19
[QR code] Nat Med 2026 Chen SF et al.
[QR code] JAMA 2025 Bedi S et al.
[Speaker panel] Daniel Truhn — Clinical evidence for AI agents: Where are we and what do we need
CADIZ AUDITORIUM - NCC
[Slide 3]
13:30 - 15:00 Transforming oncology with generative AI and autonomous tools
CHAIRS: EVANGELIA CHRISTODOULOU, JAKOB KATHER
We are now in a Transition Period
Gare Montparnasse, Paris, 22 October 1895
[photo of Montparnasse train derailment]
1895 | Conclusions for Agents today
Running late, the express entered the station too fast | Don't deploy ahead of evidence
The air brake failed, train broke through the wall | Safeguards needed
The guard was busy with paperwork and did not apply the handbrake | Don't overload the human
A woman in the street below was killed | Harm to patients?
Photo: Studio Lévy & fils, 1895 (public domain)
[Speaker panel] Daniel Truhn — Clinical evidence for AI agents: Where are we and what do we need
CADIZ AUDITORIUM - NCC
Presenting at #ESMO2026 in Madrid: Safety of LLM-Generated Chemotherapy Orders: A Multi-Model Evaluation Against International Guidelines and Standard Preparation Protocols (ePoster 247eP).
We had ChatGPT and Gemini generate chemotherapy orders across 16 regimens, then three medical oncologists scored them blinded against NCCN/ESMO, eviQ and manufacturer labels.
Key findings:
• 120/223 order sets (53.8%) had at least one clinically significant error
• No critical errors were recorded
• Errors clustered in supportive care (NK1/5-HT3 omissions, loperamide, cisplatin hydration) and route specification
• Cisplatin- and irinotecan-containing regimens (BEP, FOLFIRINOX, GEMCIS) were the highest-risk
• No detectable difference between models (p=0.42)
Takeaway: LLM errors are not random. They concentrate at identifiable points, so clinicians can focus verification where it matters most. This was a simulation study, and structured expert review remains essential.
Grateful to my co-authors Dr. R. Chanana, Dr. T. Pathan and Dr. K. Gupta, and to Apollo Hospitals Navi Mumbai.
#ESMO26 #Oncology #MedicalOncology #AIinHealthcare #LLM #PatientSafety #Chemotherapy #OncologyAI
@d_stock07734 Consider that for patients with pCR (just under 50%), adjuvant IO, by far the longest part of the regimen (neoadjuvant is just 2 doses), is not needed. https://t.co/LcMfHTk8PB
Figure S7. Pathological response rate.
Proportion of patients (%)
Local assessment: pCR 45.8% | near-pCR 10.8% | pPR 9.4% | pNR 25.0% | progression prior to surgery 2.4% | no surgery/ not reported 6.6%
Central review: pCR 47.2% | near-pCR 11.8% | pPR 8.0% | pNR 26.4% | progression prior to surgery 2.4% | no surgery/ not reported 4.2%
#ESMO2026 opening ceremony by the @myESMO president @FAndreMD https://t.co/HKGLHJBLPQ
[Slide 1]
Keeping pace with science is no longer enough
ESMO's evolution is the response
[tree diagram branching to four items]
Complexity
Fragmentation
Data
Need for guidance
MADRID 2026 ESMO congress
[Podium sign:] ESMO congress MADRID SPAIN 23-27 OCTOBER 2026
[Slide 2]
[Stage photo; screen shows slide twice flanking live video of presenter]
ESMO Roadmap 2030 levers
[gear icon] Helping to shape the scientific agenda
[folder/org-chart icon] Establishing standards and foundations
[people icon] Strengthening people, research, healthcare capabilities
[globe icon] Expanding global reach and impact
MADRID 2026 ESMO congress
[Podium sign:] ESMO congress MADRID SPAIN 23-27 OCTOBER 2026
Amazing discussion at #ESMO2026 @myESMO of Dr R Jones about intermediate mesenchymal tumours 👏🏻👏🏻 https://t.co/NfSENElsaS
Same slide also posted by @ManuPalmerini
[Slide 1]
TGCT & Desmoid: Intermediate Tumours
- Context: Sarcoma oncologists manage a variety of tumours
- "Not all sarcomas are the same"
- but we also treat a number of locally aggressive tumours
- "Oncologists are really good at treating intermediate tumours."
- Simpler biology
- Proof of principle in TGCT, giant cell tumour
- Sarcomas complex biology
- Need better understanding of biology
- Artemis trial in ESMO Plenary Monday
[Slide 2]
TGCT & Desmoid: Discussion
- Are randomized trials always required for registration/reimbursement?
- Should Patient Reported Outcomes (PROs) be the primary endpoint for clinical trials?
- Should the economic burden be more accurately quantified?
- What is the optimal duration of systemic therapy?
- What is the optimal sequence of systemic therapy?
[Slide 3]
TGCT: Randomized Phase 3 Trials
Trial | Patient Number | Response Rate RECIST 1.1 | Progression RECIST 1.1 | Tumour Volume Score Response | Quality of Life
Pexidartinib | 61 | 39% | 2% | 56% | Improvement
Placebo | 59 | 0% p<0.0001 | 2% | 0% p<0.0001 |
Vimseltinib | 83 | 40% | 0 | 67% | Improvement
Placebo | 40 | 0% p<0.0001 | 0 | 0% p<0.0001 |
Pimicotinib | 63 | 54% | 2% | 61.9% | Improvement
Placebo | 31 | 3.2% p<0.0001 | 0 | 3.2% |
Emactuzumab | 91 | 29.7% | 0 | 53.8% | Improvement
Placebo | 45 | 2.2% p<0.001 | 0 | 3% p<0.001 |
References: Tap WD et al. Lancet 394(10197): 478-487: 2019; Gelderblom H et al. Lancet 403(10445): 2709-2719: 2024; Xu H et al. Lancet 407(10533): 1072-1083: 2026; Gelderblom H et al. ESMO 2026
Really enjoyed Florian Markowetz’s talk at #ESMO26, highlighting the long and complex journey. Beyond model development, the often-overlooked challenges of technical integration, governance, regulatory approval & validation are just as critical to bringing AI safely to hospitals. https://t.co/pmtrxxBmLp
[Slide 1]
13:30 - 15:00 Transforming oncology with generative AI and autonomous tools
CHAIRS: EVANGELIA CHRISTODOULOU, JAKOB KATHER
OncoQwen (formerly Oncollama):
AI-Powered Cancer Data Extraction Across the NHS
What is OncoQwen?
• NHS open licensed product built by AI Centre with support from OneLondon
• A MESA Framework (Medical entity Extraction with Schema Alignment)
• Extracts diagnosis, staging, biomarkers & outcomes from free text
• Runs inside Trust firewalls — no patient data leaves the NHS
• Already processed 500k+ documents at GSTT
3 Impact Workstreams
Q1 Inequalities
Multi-region pan-cancer analysis of stage at diagnosis & outcomes by age, sex, ethnicity & deprivation
Q2 COSD Completeness
Compare OncoQwen vs. national cancer registry to quantify missing staging & biomarker data
Q3 Clinical Trials
Automate patient eligibility screening & auto-populate case report forms (EHR2EDC)
Scale & Partners
5 NHS Centres
20 Cancer Types
£300k Budget
3 SDEs Participating
Development phase: model trained on pan cancer synthetic documents
Validation phase: model trained on 6 cancer types: myeloma, breast, ovarian, melanoma, lung and colorectal
Lead: Dr. Joe Zhang, Guy's & St Thomas' NHS FT | OneLondon SDE | Collaboration-focused Driver Project
[Speaker panel] Florian Markowetz — Generative AI and AI biomarkers in precision medicine: Advancing regulation and clinical impact in oncology and beyond
CADIZ AUDITORIUM - NCC
[Slide 2]
13:30 - 15:00 Transforming oncology with generative AI and autonomous tools
CHAIRS: EVANGELIA CHRISTODOULOU, JAKOB KATHER
OncoQwen: the pathway from research to clinic
Governance and approvals at Cambridge University Hospital, in the order they were completed
1 AGREEMENT — Licensed — OncoQwen licensed by London AI Centre @ Guy's and St Thomas' NHS Trust
2 AGREEMENT — MOU signed — Memorandum of Understanding signed with CUH
3 APPROVAL (12/2025) — Committee sign-off — As a quality improvement project, signed off by the NHS Investment Committee
4 APPROVAL — Divisional approval — Approval given at CUH Division B Business and Improvement Meeting
5 APPROVAL — DPIA signed — Data Privacy Impact Assessment, eHospital form signed off
6 SDE GOVERNANCE — SDE access request — East of England SDE Data Access Request form, as an SDE Driver project
7 PLATFORM — Platform protocol — Protocol between Newton's Tree (the platform deploying the LLM on NHS data) and CUH
8 SDE GOVERNANCE — DAC data coverage — OncoQwen Data Coverage for SDE DAC document, alongside schema and output example
9 ACCESS — Terms of Use — Signed by everyone accessing the LLM output data in the SDE
OUTCOME (09/2026) — Governed use — OncoQwen output data accessed in the East of England SDE by approved users
Lead: Dr. Joe Zhang, Guy's & St Thomas' NHS FT | OneLondon SDE | Collaboration-focused Driver Project
[Speaker panel] Florian Markowetz — Generative AI and AI biomarkers in precision medicine: Advancing regulation and clinical impact in oncology and beyond
CADIZ AUDITORIUM - NCC
[Slide 3]
13:30 - 15:00 Transforming oncology with generative AI and autonomous tools
CHAIRS: EVANGELIA CHRISTODOULOU, JAKOB KATHER
CIN signatures to clinic: technical challenges
Moving the Drews et al. 2022 CIN signatures from academic software into NHS use
1 Code quality
• Version control and code review
• Unit and regression tests
• Locked dependencies, reproducible runs
2 QMS and ISO
• ISO 13485 quality management
• IEC 62304 lifecycle, ISO 14971 risk
• MHRA status, DCB0129/0160 safety
3 Licensing and IP
• Confirm licence allows NHS clinical use
• Audit dependency licences
• Agree IP, liability and support
4 Newton's Tree
• Containerised pipeline inside the Trust firewall
• Governed data access
• Version pinning, monitoring, rollback
Drews RM et al. A pan-cancer compendium of chromosomal instability. Nature 2022
[Speaker panel] Florian Markowetz — Generative AI and AI biomarkers in precision medicine: Advancing regulation and clinical impact in oncology and beyond
CADIZ AUDITORIUM - NCC
[Slide 4]
13:30 - 15:00 Transforming oncology with generative AI and autonomous tools
CHAIRS: EVANGELIA CHRISTODOULOU, JAKOB KATHER
CIN signatures to clinic: goals of deployment
From retrospective validation to biomarker-stratified randomised trials
1 Validation
• Lock thresholds, test archived cohorts
• Analytical and clinical validity
2 Test comparison
• Same samples, head-to-head
• CHORD, Myriad, HRDetect
3 NHS pathway study
• Live use under the QMS
• Pre-specified analysis plan
4 Stratified RCT
• CIN-guided vs standard of care
• Evidence for NHS adoption
Existing methods for comparison
Method | Features | Assay input
CIN signatures (Drews 2022) | 17 copy-number signatures | Copy-number profiles
CHORD | SNV, indel and SV signatures | Whole-genome sequencing
HRDetect | Six HRD-associated signatures | Whole-genome sequencing
Myriad myChoice CDx | LOH, TAI, LST plus BRCA1/2 | Proprietary tumour assay
Drews RM et al. A pan-cancer compendium of chromosomal instability. Nature 2022
[Speaker panel] Florian Markowetz — Generative AI and AI biomarkers in precision medicine: Advancing regulation and clinical impact in oncology and beyond
CADIZ AUDITORIUM - NCC
#ESMO26
China's growing influence in the global biotech sector https://t.co/iI3acvtcBN
4. Boom of Chinese Biotechnology Sector
KEY ISSUE
China's growing influence in the global biotech sector.
China's emergence as a global biotechnology powerhouse is increasingly driven by innovation and R&D capacity.
KEY INSIGHT
Sustaining this momentum will require deeper international scientific collaboration, talent exchange, and integration into global research ecosystems.
ESMO COMMITMENT
ESMO promotes global oncology research partnerships and international scientific collaboration to accelerate innovation and improve outcomes for patients with cancer everywhere.
China's biotech boom: why the nation must collaborate to stay ahead
Lizzi CL & Jing Qian, Nature (2026)
Improvement in Europe's Clinical Trial System
#ESMO26 https://t.co/A7djR2uy9F
5. Europe's Clinical Trials Ecosytem
KEY ISSUE
Regulatory barriers to oncology innovation in Europe.
The revision of the EU's IVD Regulation and proposed Biotech Act can streamline clinical trials, precision diagnostics and advanced therapies.
KEY INSIGHT
Faster, coordinated procedures can accelerate oncology research and patient access to innovative treatments.
ESMO COMMITMENT
ESMO has built the evidence, drafted legislative solutions and brought oncology's priorities directly to EU policy makers.
ESMO responses to the proposed revision of the In Vitro Diagnostic Medical Devices Regulation (IVDR) and the EU Biotech Act I
#ESMO26
Global health threats like war, climate change and even AI can affect how we treat cancer https://t.co/46qqiHQtXd
9. 21st Century Global Health Threats
KEY ISSUE
Growing global threats and health inequalities.
Climate change, AI, pandemics, armed conflicts and antimicrobial resistance are widening health inequalities and straining health systems.
KEY INSIGHT
Global health threats require coordinated responses to tackle health inequalities and protect the delivery of care.
ESMO COMMITMENT
ESMO is a privileged partner of the WHO and UN, and advocates for equal access to optimal cancer care for all patients.
The Lancet Commission on 21st century global threats to health
Christopher J L Murray et al.; The Lancet (2026)
The challenge: Women are underrepresented in leadership positions in oncology
#ESMO26 https://t.co/424NN6mHSn
Women underrepresented in leadership position
• Although more women than men are entering medical schools, women remain underrepresented in academic medicine1: graduates now approach 50%, female department leaders and full professors remain under 30%
• Academic medical oncology: women represented 37.1% of faculty, 31.4% of leadership positions and 21.7% of department chairs2
• Women's underrepresentation limits their opportunities for authorship, peer review, funding and promotion, further perpetuating their underrepresentation3
Women in Academic Medicine 2023–2024 [infographic: 57%, 52%, 48%, 45%, 45%, 34%, 29%, 27%, 27%, 25%; category labels illegible]
Academic medical oncology [bar chart Male/Female: Total Faculty, Chair and Program Director, Chair; y-axis Representation, %]
Vicious circle of disadvantage [illustration; small text illegible]
ESMO authorship study4
• Female authors were significantly less likely to be last than first authors (p<0.001 for all years), indicating that women were less likely to be the leaders of a study
ESMO authorship study, 2017–20224 [bar chart First author / Last author: 2017 38%/30%; 2018 37%/24%; 2019 41%/28.5%; 2020 37%/29%; 2021 36%/29%; 2022 39%/30%]
JCO Global Oncology (2015–2020)5: 645 articles
• Female (41.4%) first authors and 190 (32.1%) last authors
• Trend toward higher proportion of female first authors in the most recent years
• Variation in author gender distribution by article type
Female: 41% first author, 32% last author5 [bar chart]
Female first author by article type5 [bar chart]
Female last author by article type5 [bar chart]
JAMA Oncology (2003–2018)6: 598 RCTs
• 18% female corresponding authorship among 598 oncologic RCTs (2003–2018); lower rates for industry-funded trials (14.4%) versus cooperative group trials (25.9%)
1AAMC, State of Women in Academic Medicine 2023–2024 · 2Chowdhry M, JAMA Netw Open 2020 · 3Clark J, Lancet 2019 · 4Linardou H, Ann Oncol 2024;35(Suppl 2):S938–S940 · 5Hornstein P, JCO Glob Oncol 2021 · 6Ludmir E, JAMA Oncol 2019
Prof. Pilar Garrido
I had the pleasure of attending #ESMO2026. Incredible science and great connections all around! @myESMO https://t.co/iQdKnHBaPp
3145eP- Moroccan Oncologists' Perspectives on the Management of Rare Cancers
CHAHBAR Abdelaziz, LAYACHI Mohamed, RAHHALI Rabie, TAOUFIK Houria, MARS Ayoub, DARIF Khadija, AMZERIN Mounia, EL M'RABET Fatima Zahra
Medical Oncology Department, Ahmed Bin Zayed Al Nahyan University Hospital of Oncology, Tangier, Morocco
BACKGROUND
Rare cancers represent a major clinical challenge worldwide, in terms of both diagnosis and treatment.
In Morocco, structural and resource limitations further compound these difficulties and hinder optimal patient care.
This study aims to explore the perceptions and practices of Moroccan oncologists regarding these malignancies.
METHODS
This national, multicenter study was coordinated by the Ahmed Bin Zayed Al Nahyan University Hospital of Oncology in Tangier. An anonymous online questionnaire was sent to Moroccan oncologists involved in the care of patients with rare cancers.
A total of 77 responses were collected and analyzed anonymously.
RESULTS
Respondents' characteristics
Respondents had a mean age of 35.2 ± 6.6 years, with a female predominance (62.3%) and were specialized in medical oncology (74%) and radiation oncology (26%), practicing predominantly in university hospital centers (72.7%).
Main challenges
The most frequently reported barriers were:
Lack or insufficient clinical guidelines 83.1%
No access to an external expert tumor board 81.8%
Limited personal clinical experience 75.3%
Restricted access to diagnosis platforms 66.2%
Insufficient multidisciplinary coordination 62.3%
Reference networks unknown / poorly known 59.8%
Reimbursement issues 59.7%
Lack of investment / funding 36.4%
Information sources
Respondents relied mainly on the scientific literature (90.9%) and the websites of scientific societies (80.5%) to obtain information on rare cancers. Expert opinion or colleague networks were used by 66.2%, whereas scientific congresses were the least frequently cited source (31.2%).
Consequences
83.1% of respondents had forgone a potentially beneficial treatment because of one or more of these barriers, and 53.2% had used off-label drugs, usually after discussion in a multidisciplinary tumor board (MDT).
Suggestions for reform
The leading priorities were the development of disease-specific clinical guidelines (80.5%), the establishment of a structured referral system to designated expert centers (75.3%) and the creation of a national registry (72.7%). Overall, 94.8% of participants were willing to join a national collaborative network.
CONCLUSION
Improving the care of rare cancers in Morocco is a multifactorial challenge. Closing these gaps requires a comprehensive strategy built on tailored clinical guidelines, a dedicated national registry and accessible expert networks.
3415eP
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Honored to be an invited speaker at #ESMO2026 in Madrid, discussing advances in cancer vaccines, bispecific antibodies, ADCs, and emerging therapeutic strategies.
Exciting breakthroughs shaping the future of oncology, with personalized, #PatientCenteredCare remaining at the heart of our mission.
@myESMO
Protein- vs Messag[e]...
Feature | Protein – Centric Therapeutics (eg antibodies) | Message – Centri[c] ... (mRNA)
Mechanism | Delivers final, physical protein. | Delivers genetic instructions ("message") to cells to synthesize protein.
Manufacturing | Highly complex and slow. Cell lines, extensive purification, and strict quality control. | Fully synthetic and standardized. Produced using a cell-free in vitro transcription (IVT) process.
Versatility | Each protein requires distinct, bespoke production setup. | Chemical structure remains identical; only internal genetic sequence changes.
Development time | Years to optimize protein folding, stability and purification | Weeks to design a viable genetic sequence
Biological Bottlenecks | Post-translational modifications (PTMs) and reaching inside cells. | Host cells naturally handle PTMs and cellular placement.
Customization | Not address to individual patients | Small batch personalized medicine
MADRID 2026 ESMO congress
MRG007 (CDH17 ADC) #ESMO26
Nice to see PK...
...but the exposure comment is ridiculous 🤯!
Calculated in ng/mL based on Cmax, but MW are very different (150000 vs 435).
In reality exatecan exposure is high (6% of ADC AUC), especially for a DAR4 ADC!
Here replotted (in nM) 👇 https://t.co/azFyj7vwsA
Dose Proportional PK With High Conjugation Stability
Analyte: ADC / TAb / Payload
Dose: 2 mg/kg, 4 mg/kg, 6 mg/kg, 7 mg/kg, 8 mg/kg
Concentration (ng/mL)
Time (hr)
ADC/TAb
• Similar ADC/TAb PK profiles indicate ADC stability
• Dose-proportional increase in exposure
• ADC/TAb half-life is 3.2–4.0 days
Payload (Exatecan)
• Minimal payload exposure (<0.01% of ADC Cmax)
• Half-life is 4.6–5.8 days
• Cmax 2–4 days
Ab, antibody; ADC, antibody-drug conjugate; Cmax, maximum plasma concentration; PK, pharmacokinetic(s); TAb, therapeutic antibody
Elizabeth Mittendorf, MD, PhD, @ascopres, shares her perspective on leading teams in an increasingly complex oncology landscape during the ESMO-ASCO special session, “The Evolving Definition of the Modern Oncologist. #ESMO26 https://t.co/S4O7Xj7osg
And here's the KRAS inhibitor reimbursement picture, via Benjamin Besse #Esmo26 https://t.co/urAaa65LqW
Drug access
[World map]
Sotorasib only: Japan • Germany • Spain • Canada • Netherlands • Norway • Austria • Israel • Sweden • Czech Republic • Slovenia • South Korea • Finland
Sotorasib + adagrasib: United States • Italy • Poland
Chinese KRAS G12C inhibitors: China — Fulzerasib • Garsorasib • Glecirasib • Sosimerasib
Huge day for cancer vaccines at #ESMO26! 🧬 As Moderna shines in early-stage (#LBA1), BayVax is proud to unveil #LBA52 in ADVANCED refractory tumors. Our neoantigen vaccine BXP-001 + CLERT radiation successfully improve PFS in the iNATURE study! https://t.co/CS33GiF4Nt
The Key Members of the Study Team
Principal Investigator: Clinical PI Prof. Feng-Ming (Spring) Kong FACR, FASTRO HKU Shenzhen Hospital The University of Hong Kong President of GCOG
Co-Principal Investigator: Clinical Co-PI Prof. Caicun Zhou Tongji University School of Medicine & Shanghai East Hospital, Shanghai< China President of IASLC 2025
Study Statistician: Prof. Pingfu Fu Department of Population & Quantative Health Science, Case Western University, Cleveland, Ohio, USA; Linyu Ma, Master in Statistics HKU Shenzhen Hospital
AI Team: Dr. Zhibo Gao CEO, YuceBio Technology Co.Ltd.; Prof. Jian-Dong Huang Chair Professor, The University of Hong Kong, Hong Kong SAR
Dr. Wei Dai Associate Professor, The University of Hong Kong, Hong Kong SAR
Dr. Ye-Fan Hu CEO, BayVax Biotech Limited, Hong Kong SAR
Research & Clinical Coordinating Team: Dr. Yan Zhang Assistant Researcher, The University of Hong Kong-Shenzhen Hospital; Mr. Rui Li R&D Director, P&PMed Biotechnology Co. Ltd.
Abstract: LBA #52, Presenter: Feng-Ming (Spring) Kong, MD, PhD, FACR, FAAWR, FASTRO
MADRID SPAIN 23-27 OCTOBER 2026
.@DrUppaluri explores how surgical strategies may evolve following neoadjuvant immunotherapy, examining what these advances could mean for surgical decision-making and patient care. #ESMO26 https://t.co/OedQvxuQMS
Conclusions
• Present
• KEYNOTE-689 data is based on surgery performed to initial margins
• New strategies to manage responding and progressing tumors
• Future
• Systematic approach to surgical de-intensification
• Trials need to incorporate surgical de-intensification guidelines
• Implications for adjuvant treatment remain to be defined
Ravindra Uppaluri
🔹 #ESMO2026 starts now! 🔹
Prof. @FAndreMD, President of @myESMO, opens the congress, marking the start of several days dedicated to the latest advances in #oncology.
An opportunity for physician-researchers to showcase @GustaveRoussy’s expertise.
#ESMO #Cancer https://t.co/GY2krS4szc
What is the role of ESMO in a world where AI is predominant
A point of reference for
Cancer care providers
Patients
Decision-makers
Future AI systems
[concentric circles diagram, centre:] ESMO
We define what matters
We set the standards
We fund the work
[Slide repeated on right screen; live video of presenter in centre]
MADRID 2026 ESMO congress
@myESMO 🔹 Gustave Roussy at #ESMO26 🔹
Today's poster sessions:
• Dr Nathan El Ghazzi
• Pr Laurence @AlbigesL
@myESMO #ESMO https://t.co/KHL3WXDxhA
[Slide 1]
4395P
[Gustave Roussy Paris Cancer Campus logo] [ESMO congress logo] FPN 4395P MADRID
A 25-ge[ne T-]cell exhaustion signature refines TLS-based prediction of immunotherapy benefit
N. El Ghazzi, A. Elliott, G. Sledge, J. Xiu, E.S. Antonarakis, G. D'Amato, D. Hsieh, J.C. Trent, A. Italiano
Gustave Roussy, Villejuif, France; Caris Life Sciences, Phoenix, USA; University of Minnesota, Minneapolis, USA; University of Miami, Miami, USA; University of California San Francisco, San Francisco, USA
BACKGROUND
Immune engagement and infiltration alone do not ensure durable benefit from checkpoint blockade.
Published in 2024, the 25-gene score was derived from lung adenocarcinoma samples by identifying CD8+ T cells co-expressing PD1 and >=1 of LAG3, TIGIT or TIM3.[1]
mIF profiling 166 LUAD -> Transcriptomics 135 tumors -> 25-gene model LASSO-derived -> Prior validation NSCLC - melanoma - RCC
External validation in POPLAR/OAK, MATCH-R, CA209-038 and JAVELIN Renal 101 linked higher scores to poorer ICI outcomes.
Can this 25-gene exhaustion score refine pan-cancer ICI stratification alongside TLS?
METHODS
Retrospective Caris clinicogenomic analysis
- Whole-transcriptome RNA-seq from the Caris database (>50 cancer types)
- Endpoints: real-world time on treatment (TOT) and overall survival (OS)
- Quartile-based Kaplan-Meier analyses and Cox models adjusted for age, sex, cancer type*, PD-L1, TMB and MSI
204,231 tumors - >50 cancer types -> 41,509 ICI TOT; OS: 41,507 | 162,610 non-ICI parent cohort
*Cancer type: NSCLC vs other. TOT is not RECIST-defined PFS.
RESULTS
1 Higher exhaustion is associated with shorter ICI outcomes
TIME ON TREATMENT (Median, months): Q1 4,90; Q2 4,63; Q3 4,33; Q4 4,20
OVERALL SURVIVAL (Median, months): Q1 22,17; Q2 20,00; Q3 19,83; Q4 17,63
Q1 = lowest; Q4 = highest exhaustion. TOT n = 41,509, OS n = 41,507. Adjusted for age, sex, cancer type (NSCLC vs other), MSI, TMB and PD-L1
MULTIVARIABLE ANA[LYSIS] Q4 versus Q1 adjuste[d]: Time on treatment 1.10 (95% CI 1.06-1.[illegible]); Overall survival 1.18 (95% CI 1.13-1.23); P < 0.0001 for both endpoints
2 The association was not reproduced in the non-ICI cohort
162,610 parent non-ICI cohort: The adverse association seen under ICI was not reproduced in the non-ICI cohort.
TO ESTABLISH TREATMENT SPECIFI[CITY]: Adjusted non-ICI models and a formal [...] exhaustion interaction are nee[ded] [partially obscured]
3 Joint TLS / exhaustion classification refines ICI prognostication
TIME ON TREATMENT (TOT) Median, months: TLS-high Exh-low 5.13; TLS-high Exh-high 4.93; TLS-low Exh-low 3.63; TLS-low Exh-high 3.73
OVERALL SURVIVAL (OS) Median, months: TLS-high Exh-low 22.53; TLS-high Exh-high 21.63; TLS-low Exh-low 16.27; TLS-low Exh-high 15.70
TLS-high / Exh-low vs TLS-lo[w ...]: OVERALL SURVIVAL HR [obscured]; TIME ON TREATMENT [obscured]
Exhaustion was inversely correlated with TLS and most inferred immune populations
CONCLUSIONS / TAKE-HOME MESSAGE
1 The 25-gene T-cell exhaustion signature independently predicts poorer ICI outcomes beyond PD-L1, TMB and MSI.
2 Joint TLS/exhaustion profiling may refine ICI selection by distinguishing immune-engaged tumors with preserved versus impaired antitumor functionality.
[1] Guegan JP, Peyraud F, Dadone-Montaudie B [...] adenocarcinoma reveals a 2[...] Cell Reports Medi[cine] [partially obscured]
Contact: antoine.italiano@gustaveroussy.fr
[Presenter Nathan El Ghazzi standing beside poster]
[Slide 2]
3636TiP
LITESPARK-034: Phase 3 Study of Belzutifan Plus Zanzalintinib Versus Belzutifan in Participants with Advanced Renal Cell Carcinoma During or After Anti-PD-(L)1 Therapy and VEGF-TKI
Laurence Albiges, Bradley McGregor, Brian Rini, Lis Starkopf, Rodolfo F. Perini, Ali Rana, Robert J. Motzer [affiliations small]
Background [small text, partially legible]: Belzutifan, a potent and selective hypoxia-inducible factor 2α (HIF-2α) inhibitor ...; Zanzalintinib is a multitargeted kinase inhibitor that targets VEGF receptors, MET, and the TAM family of kinases ...; The randomized, double-blind, phase 3 LITESPARK-034 study (NCT[illegible]) is designed to evaluate the efficacy and safety of belzutifan plus zanzalintinib versus belzutifan plus placebo in participants with advanced clear cell RCC ...
Objectives
Primary: To compare the following for belzutifan plus zanzalintinib versus belzutifan plus placebo - PFS per RECIST v1.1 as assessed by blinded independent central review (BICR) - Overall survival (OS)
Key secondary: To compare ORR per RECIST v1.1 by BICR for belzutifan plus zanzalintinib versus belzutifan plus placebo
Secondary: To evaluate the following for belzutifan plus zanzalintinib and belzutifan plus placebo: - Duration of response (DOR) per RECIST v1.1 as assessed by BICR - Safety - Patient-reported outcomes (PROs)
Methods - Study design: [Key Eligibility Criteria box, small] R 1:1 -> Belzutifan 120 mg PO QD + zanzalintinib 80 mg PO QD | Belzutifan 120 mg PO QD + placebo PO QD; Primary end points: PFS per RECIST v1.1 by BICR and OS; Key secondary end point: ORR per RECIST v1.1 by BICR; Secondary end points: DOR per RECIST v1.1 by BICR, safety, and PROs
[Participant eligibility criteria, Assessments and follow-up, Analyses, Status (world map) panels: small text largely illegible]
Sites currently open to enrollment [small]
3637TiP
Phase 3 study to assess the safety and efficacy of 177Lu-girentuximab in advanced, relapsed or recurrent ccRCC (LUTEON)
Laurence Albiges, Andrew M Scott, Thea Faivre, David Cade, Sumanta Pal [affiliations small] [Telix / LUTEON logos]
Background: high unmet need for systemic therapy options for patients with advanced ccRCC who experience high recurrence rates & poor outcomes [body text small, partially legible]
Carbonic anhydrase IX (CAIX): a promising theranostic target for ccRCC; 177Lu-girentuximab: monoclonal antibody-based approach [details small]
Study design: 2-part, randomized, open-label, multicenter Phase 3 study (NCT[illegible])
Part 1: Dose optimization (Phase 2a): One 1887 MBq 177Lu-girentuximab dose every 2 months for 8 months vs One 1258 MBq 177Lu-girentuximab dose every month for 6 months [read at reduced confidence]
Part 2: Efficacy & safety evaluation (Phase 3): RP2D 1:1 -> 177Lu-girentuximab (RP2D) vs Investigators' choice (SOC)
Key patient eligibility [small, partially legible]
[Presenter Laurence Albiges standing between posters]
🔹 Gustave Roussy at #ESMO26 🔹
Dr Caroline Even presents the challenges in treating HPV-related head and neck cancers, with a focus on systemic approaches, at @myESMO.
#ESMO https://t.co/6BoZEogpmM
EGFR inhibition in LA HPV+ HNSCC
De-escalation
De-ESCALaTE: randomised phase III (Mehanna, Lancet 2019)
[low] risk HPV+ Oropharyngeal Carcinoma T3N0-T4N0, and T1N1-T4N3
168 pts with RT + cetuximab 400mg/m2 loading dose followed by 7 w cetux 250mg/m2
166 pts with RT + cisplatine 100mg/m2/3w, D1, D22, D43
[Table 2: Mean number of acute, late, and overall toxicity events per patient, by treatment group - cisplatin plus radiotherapy vs cetuximab plus radiotherapy; values too small to read reliably]
[KM A Overall survival: Cisplatin plus radiotherapy vs Cetuximab plus radiotherapy; HR 5.0 (95% CI 1.7-14.7); Log-rank p=0.0012; Number at risk: cisplatin 166, 160, 154, 147, 118; cetuximab 168, 163, 156, 144, 109; Time since randomisation (years) 0, 0.5, 1.0, 1.5, 2.0]
RTOG 1016 (Gillison, Lancet 2019)
HPV+ Oropharyngeal Carcinoma (T1-T2, N2a-N3 or T3-T4, N0-N3)
425 pts with RT + cetuximab 400mg/m2 loading dose followed by 7 w cetux 250mg/m2
424 pts with RT + cisplatine 100mg/m2/3w, D1, D22
[KM A: Intensity-modulated radiotherapy plus cisplatin (406 patients, 55 dead, 351 censored) vs plus cetuximab (399 patients, 78 dead, 321 censored); Years after randomisation 0-5; Number at risk: cisplatin 406, 372, 349, 334, 222, 100 [partially legible]; cetuximab 399, 367, 334, 305, 207, 106 [partially legible]]
Overall survival was significantly worse with cetuximab (two sided 95% CI 1.03-2.05; log-rank p=0.0163) than with cisplatin. Estimated 5-year overall survival was : 77.9% (95% CI 73.4-82.5%) in the cetuximab group and 84.6% (80.6-88.6) in the cisplatin group
Congratulations to our fellow @JavierDavidBen2 on a fantastic Rapid Oral presentation just now at the policy session at #ESMO26. https://t.co/e1sqBbEO0a
[Slide 2]
Results: reporting of planned assessments
The reporting denominator is the number meeting the full planning criterion.
Assessment | Planning fully met n / 31 (%) | Reporting fully met n / N (%)
Health-related quality of life | 23/31 (74.2%) | 3/23 (13.0%)
Chronic / low-grade toxicity over time | 7/31 (22.6%) | 1/7 (14.3%)
Patient-reported toxicity | 7/31 (22.6%) | 0/7 (0.0%)
Javier David Benitez-Fuentes | 3323RO
5/7
[Slide 3]
Results: primary endpoints and eligibility
4/7
OS primary / co-primary
All 31 trials
38.7%
12/31 trials
Primary: 12/31 (38.7%)
Not primary: 19/31 (61.3%)
ECOG PS > 1 eligible
All 31 trials
9.7%
3/31 trials
Included: 3/31 (9.7%)
Excluded: 28/31 (90.3%)
PS > 1 exclusion rationale
Among 28 PS 0-1 trials
0/28
fully justified
Limited: 3/28 (10.7%)
None: 25/28 (89.3%)
0/19 trials without primary OS met the full surrogate-validation criterion.
Javier David Benitez-Fuentes | 3323RO
[Slide 4]
Common Sense Oncology: the checklist
1/7
Phase III trials should test meaningful patient benefit.
DESIGN
[A]ppropriate comparator
[O]S or validated surrogate
[Q]uality of life
[C]linically meaningful
ANALYSIS
Censoring
Sensitivity analyses
Post-progression treatment
REPORTING
Absolute benefit
Quality of life and toxicity
Balanced interpretation
[Publ]ished in 2025: principles for design, analysis and reporting.
[...] B et al. Lancet Oncol. 2025;26:e80-e89. doi:10.1016/S1470-2045(24)00451-0.
[Javier D]avid Benitez-Fuentes | 3323RO
@A_May_MD "s(t?)imulating the tumor better than the tumor itself first" means. Could you clarify a bit? As a reminder, that's the rationale of SWOG-1801 in the cartoon. They basicallly say that using pembro as neadj would more prime T-cells at the primary (resected) tumor site, rather than https://t.co/WQNzmqPmOe
Figure S1. Cartoons of the hypothesized mechanism of action of PD-1 blockade therapy in the adjuvant and neoadjuvant settings. A, B and C) Adjuvant therapy. Before surgery, the majority of antitumor T cells inhibited by PD-1 are located at the sites of locally advanced disease (A), which are resected with surgery (B). When giving adjuvant anti-PD-1, the therapy relies on the existence of antitumor T cells inhibited by PD-1 at micrometastases sites (C). D, E and F) Neoadjuvant therapy. Administering neoadjuvant anti-PD-1 therapy is intended to activate the large numbers of antitumor T cells at the tumor site (D) before the definitive surgery (E). The locally-activated antitumor T cells then go onto induce a systemic immune response able to recognize distant micrometastatic sites (F).
[Panels A-F: illustrations, no further text]
PAPMET2 Ph2 trial initiated by @SWOG presented by @maughanonc at #ESMO26.
Builds upon #PAPMET by adding atezolizumab to cabozantinib for pRCC.
Small cohort given rare histological subtype but initial results promising: PFS 25 vs 10mo, ORR 47%, no PD as BOR.
Results for ongoing #STELLAR304, #SAMETA & #PAXIPEM nccRCC and pRCC trials eagerly awaited
@RWinayak
Objective Response Rate
Treatment Arm | PD | SD | CR | PR | ORR | Inadequate Assessment
Cabozantinib (n=16) | 3 (19%) | 9 (56%) | 0 (0%) | 3 (19%) | 3 (19%) | 1 (6%)
Cabozantinib/Atezolizumab (n=17) | 0 (0%) | 6 (35%) | 0 (0%) | 8 (47%) | 8 (47%) | 3 (18%)
Leading cancer research. Together.
SWOG
More from #ESMO2026!
VHIO researchers are sharing their expertise in scientific and educational sessions, contributing to discussions across different areas of oncology.
Great to see @alerezqallah, @judithbalmana and @crisuarez08 taking part! https://t.co/WaX8p9AV6g
A
Lifetime Absolute Risk
Age (years)
>99%
95-99%
90-95%
80-90%
60-80%
40-60%
20-40%
10-20%
5-10%
1-5%
<1%
Mavaddat N, et al. Am J Hum Genet. 2019
📌 #ESMO26 Poster
How comparable are PFS results across cancer trials?
A systematic review of 156 oncology studies found considerable variation in how intercurrent events were handled & reported, highlighting the need for greater standardisation & transparency.
#CancerResearch https://t.co/Kaf8U5yR2l
FPN: 3332P
Analysis and reporting of PFS in contemporary phase 2-3 trials in solid oncology: a systematic review
A. van Ommen-Nijhof¹, E. Blondeaux², L.E. van Rangelrooij¹, V. Delucchi², R. van den Borg¹, G.S. Sonke¹,³, S. Litière⁴
1. Dpt of Medical Oncology, The Netherlands Cancer Institute (NKI), Amsterdam, The Netherlands; 2. Clinical Trial Unit, Epidemiologia Clinica, Ospedale Policlinico San Martino, Genova, Italy; 3. Dpt of medical oncology, Amsterdam University Medical Center, Amsterdam, The Netherlands; 4. Dpt of Statistics, EORTC Headquarters, [illegible]
Background
[partially obscured by presenter] ...contemporary phase 3 trials in solid oncology use su[...] ...ts such as progression-free survival (PFS) ...ages over overall survival (OS), but is not ...ical benefit and is prone to bias ...how to analyze PFS, in particular on how ..., whereas these can greatly affect trial ...ry decisions and uptake of new treatments
[Objective, partially obscured] ...FS analysis strategies in modern-day ...(RCTs) in solid oncology, with a focus on ...rent event handling
[Methods, partially obscured] ...ew, prospectively registered on PROSPERO ...Ts with PFS (co)primary endpoint, published in ...[illegible] Lancet, Lancet Oncology, JAMA, JAMA ... Journal of Clinical Oncology, and Journal ... 2020 to Dec 2024 ...g of three intercurrent events: ...after missed assessment (1 or >1) ... PD ...ithout PD
Conclusion
• 156 studies with PFS as (co)primary endpoint (published 2020-2024, in 8 high-impact journals)
• Trial protocol and statistical analysis plan (SAP) available in 76% and 35% of studies, respectively
• Majority of studies do not report handling strategy for intercurrent events of interest
• Censoring most popular hand[...] strategy, in spite of risk of [obscured]
Table 1. Study characteristics (total n=156)
[small print; values partially legible only — Journal rows: Ann Oncol 14 (9%); JAMA/JAMA Oncol 15 (10%); JCO 47 (30%); JTO 24 (15%); Lancet/Lancet Oncol 37 (24%); NEJM 19 (12%); remaining rows illegible/obscured]
Table 2. Reporting & handling of intercurre[nt events]
Intercurrent event 1.1 — PD after 1 missed assessment
Handling strategy reported
Main manuscript | 0
Supplements | 19 (12%)
Not reported | 137 (88%)
Handling strategy in ITT analysis
Ignore | 19 (12%)
Censor | 0
Composite (i.e., event) | 0
Not reported | 137 (88%)
Sensitivity analysis
Sensitivity analysis reported | 8 (5%)
Results of sensitivity analysis reported | 0
🔹 Gustave Roussy at #ESMO26 🔹
Today's poster sessions:
• Dr. Arnaud Bayle
• Dr. Lucie Veron
• Dr. Thomas Pudlarz
@myESMO #ESMO https://t.co/wHivUNFkrp
[Slide 2]
1166P
INTERCEPTION GUSTAVE ROUSSY - Le programme de prévention personnalisée des cancers
Effectiveness of self-referral and teleconsultation as entry point to high-risk of cancer prevention pathway
Lucie Véron (1, 2), Thomas Pudlarz (1), Pamela Abdayem (1), Tarek Ben Ahmed (1), Marion Aupomerol (1), Géraldine M Camilleri (1, 3), Myriam Touren (1), Marjorie Bassail (1), Sophie Villebasse (1), Marina Di Maria (1), Clément Valarcher (1), Helene Caron (1), Chara Djellel (1), Olivier Caron (1), Suzette Delaloge (1)
(1) Gustave Roussy, Département de médecine oncologique, F-94805, VILLEJUIF France; (2) Corresponding author; (3) Université Paris Saclay, France
BACKGROUND: Self-referral and telemedicine could broaden access to personalized cancer prevention. In 2022, Gustave Roussy launched a teleconsultation (TC) offer to assess eligibility to the "Interception" program (Fig1.) for individuals at high risk (HR) of breast, lung, colorectal, pancreatic cancers, following self- or community healthcare professional (HCP) referral.
METHODS: Retrospective study of a prospective cohort of adults completing a screening TC between Oct 2022 and Jan 2026 as part of a referral to the Interception program. During the TC, a trained HCP reviewed personal/family cancer history, lifestyle, exposures and prior screening, and triaged the patients toward the Interception One Stop clinic or re-orientation. Referral was self-, HCP-, or awareness-based (flyer, restricted to lung cancer pathway). Primary outcomes are the rates of eligibility to the program and attendance to the One Stop Clinic for those eligible
RESULTS: 1164 patients (pts) attended a TC (Fig 2.) (66% women; median age 49y (IQR 37-61) (median age for pancreatic cancer et lung cancer pathway 62-61y, vs. 39y for breast cancer (BC) pathway), 63% currently employed) (Table 1). Referral mode: self 63%, HCP 17%, flyer 13%, undocumented 7%. 453/1164 (39%) were eligible for the Interception program. 345/453 eligible pts (76%) attended the One Stop (Fig. 3 and 4). 347 One Stop shops were performed, mainly for a HR of lung cancer (50%), BC (35%, 83% of whom also received online genetic counselling before the One-Stop) and pancreatic cancer (8%) (the colorectal pathway opened in 2026).
37% of women entering the BC pathway were HCP-referred, vs 8% in other pathways (Fig. 5).
The median TC–One Stop time interval was 112 days (IQR 64-205) (Fig 6.).
Eligibility/attendance by referral: self 36%/72%, HCP 45%/74%, flyer (lung) 57%/87%. Only age predicted attendance to the One Stop Clinic (per 10 years OR=1,35 IQR (1,03-0,78), p=0,031).
Fig 3 Interception pathways completed - The colorectal pathway opened in March 2026 (pie: 174, 120, 27, 12, [illegible])
Fig 4. Attendance rate by pathway (colorectal excluded): HR of lung cancer 87.8% | HR of pancreatic cancer 87.1% | HR of genetic BC 85.7% | Other 80.0% | HR of non genetic BC 72.3%
Fig 5. Referral mode by pathway (%) [values partially legible: 51, 49, 89, 37, 42, 14]
Fig 6. Delay teleconsultation – One stop by pathway
[Table 1 characteristics: illegible]
CONCLUSION: TC is a feasible, high-yield entry to a personalized cancer prevention program. These results support telemedicine combined with program-tailored communication [illegible] engagement as a scalable model to widen access to high-risk cancer prevention.
[Slide 3]
1165P - Early impact of a pilot multimodal personalized early cancer detection and prevention program for individuals at high risk of pancreatic cancer
Thomas Pudlarz (1, 10), Tarek Ben Ahmed(1), Lucie Véron (1), Pamela Abdayem(1), Géraldine M Camilleri(1,7), Bruno Duso(1,8,9), Simona Cosconea(1), Alice Boilève (1,7), Bruno Raynard(2), Helene Caron(1), André Tardieu(3), Bernard Ortolan(4, 5), Elena Fernandez de Sevilla (6), Maximiliano Gelli(6), Michel Ducreux(1,7), Olivier Caron (1), Suzette Delaloge (1)
INTRODUCTION
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers with a 5-year survival rate of approximately 10% partly due to late stage at diagnosis. Individuals identified with a high risk of PDAC (HRPDAC) are eligible for screening, but risk reduction measures could also be impactful. Interception is a French, nationally deployed, real-world pilot program that allies early detection and personalized prevention of different cancers including PDAC.
METHODS
Individuals with HRPDAC following guidelines – familial aggregation of cases, known deleterious variant in predisposition genes, and/or confirmed branch duct intraductal papillary mucinous neoplasm (IPMN) – are invited to enroll in the program. The initial One-stop-clinic includes clinical visits, a blood test, a workshops on PDAC risk, early detection and prevention, nutrition and physical activity, and settlement of a shared personalized prevention plan. Follow-up is both digital and physical. Endpoints were 1-year adherence to the screening program and modification of the WCRF score from baseline (paired t-test).
RESULTS
Between June 2023 and April 2026, 141 individuals with HRPDAC attended the One-stop-clinic (95 women, 47 men; median age 61 years IQR [53; 68]); 97 (68%) had familial aggregation, 41 (29%) had branch duct IPMN, and 31 (22%) had a P/LP variant in PDAC predisposition genes: 16 (52%) in BRCA2, 7 (23%) in CDKN2A, 6 (19%) in BRCA1, and 1 (3%) each in ATM and MSH2. Median follow-up is 16.5 months [9.6; 23.4]. Among 51 pts who filled the WCRF at 1 year so far, mean score was 4.61 ± 1.1 versus 4.34 ± 1.1 at baseline (p=0.048). 31 participants (54%) improved their score (≥ 0.25 increase) while [illegible] patients (16%) remained stable. 1-year adherence with the screening program is high (98%). One patient has been detected with a stage I pT1bN0M0 PDAC.
98% (138 / 141 participants)
"One patient has been detected with a stage I pT1bN0M0 PDAC"
16.5 months median follow-up
1 pancreatic ductal adenocarcinoma (PDAC) diagnosed - Stage I pT1b N0 M0 (1 / 141 participants (0.7%))
[Table 1 and Figures 1, 2, 4 values illegible]
CONCLUSION
In these preliminary analyses, the Interception program for individuals with HRPDAC demonstrates excellent adherence to the screening protocol and a favourable trend toward lifestyle improvement. Early detection outcomes are encouraging, with one cancer diagnosed at an early stage (stage I). These findings warrant confirmation with longer follow-up.
🔹 Gustave Roussy at #ESMO26 🔹
Dr. @derosa__lisa presents “Dynamics of the Microbiome Toposcore Following Fecal Microbiota Transplantation in Immuno-Oncology: A Longitudinal, Multi-Cohort Analysis” at @myESMO.
#ESMO https://t.co/ZSmw8HqReq
BACKGROUND
TOPOSCORE captures microbiome states associated with clinical outcome
Cell | Article: Custom scoring based on ecological topology of gut microbiota associated with cancer immunotherapy outcome
Score S = 1/2 (NSIG2/45 − NSIG1/37 + 1)
SIG1 | Gray | SIG2; High / Zero / Normal; SIG1+ | SIG2+; OS<12 | OS>12
Median OS: SIG2+ / SIG1+; HR (95% CI), 0.47 (0.35 to 0.65); p<0.0001
Overall survival (%) vs Time (Months)
Number at risk: 105, 78, 36, 12, 4, 1 / 140, 62, 29, 10, 3, 1
SIG1 bacteria (n=37) — Dysbiosis: Enterocloster genus, Streptococcaceae family, Veillonellaceae family, Lactobacillaceae family
SIG2 bacteria (n=45) — Eubiosis: Lachnospiraceae family, Oscillospiraceae family, Polyamine and Tryptophane pathways
Derosa L et al. Cell. 2024 Jun;187(13):3373-3389.e16.
Lisa Derosa, MD, PhD
🔹 Gustave Roussy at #ESMO26 🔹
Nathalie Gaspar commenting the advances of B7H3 ADC in the presidential session
#ESMO https://t.co/zYxSxoLnnL
Osteosacoma landscape
AYA disease
AYA
Chemotherapy
Standard of first-line treatment
Pre- and post-operative CT
EURAMOS-1
No improvement on survival since then
Multikinase inhibitors
Positive trials in R/R osteosarcomas
70' 80'
10' 20'
Dr Nathalie GASPAR, MD, PhD
🔹 Gustave Roussy at #ESMO26 🔹
Bruno Duso at the Early detection and prevention of cancer session
#ESMO https://t.co/pHS85Ws9aT
From records to dossiers
Two filters turn a broad and heterogeneous literature into comparable test dossiers.
Scoping review
22,194
records, each screened by at least two independent reviewers
Index-Test Qualification
• Defined assay or platform
• Specified panel/algorithm
• Pre-specified decision rule
• Explicit early-detection intent
Retention for a dossier
• Independent validation
• Screening intent; comparator
• Locked algorithm; multicentre
• Regulatory or commercial signals
Test dossiers
ESMO × covidence
Collection Tool v2.3: aligned with STARD and QUADAS-2, mirrored in Covidence
A Study and test identity, setting
B Participants and flow
C Index test and reference standard (how cancer was confirmed, e.g. biopsy or registry follow-up)
D Performance, harms, value and study quality
Built to capture the work-up a positive triggers, worst-case burden per 1,000 screened, and PPV at intended-use prevalence.
Round 1 consensus survey, statements 4.2-4.5; Covidence screening record
👀 At #ESMO26, @DrArturoAI was in the room for Abstract 170O, presented by Zhen Zhang, PhD.
RADIANT, a radiotherapy foundation model trained on nearly 120,000 cases, contours targets, generates dose plans and predicts outcomes across 4 cancer types, with higher discrimination than standard models.
Clinical utility is still to be proven in model-guided studies. ☢️
#OncologyAI #RadiationOncology #CNRealtimeReport
[Slide 1]
RADIANT, a multicancer anatomy-dose foundation model for individualised radiotherapy benefit-risk stratification
Zhen Zhang1,2,3, Tianchen Luo1, Haixia Shen1,2,3, Zhaoyu Jiang1,2,3, Ji Zhu1
1. Zhejiang Cancer Hospital, Hangzhou Institute of Medicine (HIM), Chinese Academy of Sciences, Hangzhou, Zhejiang, China
2. Maastro, Maastricht Radiation Oncology Institute, Maastricht, The Netherlands
3. Department of Radiation Oncology (Maastro), GROW Research Institute for Oncology and Reproduction, Maastricht University Medical Centre+, Maastricht, The Netherlands
23 October 2026
[Slide 2]
Conclusions
- RADIANT showed higher discrimination than clinical and DVH models across multiple outcome and toxicity prediction tasks.
- Shared anatomy-dose representations supported prediction across four cancer types after task-specific adaptation.
- Model-based risk stratification could inform personalised surveillance and prospective risk-adapted trials.
- Clinical utility remains to be established in model-guided studies.
Zhen Zhang
Very nice presentation on DDR defects, a tumor-agnostic hallmark with clinical implications.
1 pathway, 4 uses: therapeutic (PAPRi/chemo/ADCs/IO), resistance, prognostic, and genetic counseling. Interacts with all other hallmarks.
- @GhosnMd
📸 Sophie Postel-Vinay, MD, PhD
#ESMO26 @myESMO @GustaveRoussy @GRAlumni
Inserm | Université Paris-Saclay | UCL
DNA damage response (DDR) defects: a key cancer hallmark
Multiple implications in the clinic:
• Therapeutic (synthetic lethality, sensitivity to chemo- and radiotherapy; ADCs; ICI)
• Resistance
• Prognostic
• Genetic counselling
• Tumor-agnostic approach is relevant for therapeutic orientation
• Key hallmark: Interaction with multiple other cancer hallmarks
S. Postel-Vinay
EACR | ESMO congress
🔹 Gustave Roussy at #ESMO26 🔹
Dr. Sabine Mouawad presenting Complementary role of Liquid Biopsy and Imaging in Assessing Tumor Burden in Metastatic #Cancer at @myESMO.
#ESMO https://t.co/O5mh1Ac2O4
Complementary roles of liquid biopsy and imaging in assessing tumor burden in metastatic cancer
Sabine Mouawad, V. Robic, F. Frau, J. Dupont, G. Jardali, A. Choucair, L. Dawi, E. Rouleau, I. Borget, V. Letort-Le Chevalier, A. Italiano, N. Lassau
Gustave Roussy - Department of imaging
BioMaps – Université Paris-Saclay
Gustave Roussy Cancer Campus Grand Paris | Université Paris-Saclay Faculté de Médecine | École des Sciences du Cancer | BioMaps
🔹 Gustave Roussy at #ESMO26 🔹
Julien Haddoux - How to simplify the algorithm of treatment of rare endocrine tumors ?
#ESMO https://t.co/ntATSr6o8a
MADRID 2026 ESMO congress
Murcia Auditorium - Hall 3 - Monday 26 oct 26 – 15.10-15.25
How to simplify the algorithm of treatment of rare endocrine tumors?
Endocrine tumours at a glance
Dr Julien Hadoux
Endocrine oncology unit & UMR INSERM 981
Gustave Roussy, Villejuif, France
& ENDOCAN network
GUSTAVE ROUSSY
🔹 Gustave Roussy at #ESMO26 🔹
Dr. @AliceFranzoi moderating the session and discussing how to integrate AI into MDT workflows from an implementation science perspective at @myesmo.
#ESMO https://t.co/GSgeDzUBgv
From accuracy and concordance studies to the evaluation of the assisted MDT Workflow
Does the LLM recommendation agree with the MDT? → Shift → Does the assisted workflow improve MDT preparation, discussion and follow-up—for patients, staff and the organisation?
Current MDT workflow → Mapping pain points and bottlenecks → Possible LLM intervention
The real-life MDT workflow should determine the intervention, not the other way around.
Maria Alice Franzoi, MD, PhD
[Reference, small print: illegible]
Proud to hear how Brazil is approaching heath care equity through digital pathology hub-and-spoke model for diagnostics at #ESMO26 https://t.co/iDcDEAwwjB
A connected digital pathology [network to expand access,] standardise quality and reduce health [disparities in Brazil] [title partly cropped on right screen; full title on left screen: "A connected digital pathology network to expand access, standardise quality and reduce health disparities in Brazil"]
[map of Brazil with regional hubs]
NORTH
NORTH-EAST
WEST-CENTRAL
SOUTH-EAST
SOUTH
ACCC Central Hub (São Paulo)
Reference centre for complex cases and expert consultation
LEGEND
Physical sample flow (for regional hubs)
Digital images and data flow
Local Centre (hospital or laboratory)
Regional Digital Pathology Hub (slide scanning and case preparation)
ACCC Central Hub (reference for complex and expert consultation)
Tissue specimen (biopsy or surgical specimen)
[left screen also shows a right-hand step panel, mostly illegible: "Sample collection at local centres" — uncertain; "Physical shipment to regional hubs"; "Slide scanning at regional hubs"; "Digital images sent for analysis"; "Interpretation and collaboration"; "Report ..." — [illegible] small text]
The ESMO president Fabrice Andre at the opening sesion #ESMO26 Madrid.
Great talk! https://t.co/pc3rI0t5ex
[Slide 2]
Keeping pace with science is no longer enough
ESMO's evolution is the response
[tree diagram branching to four items]
Complexity
Fragmentation
Data
Need for guidance
[Slide 4]
Serving more than 52,000 oncology professionals
43
Guidelines
13
ESMO journals
Including 3 new journals:
• Artificial intelligence and oncology
• Oncology policy and science
• Genitourinary oncology
13
Meetings and congresses around the world
Including:
• 1 AI congress
• 2 new Asia congresses
30+
Webinars
🔬 First results from Module 3 of the #CCEBasketofBaskets (BoB) trial presented at #ESMO2026!
@Richard_Baird (@CRUKCamCentre), Luigi De Petris (@karolinskainst), Irene Braña (@VHIO), and Frans Opdam (@NKI_nl) shared the findings.
🔗 https://t.co/rx2h61UEm8 https://t.co/YqLFNabKL3
[Slide 1]
1037P - Amivantamab in subjects with aberrant MET and/or EGFR solid tumors – First Results from the Baskets of Baskets trial
Richard F. Schlenk1, Oriol Mirallas Viñas2, Christophe Massard3, Frans Opdam4, Luigi De Petris5, Claudio Vernieri6, Richard D. Baird7, David Tamborero5, Shubha Anand7, Etienne Rouleau3, Adria Lopez-Ferandez2, Nikos Demiris7, Petros Barmpounakis7, Paolo Nuciforo2, Editha Gnutzmann1, Arantxa Romero-Tamarit2, Elena Chavarria2, Jordi Rodon8, Irene Brana2 on behalf of the Cancer Core Europe - Basket of Baskets study team
Results
Safety: Overall safety profile across arms was consistent, with 82% treatment related AEs mostly grade 1/2, n=35 SAEs were reported with n=2 being treatment related (edema, pulmonary embolism)
Assessment at week 12 and Survival
| PR (Tumor type) | SD | PD
Arm A | 10.5% NSCLC n=2 with Met Ex14 Skipping mutation | 58% | 31.5%
Arm B | 10.5% NSCLC CN=13; EGJ adenocarcinoma CN=58 | 37% | 52.5%
Arm C | 23% endocervical adenoca, EGFR exon 20; HNSCC, EGFR exon 19; cholangiocarcinoma, EGFR exon 20 | 23% | 54%
Conclusions
Safety profile consistent, no new safety signals were identified.
Amivantamab showed best efficacy in the BoB cross histology study in patients characterized by EGFR mutations including response until day 613.
Clinicaltrials.gov identifier: NCT03767075 - EU CT number 2024-514238-19-00 - EudraCT identifier: 2017-005108-89
[Background, Methods, Characteristics table, Tumor type and survival curves: [illegible] at this distance]
[Slide 2]
Amivantamab in subjects with aberrant MET and/or EGFR solid tumors – First Results from the Baskets of Baskets trial
Characteristics of treated Patients
Patient Characteristics | Arm 3A | Arm 3B | Arm 3C
No | 19 | 19 | 13
Female | 47% | 42% | 46%
Median Age [years] (range) | 69 (44-76) | 55 (23-72) | 62 (37-79)
Molecular Inclusion marker
- MET Amplification median(range) | | 12 (7-32) |
- MET Fusions* | 6
- MET Exon 14 skipping mutations | 12
- MET mutations | 1
- EGFR mutation
- EGFR amplification
- unclear (in progress)
Previous malignancy (cured) | 3
Previous systemic treatment | 18
No of lines median | 2
Previous Radiotherapy | 7
Results
Safety: Overall safety profile across arms was consistent, with 82% treatment related AEs mostly grade 1/2, n=35 SAEs were reported with n=2 being treatment related (edema, pulmonary embolism)
Assessment at week 12 and Survival
PR (Tumor type) | SD | PD
10.5% NSCLC n=2 with Met Ex14 Skipping mutation | 58% | 31.5%
10.5% NSCLC CN=13; [illegible]GJ adenocarcinoma CN=58 | 37% | 52.5%
23% [illegible] | 23% | [illegible]
Conclusions
Safety profile consistent, no new safety signals were identified.
Amivantamab showed best efficacy in the BoB cross histology study in patients characterized by EGFR mutations including response until day 613.
[Slide 3]
1037P - Amivantamab in subjects with aberrant MET and/or EGFR solid tumors – First Results from the Baskets of Baskets trial
Results
Safety: Overall safety profile across arms was consistent, with 82% treatment related AEs mostly grade 1/2, n=35 SAEs were reported with n=2 being treatment related (edema, pulmonary embolism)
Assessment at week 12 and Survival
| PR (Tumor type) | SD | PD
Arm A | 10.5% NSCLC n=2 with Met Ex14 Skipping mutation | 58% | 31.5%
Arm B | 10.5% NSCLC CN=13; EGJ adenocarcinoma CN=58 | 37% | 52.5%
Arm C | 23% endocervical adenoca, EGFR exon 20; HNSCC, EGFR exon 19; cholangiocarcinoma, EGFR exon 20 | 23% | 54%
Abbreviations: PR, partial remission; SD, stable disease; PD, progressive disease; CN, copy number
Tumor type
In A, most pts had lung cancers (63%), whereas arms B and C were cross histology with exclusion of lung cancer in arm C.
Conclusions
Safety profile consistent, no new safety signals were identified.
Amivantamab showed best efficacy in the BoB cross histology study in patients characterized by EGFR mutations including response until day 613.
Acknowledgement
To the patients and their caregivers. This research has been funded by CaixaResearch Advanced Oncology Research Program supported by Fundació La Caixa, by the Comprehensive Program of Cancer Immunotherapy & Immunology II (CAIMI-II) supported by the BBVA Foundation (grant 53/2021). J&J supports the study with an unrestricted grant and Amivantamab free of charge.
[...].gov identifier: NCT03767075 - EU CT number 2024-514238-19-00 - EudraCT identifier: 2017-005108-89
Early clinical milestones opens more questions than it answers. These are the discussions that turn early progress into a credible path forward at #ESMO26. Next question is where this profile matters most for patients.
w/@gulsahnomak11
#CureWithASmile #DrugDelivery @OncoAlert https://t.co/fghDjvjgeI
#ESMO26 by the numbers. A global family of 40K delegates! https://t.co/SYFGCNJe07
ESMO 2026 IN NUMBERS
4,414 Abstracts:
• 12 in Presidential Symposia
• 147 Proffered Papers
• 242 Rapid Oral
• 2,025 Posters
• 1,988 ePosters
296 Sessions, of which:
• 230 Programme Sessions
• 66 Industry Satellite Symposia
~ 40,000
Professionals attending
Now public at @myESMO: In our phase Ia/Ib study, patients received RS-0139 at 40–60 mg/m² without a single case of neutropenia of any grade and without G-CSF support. Find the e-poster 1095eP or reach out to continue the conversation.
#ClinicalTrials #ESMO26 #CureWithASmile https://t.co/RQ7mZu4xf2
🏛️Hemos presentado en #ESMO2026 los resultados preliminares de nuestro programa de formación oncológica para pacientes con #CáncerMetastásico Oncology Education 360º #OE360
https://t.co/MrkBQ5JoXY https://t.co/WpQUptyqPY
EVENTO | ALMIA presenta en ESMO 2026 los primeros resultados de OE360°
Supported by ALMIA
DECISION PARTNER:
Preliminary Feasibility Results of a Structured Oncology Education and Shared Decision-Making Programme for Metastatic Cancer Patients Delivered via a Digital Learning Platform
FINAL PUBLICATION NUMBER 4075eP
CAN STRUCTURED ONCOLOGY EDUCATION MEASURABLY IMPROVE SHARED DECISION-MAKING IN METASTATIC CANCER?
89.7% programme completion, with encouraging early signals in knowledge acquisition and patient-reported outcomes.
THE CHALLENGE
THE INTERVENTION
Modular education | 10 workshops | Meet the Expert | Consultation guides | Glossary & support
METHODS & DESIGN
Design: Single-arm feasibility pilot
Duration: 5 weeks
Population: Patients with metastatic cancer
Platform: Moodle LMS (open source)
Faculty: 9 specialists
Analysis: Descriptive; no inferential testing
Ethics: Informed consent · GDPR compliant
OUTCOMES
PRIMARY: Feasibility — enrolment and module completion — and acceptability.
SECONDARY - EXPLORATORY: Knowledge; PREMs — 5 domains; Anxiety & tension
THE DECISION PARTNER MODEL
UNDERSTAND · PREPARE · PARTICIPATE · REFLECT
FEASIBILITY & ENGAGEMENT
68 ENROLLED | 61 COMPLETED | 10.3% DROPOUT
89.7% COMPLETION
KNOWLEDGE & PATIENT-REPORTED OUTCOMES
PRE 4.0 | POST 8.5
+4.5 POINTS +112.5%
PATIENT-REPORTED EXPERIENCE
STRUCTURED ONCOLOGY EDUCATION SUPPORTS METASTATIC CANCER PATIENTS IN BECOMING DECISION PARTNERS.
The next step is prospective validation of the complete nine-module programme using validated outcomes and longitudinal follow-up.
Secondary commentary
KOL infographics 54
Summary graphics that physicians, media and companies designed themselves (branded cards, redraws, watchlists and top-10 lists). They are commentary, not the presented data, so they sit here in compact form. Click a thumbnail to enlarge it on this page.
Heme & Myeloma 3
Henry C Fung| MM, lymphoma, leukemia & CART @HenrychihangFu1Post text
🩸🇪🇸 ESMO 2026 MYELOMA + MADRID GUIDE
Myeloma in the morning. Tapas at night. 😆
📍 Madrid | Oct 23–27
⭐ Essential session: Sat Oct 24, 08:30–10:00
Salamanca Auditorium, Hall 10
Three myeloma oral presentations:
1️⃣ 1454O—Bela-DRd in transplant-ineligible NDMM
High MRD negativity sounds excellent—but what does belamaf truly add beyond DRd? We need durable PFS, tolerability and ocular-treatment burden—not another impressive MRD snapshot.
2️⃣ 1455O—Long-term BelaRd
The important question is durability. Is frontline BCMA exposure justified when CAR-T and bispecific antibodies may be needed later?
3️⃣ 1456O—LBL-034, a new GPRC5D×CD3 bispecific in heavily pretreated RRMM
Phase I and single-arm: promising, not practice-changing. Watch duration of response, infections, EMD activity and the familiar GPRC5D taste/skin/nail toxicities.
BOTTOM LINE:
ESMO myeloma is small but focused:
➡️ Belamaf moving earlier
➡️ Another GPRC5D bispecific moving forward
➡️ No phase III result likely to change practice immediately
🍖 NOW THE IMPORTANT SESSION: IBÉRICO!
Easiest post-ESMO stop:
🥇 Cinco Jotas Padre Damián—excellent 100% ibérico de bellota and convenient after taking Metro Line 8 from IFEMA toward Nuevos Ministerios.
For the complete Madrid experience:
🥓 Joselito’s Velázquez—destination-quality jamón
🍤 La Casa del Abuelo—gambas al ajillo
🍳 Casa Lucio/Huevos de Lucio—huevos rotos
🍺 Bodega de La Ardosa—tortilla, vermouth and old-Madrid atmosphere
Scientific rule: Do not confuse MRD negativity with cure.
Madrid rule: Do not confuse ordinary ham with jamón ibérico de bellota. 😆
#ESMO2026 #MultipleMyeloma
ESMO 2026: MYELOMA + MADRID
MYELOMA IN THE MORNING • TAPAS AT NIGHT
SAT OCT 24 • 08:30–10:00
Salamanca Auditorium • Hall 10
1454O Bela-DRd — Does deeper MRD become durable benefit?
1455O BelaRd — Durability vs ocular burden
1456O LBL-034 • GPRC5D×CD3 — Promising Phase I—not practice changing
THE IBÉRICO ROUTE
1 Cinco Jotas Padre Damián — 100% ibérico de bellota • easiest from IFEMA
2 Joselito's Velázquez — Destination-quality jamón
3 Casa Lucio — Huevos rotos
4 La Casa del Abuelo — Gambas al ajillo
Do not confuse MRD negativity with cure.
Do not confuse ordinary ham with jamón ibérico de bellota. 😆
Henry C Fung| MM, lymphoma, leukemia & CART @HenrychihangFu1Post text
Figure 2/2: Not only myeloma!
The same Saturday session includes new approaches in B-cell lymphoma, transformed DLBCL and R/R MDS/AML. Interesting early-phase signals—but novel mechanism ≠ new standard.
Spanish wine, however, needs no Phase III trial. 🍷😆
#ESMO26 #HemeTwitter #Lymphoma #AML #MDS
ESMO 2026: BEYOND MYELOMA + SPANISH WINE
NOVEL TARGETS IN THE MORNING • SPANISH WINE AT NIGHT
SAT OCT 24 • 08:30-10:00
Salamanca Auditorium • Hall 10
1457O Rocbrutinib + R-CHOP - Frontline B-cell lymphoma • Phase Ib
1458O TRS005 • anti-CD20 ADC - Transformed DLBCL • ORR 50% • mPFS 8.7 mo
1459O LYT-200 • anti-Galectin-9 - R/R high-risk MDS/AML • Phase Ib
THE SPANISH WINE FLIGHT
1 Rioja Gran Reserva - Elegant • mature • classic
2 Ribera del Duero - Bold • structured • powerful
3 Albariño • Rías Baixas - Fresh • mineral • seafood-ready
4 Fino Sherry • Jerez - Dry • salty • perfect with jamón
Novel mechanism ≠ new standard.
Good Spanish wine needs no Phase III trial.
MedJ @MedJ0401Post text
TRS005 achieved a 50.0% ORR in transformed DLBCL, with median OS of 19.29 months—but grade ≥3 neutrophil decrease in 58.1% underscores the efficacy–safety trade-off.
At ESMO Congress 2026, organized by the European Society for Medical Oncology @myESMO, Prof. Yuankai Shi of the National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences presented Zhejiang Teruisi’s phase 1 data.
Among 28 evaluable patients, DCR was 71.4%.
Median PFS was 8.67 months; median DoR was 12.91 months.
The recommended phase 2 dose was 1.8 mg/kg.
Peripheral neuropathy was limited to grade 1–2 across 146 patients.
These early, non-peer-reviewed subgroup results support phase 2 evaluation but cannot yet change practice. Larger studies will determine TRS005’s clinical role.
🔗 Read the full article via the link in the comments below.
#MedJ #ESMO26 #DLBCL #Lymphoma #AntibodyDrugConjugate #ClinicalTrials #Hematology
MEDJ | ESMO 2026 HIGHLIGHTS
PROF. YUANKAI SHI
TRS005 Shows 50% ORR in Transformed DLBCL Phase 1 Study
Key Points:
1. Prof. Yuankai Shi presented the first-in-human phase 1 results at ESMO 2026.
2. The study treated 146 patients across 29 Chinese hospitals, including 31 with t-DLBCL.
3. Among 28 evaluable patients, DCR reached 71.4% and target lesions shrank in 64.3%.
4. Median PFS, DoR, and OS were 8.67, 12.91, and 19.29 months, respectively.
5. RP2D was 1.8 mg/kg; grade ≥3 neutrophil decrease occurred in 58.1%.
MedJ
ESMO
Other 51
Oncology Brothers @OncBrothersCLARITY-Gastric01DeLLphi-305SAFFRONVOLGAINTerpath-001TroFuse-005NATALEELITESPARK-011VIKTORIA-1DASL-HiCaPMOIOpostMONARCHTRIO-US B-12 TALENT
Post text
We are all done with #ESMO26! 10+ studies that were on our radar and the updated data around them.
Out in the community settings, it’s tough to keep up with all that is happening here in the world of cancer (and this was just ONE conference). Really appreciate you all sharing the data and importantly your take around this: @OncoAlert @weoncologists @DrChoueiri @StephenVLiu @SuyogCancer @dr_yakupergun @drsarahsam @PTarantinoMD @GIMedOnc @BijoyTelivala @RenoHemonc @nlindenberg @jryckman3 @ErikaHamilton9 @myESMO @LorenzaRimassa 🙏🏽🙏🏽
Top 10 Anticipated Practice Changing/Informing Abstracts for ESMO 2026 from Community Oncology's (@OncBrothers) perspective
1 #INTerpath001: Ph III, Intismeran autogene (individualized mRNA neoantigen therapy) + Pembro vs. Pembro in adjuvant resected stage IIB–IV Melanoma. RFS HR 0.58 (42% risk reduction); 2-yr RFS 82.2% vs 70%. DMFS HR 0.62; 2-yr DMFS 88.5% vs 80.2%. OS immature. Landmark personalized vaccine result.
2 #VOLGA: Ph III, NeoAdj Durva + EV +/- Treme → Surgery → Durva +/- Treme in platinum-ineligible muscle-invasive Bladder Cancer. Durva+EV: 24-mo EFS 63.5% vs 45.1% (HR 0.51); 24-mo OS 78.4% vs 69.4% (HR 0.58). Treme added no clear OS benefit. New peri-operative option.
3 #ANZUP1801 (DASL-HiCaP): Ph III, Darolutamide + ADT + XRT vs. ADT + XRT for very high-risk localized Prostate Cancer. MFS HR 0.42 (58% reduction); 4-yr MFS 95% vs 88%. OS immature. Practice-changing for high-risk localized disease.
4 #LITESPARK011: Ph III (Update), Belzutifan + Lenvatinib (FDA approved Sep 24, 2026) vs. Cabozantinib in 2L (after IO) advanced/metastatic Renal Cell Carcinoma. Final analysis: mPFS 14.8 vs 10.8 mo (HR 0.74); ORR 53% vs 40%. OS numerical only (33.7 vs 28.6 mo, HR 0.85, NS). Confirmed PFS/ORR benefit.
5 #DeLLphi305: Ph III, Durvalumab + Tarlatamab vs. Durvalumab maintenance (after chemo + IO induction) in extensive-stage Small Cell Lung Cancer. mOS 21.1 vs 12.7 mo (HR 0.42); mPFS 7.4 vs 1.9 mo (HR 0.34). Unprecedented OS gain in ES-SCLC.
6 #SAFFRON: Ph III, Osimertinib + Savolutinib vs. Chemo (platinum + Pemetrexed) in MET overexpressed/amplified after Osi in mEGFR Non-Small Cell Lung Cancer. mPFS 7.6 vs 5.4 mo (HR 0.55); mOS 17.8 vs 12.9 mo (HR 0.68). New standard after osimertinib progression.
7 #CLARITYGastric01: Ph III, Sonesitatug Vedotin (sone-ve, CLDN18.2-targeting ADC) vs. physician's choice chemo in 2L+ CLDN18.2+ advanced/metastatic GE Junction or Gastric Adenocarcinoma. 3L+ mOS 10.0 vs 5.0 mo (HR 0.47); ITT mOS 10.6 vs 6.4 mo (HR 0.58). BICR PFS not significant. Strong OS signal.
8 Updates in Breast Cancer:
• #TALENT: Ph II, NeoAdj T-DXd +/- ET for early-stage HER2-low, HR+. Low pCR rates (≈3–9%); modest activity, limited path CR.
• #NATALEE: Ph III, Adj Ribo + ET in resected HR+. 6-yr update. OS HR 0.809 (~19% risk reduction); 6-yr OS 91.9% vs 89.7%. iDFS benefit continues to widen.
• #postMONARCH: Ph III, Abema + Fulvestrant after 1L CDK4/6i + ET in metastatic HR+, final OS. mOS 32.1 vs 24.6 mo (HR 0.80, p=0.11, NS). Numerical benefit only.
• #VIKTORIA1: Ph III, Gedatolisib + Fulv +/- Palbo after 1L CDK4/6i + ET (PIK3CA-mutant focus). Strong PFS benefit maintained (e.g., triplet ORR 59% vs 33%; durable responses even with visceral disease).
9 #MOIO: Ph III non-inferiority trial, Standard Immunotherapy dosing vs. Reduced frequency (once every 3 months) after 6 months of standard dosing and achieving Partial or Complete response in Metastatic Cancer (multiple primaries). Non-inferiority NOT met. PFS HR ~1.35; OS HR 2.0. Caution against de-escalation.
10 #TroFuse005: Ph III, Sacituzumab Tirumotecan (Sac-TMT, Trop-2 targeting ADC) vs. physician's choice chemotherapy in 2L+ (after chemo + IO) in recurrent/metastatic Endometrial Cancer. Statistically significant, clinically meaningful improvement in both OS and PFS (plus ORR). First TROP2 ADC to show this in post-chemo/IO endometrial cancer.
www.oncbrothers.com @Oncbrothers @Oncbrothers @Oncbrothers
Toni Choueiri, MD @DrChoueiriPost text
It was a fantastic #ESMO26 full of practice changing clinical trial and data that will make an impact for cancer patients. I can’t wait for #ESMO27 in Barcelona.
@myESMO @DanaFarber @DanaFarber_GU @OncoAlert https://t.co/fJv47eB5x1
Same image also posted by @OncoAlert
DAY 4 · SOCIAL PULSE •LIVE
#ESMO26
Madrid
23–27 OCTOBER 2026 | IFEMA MADRID
POTENTIAL REACH
83.9M
5.2K Posts on X clean, no bots or dupes
884 Participants voices in the conversation
32 Countries a global conversation
50.9 Posts / hour across the meeting days
5.9 Posts / HCP engagement depth
44% Positive of scored posts
TOP INFLUENCERS impressions + mentions + engagement · X-weighted
1 OncoAlert @OncoAlert
2 ESMO - Eur. Oncolo... @myESMO · esmo_eur_oncology
3 Toni Choueiri, MD @DrChoueiri
4 NEJM @NEJM
5 Stephen V Liu, MD @StephenVLiu
6 Yakup Ergün @dr_yakupergun
7 Paolo Tarantino @PTarantinoMD
8 Hidehito Horinouchi @HHorinouchi
9 Zach Klaassen @zklaassen_md
10 Yüksel Ürün @DrYukselUrun
11 Tom Powles @tompowles1
12 Nieves Martinez La... @DraMartinezLago
13 Arndt Vogel @ArndtVogel
14 Adam Feuerstein @adamfeuerstein
ACUVOX real-time congress metrics · by OncoBites x OncoAlert
WHERE IT CAME FROM
North America 1,669
Europe 1,467
Asia-Pacific 433
Latin America 124
Middle East & Africa 27
TOP COUNTRIES
United States 1,559
Turkey 252
United Kingdom 226
Italy 135
Spain 500
Japan 227
Switzerland 171
Canada 110
TOP CITIES
Boston 294
London 174
New York 174
Madrid 172
Tokyo 166
Diyarbakır 108
LANGUAGES
English 89%
Spanish 5%
Japanese 3%
Italian · Indonesian · French · other 4%
ONCOLOGY INSIGHTS. REAL-TIME IMPACT.
Dr Rishabh Jain @DrRishabhOncoPost text
🇮🇳 A major win for Indian oncology at #ESMO26!
LBA44 | Phase III | 475 patients
Pacli-Carbo + metronomic therapy vs DCF:
✅ Non-inferior OS
✅ Grade ≥3 toxicity: 43% vs 86%
✅ Resectability: 57% vs 34%
🔥 Less toxicity. More patients becoming operable!
👏 @VanitaNoronha
@myesmo @ESMO_open @ASCO @oncoalert
Full paper link in comment below ⬇️
ESMO 2026 | LBA44
Less Toxic Neoadjuvant Option for Unresectable Oral Cancer
Phase III RCT (475 patients)
Technically unresectable oral cancers
• Extensive local disease
• Skin involvement
• Bulky nodes
DCF (Standard): Docetaxel + Cisplatin + 5-FU; Every 3 weeks × 2–4 cycles
VS
PCm (Novel regimen): Weekly paclitaxel + carboplatin + Metronomic oral therapy (methotrexate + celecoxib + erlotinib); Weekly × 6–9 cycles
Median overall survival: DCF 13.99 months | PCm 13.31 months
HR 0.826 (Non-inferiority, P = 0.0002)
Grade ≥3 toxicity: DCF 86.4% | PCm 43.2%
Objective response rate: DCF 23.4% | PCm 45.6%
Resectability after NACT: DCF 33.9% | PCm 57.3%
Non-inferior survival with less toxicity and more patients becoming resectable
@DrRishabhOnco
Jeff Ryckman @jryckman3Post text
OPTIMAL is asking whether selected oral cavity cancer responders can skip postoperative RT. Still awaiting primary endpoint, 2y EFS (not reported just yet)
Randomized phase II, 116 pts with resectable locally advanced oral cavity SCC, 1:1, stratified by stage III vs IVA:
Surgery→ standard postoperative RT/CRT
vs.
Tislelizumab + nab-paclitaxel + cisplatin x3c→ surgery→ response-adapted adjuvant treatment.
Neoadjuvant doses: tislelizumab 200 mg, nab-paclitaxel 260 mg/m², cisplatin 75 mg/m² q3w. Pts with "aMPR" and no positive margins/ENE received tislelizumab x6c without RT. Other operated pts received postoperative RT/CRT. aMPR isn't defined in the report; the registry uses MPR.
📌 Experimental ORR 81% (47/58). Among 55 pts who underwent surgery, pCR 45.5% (25/55).
G3+ TRAEs 36.2→ 25.9% (control→ experimental), described as mainly related to RT and surgery.
At the 6 Sep 2026 cutoff, control had 19 EFS events, including 8 deaths. The reported neoadjuvant-plus-RT subgroup had 9 EFS events: 3 PD during neoadjuvant treatment, 5 relapses, and "1 died due to radiotherapy complications, 3 deaths" as written. I'm not sure how the death counts reconcile. The RT-free subgroup had 2 EFS events and 0 deaths.
The primary endpoint, 2y EFS, is NOT reported. EFS is immature, with no rates or HR and no MFU given. Those raw counts can't answer the RT question: the RT-free pts were selected responders without positive margins/ENE, not a separately randomized group, and the subgroup denominators aren't given.
I'd also want the control-arm RT/CRT details and RT dose/fx, which aren't reported. Interesting response-adapted strategy, with substantial pathologic response, but this doesn't establish that we can safely omit RT.
https://t.co/QTqFcVVZbM
#radonc #ESMO26 #HeadAndNeckCancer
OPTIMAL
Surgery / postoperative RT/CRT vs neoadjuvant chemo-IO / response-adapted therapy
Resectable LA Oral cavity SCC Stage III / IVA Randomized phase II n=116
RANDOMIZE 1:1
| 2y EFS* | MPR† | pCR
Surgery→ PORT/POCRT G3+ TRAEs 36.2% Standard postoperative RT or CRT | Not reported | — | —
Tislelizumab + chemo x3c→ surgery G3+ TRAEs 25.9% 58 evaluable; 55 underwent surgery ORR 81.03% (47/58) aMPR, no positive margins/ENE: tislelizumab x6c without RT Other operated pts: postoperative RT/CRT | Not reported | 65.45% 35/55; as reported† | 45.45% 25/55
ESMO '26 #LBA47 | *Primary: 2y EFS not reported; immature. No EFS rates/HR; MFU not reported.
RT-free pathway: selected, nonrandomized; no subgroup denominators. Counts cannot establish safe RT omission.
†MPR percentage/count disagree; shown as reported. aMPR undefined. RT dose/fx and control RT/CRT details not reported.
Rohit Malde @roxboxfixPost text
ESMO 2026
TMH study
Unresectable LAHNSCC
Weekly C+P +OMC Vs. DCF
Non inferior
Low toxicity
Higher ORR
More conversion to resectability https://t.co/0qivxsKjjC
ESMO Congress 2026 (LBA44)
DCF/TPF versus a novel regimen of paclitaxel, carboplatin and oral metronomic chemotherapy (PCm) as neoadjuvant treatment for technically unresectable oral cancers: A multicentric phase III randomized non-inferiority study
Vanita Noronha (on behalf of Solid Unit 2 group and all investigators) | Tata Memorial Hospital, Mumbai and collaborating centres
STUDY DESIGN: Multicentric, phase III, randomized non-inferiority trial; 475 patients 1:1 randomization; DCF/TPF arm n = 236; PCm arm n = 239
ELIGIBILITY CRITERIA: Age > 18 years; Oral cavity cancers deemed technically unresectable by MDT; ECOG performance status 0–1; Adequate organ and bone marrow function
Examples of technically unresectable tumours: Buccal mucosa primaries with soft tissue involvement or edema extending to zygomatic arch; Oral tongue primaries with soft tissue involvement up to oropharynx or hyoid; Extensive skin or nodal involvement; Involvement of high infratemporal fossa
STRATIFICATION FACTORS: Not reported in the material reviewed — verify official protocol.
TREATMENT REGIMENS (NEOADJUVANT)
DCF / TPF (Conventional triplet): Docetaxel 75 mg/m² IV day 1; Cisplatin 75 mg/m² IV day 1; 5-FU 750 mg/m²/day continuous IV infusion days 1–5; Every 3 weeks for 2–3 cycles; Typically inpatient, Central line required (for 5-FU infusion)
PCm (Novel metronomic regimen): Paclitaxel 80 mg/m² IV day 1; Carboplatin AUC 1.5 IV day 1; Celecoxib 200 mg orally twice daily; Erlotinib 150 mg orally daily; Methotrexate 9 mg/m² orally weekly; Weekly cycles for 6–9 cycles; Outpatient regimen, No central line or infusion pump
REASSESSMENT AND FURTHER MANAGEMENT: After completion of neoadjuvant treatment - Clinical assessment + Radiological assessment + MDT discussion; If resectable: Surgery followed by indicated adjuvant therapy; If unresectable: MDT decision for radical chemoradiotherapy, radical radiotherapy alone, palliative therapy, best supportive care. Resectability is an MDT decision based on overall clinical and radiological assessment, not imaging response alone. The fixed timing of interim assessment is not clearly specified in the supplied ESMO slide.
OVERALL SURVIVAL RESULTS
Outcome | DCF (n = 236) | PCm (n = 239)
Events (deaths) | 194 | 177
Median OS (months, 95% CI) | 14.0 (12.0 – 16.7) | 13.7 (12.4 – 18.3)
Hazard ratio (PCm vs DCF) | 0.82 (95% CI 0.64 – 1.03)
One-sided non-inferiority P value | 0.0002
KM labels: 12 months 58.1% (PCm) / 56.4% (DCF); 24 months 36.0% (PCm) / 29.4% (DCF)
Number at risk: DCF 236 153 97 64 42 21 13 5 1 0; PCm 239 174 104 67 47 29 15 9 1 1
Landmark OS rates (approximate readings from slide): 12-month OS DCF 56.4%, PCm 58.1%; 24-month OS DCF 29.4%, PCm 36.0%
RESPONSE AND RESECTABILITY: Investigators report significantly higher response rate with PCm than DCF. Significantly higher conversion to resectability with PCm. Significantly fewer toxicities with PCm. Exact number/percentage converted to resectability is not legible in the supplied ESMO slides and was not verified in the accessible abstract. Do not substitute results from earlier PCm cohorts.
INTERPRETATION: Non-inferiority for overall survival reported (one-sided P = 0.0002). Median OS is similar between arms. HR 0.82 suggests a numerical trend in favour of PCm, but the 95% CI includes 1.0, so OS superiority is not established. Landmark OS rates appear higher with PCm (approximate readings).
KEY CONCLUSIONS: PCm is a promising, potentially less toxic and logistically simpler neoadjuvant option for technically unresectable oral cancers. Survival appears non-inferior, but superiority is not established. Patients must be managed in a multidisciplinary setting with definitive treatment chosen by MDT.
PRACTICAL ADVANTAGES OF PCm: Outpatient delivery; No central line or infusion pump; Reduced logistic and resource burden
IMPORTANT CAVEATS: Verify exact conversion-to-resectability rate, actual surgery/R0 rates. Verify grade 3–4 toxicity rates. Verify the prespecified non-inferiority margin. Stratification factors not reported — confirm in official protocol.
Based on supplied ESMO 2026 slides; unverified fields are explicitly flagged.
Dr Rohit Malde, MD, DNB, FRCR (UK) — Consultant Clinical Oncologist
MV Chandrakanth @ChandrakanthMvPost text
🇮🇳 MORE SURGERY. LESS TOXICITY. SAME SURVIVAL!
DCF vs PCm | ESMO 2026 | Noronha et al.
An important Indian multicentre Phase III non-inferiority trial in technically unresectable oral cavity cancer (n=475).
🎨 THE CARTOON TELLS THE STORY!
🔴 DCF — THE HEAVY ROAD
- Docetaxel + Cisplatin + 5-FU
- Grade ≥3 toxicity: 86.4%
- Growth-factor use: 100%
- Intensive, infusion-based treatment.
🟢 PCm — THE LIGHTER ROAD
- Weekly paclitaxel–carboplatin + oral metronomic therapy
- Grade ≥3 toxicity: 43.2%
- Growth-factor use: 20.5%
- Outpatient-friendly, reduced treatment burden.
🏁 SAME SURVIVAL DESTINATION!
- Median OS: 13.99 vs 13.31 months
- HR 0.826 | Non-inferiority p=0.0002
- Non-inferior OS — NOT proven superior.
🚪 MORE PATIENTS REACH SURGERY!
- Response: 23.4% → 45.6%
- Resectability: 33.9% → 57.3%
- Surgery performed: 26.0% → 45.6%
All comparisons: DCF → PCm.
💡 THE TAKE-HOME
Two different roads. A non-inferior survival outcome.
PCm delivered more responses, more surgical opportunities and approximately HALF the severe toxicity.
A compelling Indian neoadjuvant alternative for selected patients — not a replacement for upfront surgery in resectable disease.
📚 Reference: Noronha V et al. ESMO 2026; LBA44. CTRI/2023/08/056693.
@myESMO @OncoAlert @larvol
#ESMO2026 #OralCancer #HeadNeckCancer #MedicalOncology #IndianOncology #MVOnco
MORE SURGERY. LESS TOXICITY. SAME SURVIVAL!
MV Onco
DCF vs PCm | ESMO 2026 | Noronha et al.
Technically unresectable oral cavity cancer | Indian Phase III trial
GRADE ≥3 TOXICITY 86.4% | Growth-factor use 100% (DCF)
OVERALL SURVIVAL: 13.99 mo (DCF) vs 13.31 mo (PCm) | HR 0.826 | NI' p = 0.0002 | NON-INFERIOR — NOT SUPERIOR
GRADE ≥3 TOXICITY 43.2% | Growth-factor use 20.5% (PCm)
WHAT A BURDEN! | LIGHTER PATH. SAME SURVIVAL!
DCF: Docetaxel + Cisplatin + 5 FU | PCm: Paclitaxel + Carboplatin + Metronomic therapy
SURGERY | BETTER TOLERABILITY | OUTPATIENT FRIENDLY
RESPONSE 23.4% → 45.6%
RESECTABILITY 33.9% → 57.3%
SURGERY 26.0% → 45.6%
26.0% to surgery | 45.6% to surgery
MORE SURGERIES. LESS TOXICITY. NON-INFERIOR SURVIVAL.
Jeff Ryckman @jryckman3Post text
RADIANT trained on 119,782 RT cases and tested segmentation, dose and outcome prediction across sites.
What I want next is clinical utility: does using it improve planning decisions, toxicity or outcomes? Accuracy alone isn't enough.
#ESMO26 #radonc
https://t.co/0MTMp2F6iI https://t.co/eczRhHiVI8
RADIANT
Radiotherapy foundation model development and validation
CT, structures,
dose
14 centers
Pretraining cohort
n = 119,782 cases
→ Hold-out + external
validation
GTV Dice CTV Dice
83.52% 81.53%
Hold-out cohort: 22,058 cases across 10 disease sites; external retrospective/prospective cohorts in 3 countries.
21 downstream tasks include segmentation, dose and outcome prediction. No randomized clinical utility evaluation.
Zhang et al. ESMO 2026, 170O. AI model study; reported predictive performance does not establish patient benefit.
MV Chandrakanth @ChandrakanthMvPost text
NeoLOCUS vs PCm/DCF | Phase II Promise vs Phase III Evidence!
Two Indian studies exploring neoadjuvant strategies in oral cavity cancer.
🔹 NeoLOCUS | Marimuthu et al.
Single-arm Phase II (n=34), incorporating low-dose nivolumab + chemotherapy + oral metronomic therapy.
ORR 66.6% | Surgery 87.9% | 2-year OS 67.1%.
🔹 PCm vs DCF | Noronha et al.
Randomized Phase III (n=475).
PCm demonstrated OS non-inferiority to DCF, with higher response and surgery rates and substantially less grade ≥3 toxicity (43.2% vs 86.4%).
🎯 Take-home: PCm has randomized Phase III evidence. NeoLOCUS is promising but needs Phase III validation.
⚠️ Different populations and study designs — cross-trial comparisons are not head-to-head.
References: Marimuthu et al.; Noronha et al. ESMO 2026.
@myESMO @OncoAlert @larvol
#MVOnco #ESMO2026 #HeadNeckCancer #OralCancer #Immunotherapy
NeoLOCUS vs PCm/DCF
PHASE II PROMISE vs PHASE III EVIDENCE
Marimuthu et al. | Noronha et al. | 2026
Parameter | NeoLOCUS | PCm vs DCF
Design | Phase II, single-arm | Phase III, randomized
Patients | 34 | 239 vs 236
Population | Borderline resectable | Technically unresectable
Regimen | Carbo + nab-P + LOW-DOSE NIVO + OMT | P-Carbo + OMT vs DCF
ORR | 66.6% | 45.6% vs 23.4%
Surgery | 87.9% | 45.6% vs 26.0%
R0 resection | 84.8% | NR
pCR | 13.8% | 5.5% vs 6.6%
Grade ≥3 AEs | 14.7% | 43.2% vs 86.4%
Median OS | NR | 13.31 vs 13.99 mo
2-year OS | 67.1% | 38.9% vs 28.4%
Evidence | PROMISING PHASE II | PHASE III NON-INFERIORITY
Different populations: cross-trial comparisons are descriptive, not head-to-head. pCR denominators differ.
OMT = oral metronomic therapy; NR = not reported.
PCm: RANDOMIZED EVIDENCE.
NeoLOCUS: PROMISING, PHASE III NEEDED.
MV Onco
Jeff Ryckman @jryckman3Post text
R2810-ONC-1901
Neoadjuvant cemiplimab: single-arm phase II, resectable II-IV (M0) cSCC → surgery.
pCR 51%; 54-mo EFS 76.2%, OS 79.4%.
Postop RT, cemiplimab or observation: investigator choice. This can't establish safe RT omission.
#ESMO26 #OncTwitter
https://t.co/vIOmvaCRx7
Cemiplimab cSCC
Neoadjuvant therapy: final follow-up
Resectable cutaneous SCC Stage II-IV (M0) n = 79 -> ENROLL -> Cemiplimab then surgery
pCR* 51%
Single-arm phase II
*Primary pCR. 54-mo EFS 76.2%, OS 79.4%: descriptive, not powered.
No randomized HR. Adjuvant RT discretionary; safe RT omission not established.
Gross et al. JCO '26. DOI: 10.1200/JCO-26-02166.
Jeff Ryckman @jryckman3Post text
FURTHER enrolled 69/129 planned pts.
At 2wk, pain response 50% in pooled MR-HIFU arms vs 38% with EBRT (P=.41).
Just refer these folks for EBRT. Most data for invasive ablation is confounded by receipt of EBRT. Love me some kypho after EBRT (for select cases), though
#ESMO26 #radonc
https://t.co/D7WeSP7cEe
FURTHER
MR-guided focused ultrasound with or without RT for bone pain
Painful non-spinal
Bone metastases
NRS >=4
n = 69
→ RANDOMIZE
EBRT (n = 24)
MR-HIFU (n = 22)
EBRT + MR-HIFU (n = 23)
*Primary endpoint: pain response at 2 weeks. Pooled MR-HIFU arms 50% vs EBRT 38% (P = .41), not significant.
Accrued 69/129 planned; underpowered. Pain response incorporates pain score and opioid use.
Braat et al. ESMO 2026, 3084O. 1:1:1 randomized; combined arm: MR-HIFU within 1 week of EBRT. RT dose unreported.
Jeff Ryckman @jryckman3Post text
Swallowing QoL matters.
QoLATI-DAHANCA34 (LBA45):
2:1 randomized TORS + staging neck dissection vs (C-)RT in early OPSCC.
12-mo MDADI difference 5.1 points favored TORS (p=0.04), below the prespecified clinical-relevance threshold.
16% assigned to TORS were redirected to (C-)RT after neck dissection.
#ESMO26 #radonc
https://t.co/EEqA74vrnZ
QoLATI-DAHANCA34
TORS + staging neck dissection vs (C-)RT (2:1)
T1-2 N0-1 M0 OPSCC n=138 randomized n=136 analyzed -> 2:1 RANDOMIZE
| 12-mo MDADI* Adjusted difference | TORS alone
(C-)RT (n=44) Registry IMRT: 66 Gy/33 fx or 76 Gy/56 fx BID Nimorazole ± weekly cisplatin | Reference |
TORS (n=92) + staging neck dissection | +5.1 points | 73 (79%)
15 (16%) redirected to (C-)RT after staging neck dissection
Channir. ESMO 2026, LBA45. cslide: https://cslide.ctimeetingtech.com/esmo2026/attendee/confcal/presentation/list?q=LBA45
*Primary: 12-mo MDADI. Difference 5.1 (95% CI 0.3-9.9), p=0.04. RT prescription: NCT04124198.
Abstract only. Below clinical-relevance threshold (value not reported). Abstract phase 2; registry NA.
MV Chandrakanth @ChandrakanthMvPost text
🇮🇳 LESS TOXICITY. MORE SURGERIES. SAME SURVIVAL!
An important Indian Phase III trial at #ESMO2026!
DCF/TPF vs PCm in technically unresectable oral cavity cancer (n=475).
📘 PART 1 | WHY THIS TRIAL?
Can weekly paclitaxel–carboplatin + oral metronomic therapy replace intensive DCF without compromising survival?
📘 PART 2 | EFFICACY
✅ OS non-inferior: HR 0.826; p=0.0002
✅ Response: 45.6% vs 23.4%
✅ Resectability: 57.3% vs 33.9%
✅ Surgery: 45.6% vs 26%
📘 PART 3 | SAFETY
✅ Grade ≥3 toxicity: 43.2% vs 86.4%
✅ Growth-factor use: 20.5% vs 100%
✅ Outpatient-friendly, without routine infusion-pump requirements.
📘 PART 4 | THE VERDICT
More responses and surgical opportunities, with substantially less toxicity — but no proven OS superiority.
A compelling alternative for selected patients, not a replacement for upfront surgery in resectable disease.
Less treatment burden. More surgical opportunities.
📚 Reference: Vanita Noronha et al. Multicentre Phase III randomized non-inferiority study. ESMO Congress 2026, LBA44. CTRI/2023/08/056693.
@myESMO @OncoAlert @larvol
#ESMO2026 #HeadNeckCancer #OralCancer #IndianOncology #MVOnco
[Slide 1]
DCF vs PCm | ESMO 2026
CAN WE DO BETTER WITH LESS?
MV Onco
PART 1/4 | RATIONALE & DESIGN
1 WHY THIS TRIAL?
TECHNICALLY UNRESECTABLE ORAL CANCER
WHY NACT?
• Some patients are initially unresectable.
• NACT may convert selected patients to resectability -> enabling surgery.
THE PROBLEM?
• DCF/TPF can achieve tumour shrinkage – but is toxic and cumbersome.
THE QUESTION?
CAN WE DO BETTER WITH LESS?
Heavy duty! (DCF) | Let's simplify! (PCm)
2 WHO ENTERED?
475 PATIENTS
• Technically unresectable oral cavity SCC
• ECOG 0-1
• Stage IVA/IVB
Randomized 1:1
3 WHAT WAS COMPARED?
DCF | n = 236
Docetaxel 75 mg/m² D1
Cisplatin 75 mg/m² D1
5-FU 750 mg/m²/day D1-5
Every 3 weeks × 2-4 cycles
VERSUS
PCm | n = 239
Paclitaxel 80 mg/m² weekly
Carboplatin AUC 1.5 weekly
Plus oral metronomic therapy:
Methotrexate 9 mg/m² weekly
Celecoxib 200 mg twice daily
Erlotinib 150 mg daily
6-9 weekly cycles
4 WHAT HAPPENED NEXT?
NEOADJUVANT THERAPY -> REASSESSMENT -> Resectable -> Surgery ± adjuvant therapy; Unresectable -> Multidisciplinary treatment
TAKE-HOME
PRIMARY ENDPOINT: OVERALL SURVIVAL
Could PCm preserve survival while reducing treatment burden?
[Slide 3]
DCF vs PCm | ESMO 2026
MV Onco
PART 3/4 | SAFETY & PRACTICALITY
1 WAS PCm LESS TOXIC?
GRADE ≥3 TOXICITY
DCF 86.4%
PCm 43.2%
p < 0.001
HALF THE TOXICITY!
2 LESS GROWTH-FACTOR SUPPORT?
GROWTH-FACTOR USE
DCF 100%
PCm 20.5%
DRAMATIC REDUCTION!
3 WHY IS PCm PRACTICAL?
DCF: Multi-day 5-FU infusion; Central line / infusion pump; Greater supportive-care burden
PCm: Weekly outpatient treatment; No routine 5-FU infusion pump; Less logistical complexity
4 A SMALLER BURDEN IN REAL LIFE
WHAT A BURDEN! (DCF) | TRAVEL LIGHT! (PCm) | OUTPATIENT TREATMENT
TAKE-HOME: LESS TOXICITY. LESS SUPPORT. EASIER DELIVERY.
PCm is less toxic – NOT toxicity-free.
[Slide 4]
DCF vs PCm | ESMO 2026
A NEW INDIAN STANDARD?
PART 4/4 | THE VERDICT
MV Onco
1 WHAT DID PCm ACHIEVE?
✓ NON-INFERIOR OS
✓ NEARLY DOUBLE THE RESPONSE
✓ MORE PATIENTS TO SURGERY
✓ HALF THE SEVERE TOXICITY
2 WHAT IS THE BIG PARADOX?
MORE SURGERIES – BUT NO PROVEN OS SUPERIORITY!
Better tumour response ≠ Proven survival advantage
3 WHAT SHOULD MAKE US CAUTIOUS?
IMPORTANT LIMITATIONS
• Non-inferiority margin: HR 1.30
• Open-label trial
• ECOG 0-1; selected patients
• Mature survival and detailed outcomes needed
4 WILL THIS CHANGE PRACTICE?
POTENTIALLY YES!
For selected patients with:
TECHNICALLY UNRESECTABLE ORAL CAVITY SCC
PCm offers a promising, less toxic, outpatient-friendly neoadjuvant alternative.
NOT evidence to replace upfront surgery in resectable disease.
TAKE-HOME
SAME SURVIVAL STANDARD. MORE SURGICAL OPPORTUNITIES. LESS TREATMENT BURDEN.
PCm: A compelling Indian alternative – not yet a universal standard.
Jeff Ryckman @jryckman3Post text
MOIO (LBA10): IO every 3 months did not achieve PFS noninferiority.
📌 Randomized phase 3 noninferiority trial, 340 pts w/ advanced/metastatic cancer in PR/CR after 6 mo of standard IO; melanoma CR excluded.
📌 Continue standard IO vs the same dose every 3 mo. Interim mITT n=308; median follow-up 18.6 mo.
📌 mPFS 25 vs 21.9 mo; HR 1.35 (95% CI 0.9-2.0), reduced vs standard IO. Prespecified futility boundary exceeded.
📌 Death HR 2.0 (95% CI 1.1-3.9), reduced vs standard IO.
📌 G3-4 irAEs 10.5% vs 9.5%; serious AEs 26.3% vs 25.0% (standard vs reduced IO).
https://t.co/cLGRcK0dg9
#ESMO26
MOIO
Reduced-frequency IO after response: interim noninferiority analysis
Advanced/metastatic cancer responding after 6 mo standard IO
Phase III noninferiority
n=340 randomized
RANDOMIZE
1:1
Median PFS* | Interim result
Standard IO | 25 mo | Reference
G3-4 irAEs 10.5%
Same IO every 3 months | 21.9 mo | Futility boundary exceeded
G3-4 irAEs 9.5%
PFS HR 1.35 (95% CI 0.9-2.0); prespecified futility boundary exceeded
Death HR 2.0 (95% CI 1.1-3.9); reduced-frequency vs standard IO
Gravis G, ESMO 2026 LBA10 (abstract)
*Primary: PFS noninferiority; interim mITT n=308; NI margin 1.3 (protocol).
MFU 18.6 mo; PFS noninferiority not achieved.
Pablo Jiménez @PaulJiLPost text
#ESMO26 is here with plenty of studies to digest in the Head & Neck space
⛳️Great interest in the potential addition of neo chemo to periop IO
📢Novel analyses from #KEYNOTE689
📡Cohort 5 from #Origami4
🎯Surge of several ADCs in ongoing research
Here is my take👇 for #HNSCC #NPC #SalivaryGlandCancers #Sinonasal
#headandneckcancer
@myESMO @OncoAlert @brunolarvol
@FundacionTTCC @SGCancerUK
[Slide 1]
Head & Neck SCC @PaulJiL [ESMO Congress Madrid 2026 logo]
Early disease
- Induction CarboTaxolPembro followed by RT and consolidation pembro for LA larynx (SMARTKey Ph2)
43 pts. 2y OS 74.4%. Alive with larynx 65.1%. Cisplatin-free!
- Perioperative toripalimab plus cetuximab in LA resectable followed by tori or tori-cetu. Single-arm Ph II.
52 pts. ORR 61%. MPR 42%. PORT avoidance unclear.
- LBA Perioperative tislelizumab in resectable LA oral cavity (OPTIMAL Ph 2 RCT)
- Neoadjuvant 2 vs 3 chemoIO cycles LA resectable SCC
178 pts. ORR 95 vs 80%. pCR 72 vs 55%. No EFS data.
- LBA Induction combo of metronomic chemo, carboplatin and paclitaxel vs TPF for unresectable oral cancer. Non-inferiority RCT Phase III
- AntiPD1 +/- AntiEGFR ADC*topo1 MRG003 followed by CRT with or without adj antiPD1 in LA resectable (IDEAL)
49 pts. Awaiting updated safety&efficacy during presentation.
- LBA Niraparib and dostarlimab plus RT in LA-HNSCC (Radian Phase Ib/II trial)
- Post-hoc ctDNA analysis KEYNOTE-412 (CRT +/- pembro).
473 pts. Prognostic value in HPV- pts but not seen in HPV+ pts
[Slide 2]
Head & Neck SCC [ESMO Congress Madrid 2026 logo]
Early disease @PaulJiL
- Post-op residual viable tumor (RVT) in the KN689 trial
EFS benefit across all the RVT cutpoints, even in non-responders
- Post-surgical stage reassignment in KN689 trial
Downstaging primary T demonstrated the strongest EFS benefit
- Neoadj platinum-taxane and periop finotonlimab (antiPD1) in resectable HPV negative LA. Ph 2.
35 pts. ORR 96%. pCR 38%. pCR 38%. MPR 84%.
Advanced disease
- Amivantamab, carboplatin plus pembrolizumab in 1st line R/M (Phase Ib/2 OrigAMI-4)
22 HPV- patients. ORR 77% (3 pts CR). Role of ami in 7 HPV+ pts (?) ORR 29%.
- Iza-Bren (EGFRxHER3 ADC*topo1) plus pembro in 1st line R/M. Phase 2 trial
78 pts. cORR 48%. mDOR 13.6. mPFS 7.1. Chemo toxicity
- Pembro +/- petosentamab in 1st L R/M Ph 2
45 pts. ORR 63%. mPFS 9 months. DoR&OS NR.
- LBA HexAgonHN: RCT 2/3 Pembro +/- ordastobart in PDL1-high 1stL R/M.
- End-of-trial results LEAP-009 Ph2 trial (Lenva Pembro vs Lenva vs SoC in refractory R/M patients).
↑G3-5 trAEs in LenvaPembro or Lenva VS SoC
[Slide 3]
Nasopharyngeal Ca [ESMO Congress Madrid 2026 logo]
@PaulJiL
- Radiotherapy vs CRT after induction chemotherapy obtaining PR/CR. Phase 3 RCT
109 vs 111 pts. FUP 57m. 5y PFS 87% vs 80% (p=.21). Early termination. Hypothesis generating study.
- LBA Tam-Peli (Anti B7-H3 ADC*topo1) vs chemo in heavily pretreated R/M patients. Phase III RCT (TAISHAN-301)
- Sequential vs simultaneous integrated boost in pts with NPC treated with photon or proton.
268 pts. Seq provided less tox, with no recurrence excess
- Induction sintilimab and bevacizumab plus nab-paclitaxel and cisplatin for N2-3 NPC Ph 2 trial.
45 pts. 36% CR. 59% PR.
- Anti LMP2 protein TCR-T cell for Epstein-Barr virus-related R/M disease. Ph 1
29 pts. No DLT. ↓EBV load in 86% pts. ORR 0%. DCR 63%. Still premature drug development.
- 9th TNM and phenotypic staging across endemic vs Non-endemic NPC
TNM distribution was comparable. Phenotype differs
[Slide 4]
Salivary gland & Paranasal [ESMO Congress Madrid 2026 logo]
@PaulJiL
- Neoadjuvant nivo, cisplatin plus docetaxel followed by surgery and PORT in resectable LA high-grade SGC
50 pts, pdm Ductal (74%). ORR 52%. MPR 60%
- Phase 1a/1b FAP-Dox (AVA600- AntiFAP ADC*Doxo) in SGCs
No high activity. 2 pts (AdCC and SDC) with PR among 11+27 pts treated in dose escalation. ↑Tumour penetration.
- Emi-Le (B7-H4 ADC*auristatin) in aggressive adenoid cystic carcinoma EMBLEM-1 trial in progress
- Phase 1 Rgenta trial: A MYB degrader for R/M AdCC
↓MYB expression. Overall safe. 3 PR across 40 patients
- Pembrolizumab plus cisplatin and nab-paclitaxel as 1st line R/M sinonasal SCC. Ph 2.
20 pts. ORR 60%. Encouraging 3yOS 54.5%.
- RWD Neoadjuvant strategies for sinonasal ca
PE ORR 65% in olp neurob. TPF ORR 72% in G3 carcinoma
- RWD Adenoid cystic carcinoma
90 patients. No PFS difference among type I and II despite different type of treatment. Distinct biology
Alicia Castelo @alicastletreePost text
3/4 Documented geriatric assessment was strongly linked to interventions:
🏃 Exercise: 57.1% vs 2.7%
🥗 Nutritional intervention: 71.4% vs 24.3%
💊 Adapted chemotherapy: 52.0% vs 16.1%
Assessment should translate into action. #ESMO2026 https://t.co/bIfgH0LlFJ
GA was documented in under 3 in 10 patients and varied by centre. It was strongly linked to interventions.
Outcomes associated with documented geriatric assessment
Not documented (n=73) Documented (n=29)
aOR 51.32 (11.76–357.29) *
2/73 (2.7%)
16/28 (57.1%)
aOR 6.63 (2.58–18.36) *
17/70 (24.3%)
20/28 (71.4%)
+centre 1.88 (0.35–9.25), ns
aOR 3.52 (1.14–11.19) *
9/56 (16.1%)
13/25 (52.0%)
[illegible] [illegible] [illegible]
Jeff Ryckman @jryckman3Post text
Trotabresib added toxicity without helping newly diagnosed GBM.
12mo PFS 22% vs 39% w/ RT+TMZ alone (P=.048); OS similar.
G3+ thrombocytopenia 37% vs 15%.
#ESMO26 #radonc
https://t.co/fvr6SiCBoc https://t.co/cdf8w6jkIe
Trotabresib
Adding a BET inhibitor to chemoradiotherapy in glioblastoma
Newly diagnosed IDH-wildtype GBM
After surgery
n = 184
→ RANDOMIZE (Randomized phase II; 2:1)
RT + TMZ (n = 60) | 12-month PFS* 38.9%
+ trotabresib (n = 124) | 12-month PFS* 22.2%
*Primary endpoint: PFS by local RANO. 12-month PFS favored control (P = .048); HR not reported.
Median OS 16.7 vs 16.9 months (P = .898), not statistically significant. G3+ thrombocytopenia: 15.3% vs 37%.
Dipasquale et al. ESMO 2026, 692O. RT dose not reported in abstract; median follow-up 15 months.
Jeff Ryckman @jryckman3Post text
KEYNOTE-412 ctDNA: clearance after 5wk CRT was more frequent w/ pembro, but outcome associations varied by HPV status and arm.
Interesting biomarker work. Without an interaction test, I wouldn't call this predictive of pembro benefit.
#ESMO26 #radonc
https://t.co/HAS3ZYi4lX https://t.co/7rlojMGpuJ
KEYNOTE-412 ctDNA
Exploratory clearance analysis in a paired-sample subset
Locally advanced
Head and neck SCC
Paired plasma
samples
n = 473 of 804
Parent trial randomized
Subset not re-randomized
→ RANDOMIZE
ctDNA clearance HPV-negative ctDNA clearance HPV-positive
CRT + placebo
(n = 240) 63.6% 62.7%
CRT + pembro
(n = 233) 72.6% 76.8%
Clearance assessed after 5 weeks of CRT (baseline to cycle 3 day 1). Exploratory, retrospective analysis.
Outcome associations varied by HPV status and arm. No treatment-interaction test reported; not proof of prediction.
Machiels et al. ESMO 2026, 1536RO. Parent primary endpoint: EFS; these percentages are biomarker outcomes.
Mustafa Özdoğan, MD @ozdogan_mdPost text
4 studies I’m watching today at #ESMO26
Presidential Symposium III (16:30 CET):
ARTEMIS-011,
MIOIO,
TroFuse-005 and KEYNOTE-C93.
Which one are you waiting for?
I’ll post notes right after each LBA. #Oncology https://t.co/LXz7BxcQsz
drozdogan.com · Evidence Notes
#ESMO26 · PS III
4 STUDIES I AM WATCHING TODAY
Presidential Symposium III · 16:30 CET
Notes shared right after each LBA
MADRID • CONGRESS NOTES
MUSTAFA ÖZDOĞAN MD · MADRID 2026
Curious about all four · absolute benefit first, then HR, then what stays open
LBA9 Sarcoma
ARTEMIS-011
Heavily pretreated relapsed or refractory osteosarcoma
risvutatug rezetecan vs gemcitabine + docetaxel
THE QUESTION
Can a new agent beat chemotherapy in heavily pretreated osteosarcoma?
LBA10 Solid tumours
MIOIO
Responding patients, advanced or metastatic solid tumours · phase III non-inferiority
reduced-frequency vs standard checkpoint inhibitor dosing
THE QUESTION
Can immunotherapy be given less often without losing efficacy?
LBA11 Endometrial
TroFuse-005
Previously treated advanced or recurrent endometrial cancer
sacituzumab tirumotecan
THE QUESTION
How much can it add after prior therapy in endometrial cancer?
LBA12 Endometrial
KEYNOTE-C93
First-line dMMR advanced or recurrent endometrial carcinoma
pembrolizumab vs carboplatin + paclitaxel
THE QUESTION
Can immunotherapy alone replace carboplatin–paclitaxel in first-line dMMR disease?
YOUR TURN
Which one are you waiting for?
Independent commentary · INN only · session details may change
@ozdogan_md
Jeff Ryckman @jryckman3Post text
GORTEC IDEAL is early: induction EGFR-ADC +/- anti-PD1, then 70 Gy/cisplatin. G3 TEAEs in 6/10 combination pts vs 2/10 ADC alone.
20 pts in this safety analysis.
#ESMO26 #radonc
https://t.co/WXt5sKlK9W https://t.co/lXFU9CQGPS
GORTEC IDEAL
Induction EGFR-ADC with or without anti-PD1 before CRT
Locally advanced
Head and neck SCC
n = 49 randomized
→ RANDOMIZE
Grade 3 TEAEs, safety subset
EGFR-ADC, then CRT 2/10
+ anti-PD1 6/10
Becotatug vedotin x3 +/- pucotenlimab, then 70 Gy + cisplatin; combination arm also receives adjuvant anti-PD1.
Phase II; 106 planned. First 20 safety-evaluable pts only. Primary CR at 12 weeks after CRT remains immature.
Tao et al. ESMO 2026, 1538RO. No grade 4 AEs; one death in ADC-only arm deemed unrelated. No efficacy conclusion.
Jeff Ryckman @jryckman3Post text
RADIAN (LBA46)
Non-randomized cohorts by cisplatin eligibility, each vs historical controls.
1y DFS: CRT-eligible A 88.2% vs 65% (HR 0.19); cisplatin-unfit B 61% vs 55% (HR 0.72).
Continuous niraparib + 70 Gy/35 fx in B caused prolonged RT adverse events, including 2 niraparib-RT-related deaths.
#ESMO26 #radonc #OncTwitter
https://t.co/X7xkSq8XMv
RADIAN
Niraparib + dostarlimab with definitive CRT or RT: non-randomized cohorts
LA-HNSCC
PD-L1 CPS ≥1
ECOG 0-1
n=34
-> Cisplatin eligibility
| 1y DFS* Cohort | 1y DFS* Historical | DFS HR* vs historical
A: CRT-eligible (n=17) Cisplatin 100 mg/m² + RT 70 Gy/35 fx | 88.2% | 65% | 0.19
B: cisplatin-unfit (n=17) RT 70 Gy/35 fx + continuous niraparib No cisplatin | 61% | 55% | 0.72
Both: dostarlimab + niraparib induction, then maintenance after RT
Oliva. ESMO 2026, LBA46. cslide: https://cslide.ctimeetingtech.com/esmo2026/attendee/confcal/presentation/list?q=LBA46
*Primary: 1y DFS vs historical controls. A p=0.01; B p=0.19. RT regimen: NCT05784012.
Abstract only; historical comparisons. Cohort B: prolonged RT toxicity, 2 niraparib-RT-related deaths.
Jeff Ryckman @jryckman3Post text
In resected brain mets progressing after RT: fewer CD8+ cells and more FOXP3+ cells than untreated tumors.
These are selected treatment failures. I wouldn't read this as evidence that RT broadly suppresses antitumor immunity.
#ESMO26 #radonc
https://t.co/dnJu8C8P22 https://t.co/Yu1JJE74mE
Progressive brain metastases
Molecular profiling of resected tumors by prior treatment
Resected brain mets
Progression after RT
or systemic therapy
+ untreated controls
n = 153
→ GROUPS
No prior therapy (n = 63)
Prior RT (n = 43)
Prior systemic therapy (n = 37)
Both (n = 10)
Exome sequencing, methylation profiling and immunohistochemistry; 35 paired initial/recurrent samples.
Prior-RT tumors had fewer CD3/CD8/CD45RO+ cells and more FOXP3+ cells than untreated tumors.
Steindl et al. ESMO 2026, 703RO. Observational, selected resected failures; no causal treatment comparison.
Richard Fitzgerald 💙 🦀💚 @r1chardf1tzg3r1Post text
#ESMO2026
“Beyond Guidelines”
Include Impact Of
🇬🇧 #DoctorSubstitution On
#Oncology Patient Outcomes
“ADVANCED PRACTITIONERS”
“PHYSICIAN ASSOCIATES “
@myESMO @ESTRO_RT @CPME_EUROPA @UEMSEurope
@AliceIndini @AndriPapakonst @AndrewWardley @TheLancetOncol
@TheBMA https://t.co/UlYlAbm2YW
[Slide 3]
Example 1
A cancer diagnosis was missed
One doctor reported that a patient with red-flag symptoms was repeatedly seen by a non-doctor, delaying diagnosis by around six weeks.
[Photo of man in waiting room]
[Slide 4]
Example 3
A patient wrongly admitted to end-of-life care
An ACP reviewed a cancer patient, determined she was at the end of life and admitted her to an end-of-life care room. She was later found to have treatable hypercalcaemia, improved with treatment and was discharged.
[Photo of patient in hospital gown]
Mustafa Özdoğan, MD @ozdogan_mdPost text
Osteosarcoma: few options for years.
#ESMO26 ARTEMIS-011 says a new ADC beats chemo on PFS. Follow-up is short, toxicity is real.
Hope or hype?
Dr Lu Xie
#Sarcoma https://t.co/XlZoO434Ju
drozdogan.com · Evidence Notes
#ESMO26 · LBA9
ARTEMIS-011
Relapsed or refractory osteosarcoma · progressed after ≥2 prior lines
risvutatug rezetecan vs gemcitabine + docetaxel · Lu Xie
PFS met · OS immature · small open-label trial
STUDY DESIGN
Patients n = 122
Arms (2:1) 80 vs 42
Primary BICR PFS
Median FU 7.1 mo
ABSOLUTE OUTCOMES
PFS (BICR)
Risvutatug 5.5
Chemo 1.4
months (median)
Absolute Δ +4.1 mo
Relative HR 0.33
p < 0.0001 · 4-mo PFS 65% vs 33%
Response (BICR)
Risvutatug 15
Chemo 2
ORR, %
Absolute Δ +13 pts
Overall survival HR 0.51 (0.21–1.23)
immature · not significant
Chemo = gemcitabine + docetaxel · DCR 76% vs 33% · median DoR 7.6 mo
THE TAKE
A large PFS gain in heavily pretreated osteosarcoma, with high haematologic toxicity and short follow-up
SAFETY
Serious TRAEs 63.8% vs 28.6% mainly haematologic
Dose reductions 71% vs 26% treatment-related
Stopped for TRAE 3.8% vs 2.4% no treatment-related deaths
PFS HR 95% CI not reported · crossover allowed, number not reported · one grade 2 ILD, resolved
HOW TO READ
Absolute first: +4.1 mo PFS and +13 pts ORR. Small trial (n = 122) with 7.1 mo follow-up, OS immature. Dose reductions were common, so check haematologic AEs and crossover on the slides.
Mustafa Özdoğan, MD @ozdogan_mdPost text
Can we give immunotherapy less often?
#ESMO26 MIOIO asked exactly that. The answer was not the one we hoped for.
Would you still stretch the interval?
Dr Gwenaëlle Gravis
#Immunotherapy https://t.co/bFnSrfLKoD
drozdogan.com · Evidence Notes
#ESMO26 · LBA10
MIOIO
Advanced or metastatic solid tumours · responding after 6 months of checkpoint inhibitor
dosing every 12 weeks vs standard dosing · phase III non-inferiority · Gwenaëlle Gravis
Non-inferiority not established · interim analysis
STUDY DESIGN
Randomized (1:1) n = 340
Analysed (mITT) n = 308
NI margin HR 1.30
Median FU 18.6 mo
ABSOLUTE OUTCOMES
PFS (primary)
Standard 25.0
Every 12 wk 21.9
months (median)
Absolute (reduced vs standard) Δ −3.1 mo
Relative (reduced vs standard) HR 1.35 (0.90–2.00)
CI includes 1 and the 1.30 margin
Overall survival (secondary)
Medians Not reported interim analysis
Direction Favors standard
Relative (reduced vs standard) HR 2.00 (1.10–3.90)
p = 0.0143
Standard = usual checkpoint inhibitor schedule · reduced = every 12 weeks
THE TAKE
The interim data do not support routinely extending checkpoint inhibitor dosing to every 12 weeks
SAFETY · ENROLMENT
Grade 3–4 irAEs 10.5% vs 9.5% standard vs reduced
Serious AEs 26.3% vs 25.0% standard vs reduced
Enrolment 340 of 646 planned, randomized
Per-arm numbers and OS medians not reported · tumour-type subgroups imprecise
HOW TO READ
Absolute first: median PFS 25.0 vs 21.9 mo. Non-inferiority was not shown and the OS signal favors standard dosing. It is an interim analysis with 340 of 646 planned patients, so [cut off]
Dr. Iván R. González @Dr_IvanoncologoPost text
At #ESMO26, the ESMO–EACR session highlighted a key challenge in cancer immunotherapy: tumor antigenicity alone is not enough. Impaired antigen presentation and immunosuppressive dendritic cells, macrophages and B cells may limit T-cell priming and immune recognition. https://t.co/PpcehVViK6
ESMO Congress 2026 Special Session Recap
Tumor Microenvironment
Tumor antigens, antigen presentation, and immune suppresssion
SCIENCE PEOPLE PROGRESS A HEALTHIER TOMORROW
CORE THEME: Antitumor immunity depends not only on the presence of tumor antigens, but also on effective antigen processing and presentation within a permissive immune microenvironment.
KEY SCIENTIFIC INSIGHTS
1 Tumor antigens arise from multiple sources: Tumor-specific antigens and neoantigens may result from genomic, transcriptomic, translational, and post-translational alterations.
2 Antigen presentation is a critical checkpoint: Peptide processing and HLA-mediated presentation determine whether tumor antigens can be recognized by T cells.
3 Professional APCs can be rewired: Dendritic cells, macrophages, and B cells may shift from antitumor activity toward immunosuppressive phenotypes in the tumor microenvironment.
4 Immune escape has therapeutic consequences: Defects in antigen presentation and suppressive immune niches may limit T-cell priming, promote resistance, and shape vaccine strategies.
MICROENVIRONMENTAL REPROGRAMMING
Dendritic cells: Tolerogenic DCs may reduce effective T-cell priming.
Macrophages: Tumor-associated macrophages can support immune suppression.
B cells: Regulatory B-cell phenotypes may modulate CD4+ T-cell responses.
CLINICAL RELEVANCE: Explains why antigenicity alone may not translate into effective immunity. Provides a framework for resistance to immunotherapy. Supports the rationale for improved cancer vaccine development.
TAKE-HOME MESSAGE: In the tumor microenvironment, generating antigens is only part of the story: effective antitumor immunity requires successful antigen presentation and immune cells that remain functionally antitumor rather than suppressive.
#ESMO26 #TumorMicroenvironment #CancerImmunology #Immunotherapy
Jeff Ryckman @jryckman3Post text
Plasma miR371 and relapse detection during active surveillance in S1823/GCC.1 (LBA58).
📌 Prospective observational cohort, 631 pts w/ newly diagnosed early-stage GCT on active surveillance; serial plasma miR371 at baseline, follow-up and relapse.
📌 Median follow-up 35.9 mo; 104 relapses, 90 confirmed as unequivocal.
📌 Baseline: sensitivity 0.20 (95% CI 0.10-0.29), specificity 0.90 (0.87-0.92), PPV 0.21 (0.11-0.31), NPV 0.90 (0.86-0.92), AUC 0.55 (0.50-0.61).
📌 At relapse: sensitivity 0.54 (95% CI 0.43-0.65), PPV 0.46 (0.35-0.56), NPV 0.92 (0.90-0.95), AUC 0.74 (0.67-0.80); all intervals are 95% CIs. Specificity at relapse not reported.
📌 False positives: 10.3% at baseline, 4.4% at 12 mo. Positive baseline miR371: relapse HR 2.04 (p=0.02).
📌 Adverse events not reported.
https://t.co/M4VeT0LFaZ
#ESMO26 #GCT
S1823 / GCC.1
Serial plasma miR371 during active surveillance for early-stage GCT
Sensitivity | NPV | AUC
Baseline | 0.20 95% CI 0.10–0.29 | 0.90 95% CI 0.86–0.92 | 0.55 95% CI 0.50–0.61
Newly diagnosed early-stage GCT Active surveillance n=631
Serial plasma miR371 Baseline, follow-up, at relapse
104 relapses (90 unequivocal) MFU 35.9 mo
At relapse | 0.54 95% CI 0.43–0.65 | 0.92 95% CI 0.90–0.95 | 0.74 95% CI 0.67–0.80
Positive baseline miR371: relapse HR 2.04 (p=0.02)
95% CI not reported
Prospective observational study. False positives: 10.3% at baseline; 4.4% at 12 mo.
How best to integrate miR371 into routine practice remains unknown.
ESMO 2026 LBA58
Nicolò Battisti, MD @nicolobattistiMOIONSABP B-42KEYNOTE-905 / EV-303NATALEEAZUR-1KEYNOTE-C93lidERADESTINY-Breast05GIM3 FATATRIO-US B-12 TALENTDEWI (GERCOR-GONO)
Post text
Older adults at #ESMO26:
MOIO (LBA10) on 3-monthly checkpoint inhibitors, TOP-1 (545RO) on omitting RT in older women with ER+ breast cancer, B-42 (LBA24) on extended letrozole, EV-302 in older patients (4761P).
De-escalation is the theme this year.
#GeriatricOncology
#gerionc
@myESMO
@SIOGorg
@siognah
@SIOGnursing_AH
@YoungSIOG
@AlumniSiog
@royalmarsdenNHS
@ICR_London
@royalmarsden
ESMO CONGRESS 2026 · MADRID · 23-27 OCTOBER
Older adults with cancer at #ESMO26
10 presentations I will not miss
1 MOIO LBA10
Phase III non-inferiority trial of immune checkpoint inhibitors every 3 months in responding patients. Gwenaëlle Gravis.
Mon 26 Oct · 16:30-18:15 · Presidential Symposium III · Alicante Auditorium, Hall 6
2 TOP-1 (BOOG 2016-01) 545RO
5-year results of omitting radiotherapy after breast-conserving surgery in systemically untreated older women with ER+ early breast cancer. Lotte Bouwman.
Fri 23 Oct · 16:15-17:45 · Rapid oral, early breast cancer · Alicante Auditorium, Hall 6
3 NRG Oncology/NSABP B-42 LBA24
Final analysis of extended letrozole after 5 years of aromatase inhibitor-based therapy in postmenopausal women. Eleftherios P. Mamounas.
Fri 23 Oct · 13:30-15:00 · Proffered paper 1, breast cancer · Alicante Auditorium, Hall 6
4 GIM3 FATA 544RO
Final analysis: upfront versus switch schedule and three aromatase inhibitors head to head in postmenopausal HR+ early breast cancer. Pietro De Placido.
Fri 23 Oct · 16:15-17:45 · Rapid oral, early breast cancer · Alicante Auditorium, Hall 6
5 GERCOR-GONO DEWI 2877RO
Dostarlimab with watch-and-wait in localised dMMR/MSI-H gastro-oesophageal cancer, including a cohort of patients over 70 unfit for surgery. Thierry André.
Fri 23 Oct · 16:15-17:45 · Rapid oral, upper GI · hall to be confirmed
6 EV-302 in older patients 4761P
Updated exploratory analysis of enfortumab vedotin plus pembrolizumab in older patients and those with comorbidities. S. S. Sridhar.
Fri 23 Oct · poster on view 09:00-17:00, presenter 15:15-16:00 · Poster Area, Hall 5
7 KEYNOTE-C93 / GOG-3064 / ENGOT-en15 LBA12
Phase III first-line pembrolizumab versus carboplatin-paclitaxel in dMMR advanced or recurrent endometrial cancer. Brian M. Slomovitz.
Mon 26 Oct · 16:30-18:15 · Presidential Symposium III · Alicante Auditorium, Hall 6
8 AZUR-1 LBA87
First results of dostarlimab monotherapy for clinical complete response in dMMR/MSI-H locally advanced rectal cancer. Andrea Cercek.
Sun 25 Oct · 10:15-11:45 · Proffered paper, lower GI · hall to be confirmed
9 AIUR LBA28
Randomised trial of compression with standard surgical gloves to prevent paclitaxel-induced peripheral neuropathy. Young-Joon Kang.
Fri 23 Oct · 16:15-17:45 · Rapid oral, early breast cancer · Alicante Auditorium, Hall 6
10 HOPE LBA92
Phase III trial of a personalised digital supportive-care pathway for endocrine therapy symptoms in early breast cancer.
Mon 26 Oct · 08:30-10:00 · Proffered paper, supportive and palliative care · hall to be confirmed
Also on my list
Beyond guidelines: grey zones of oncology practice, with decision making in elderly and frail patients, Sat 24 Oct 10:15-11:45, Murcia Auditorium, Hall 3 · Overcoming barriers of access to clinical trials, Sat 24 Oct 08:30-10:00, Seville Auditorium · LOMAC (LBA81), 4 versus 6 months of adjuvant XELOX in gastric cancer · HER2CLIMB-05 HRQoL (1766RO), Sat 24 Oct 10:15-11:45, Almeria Auditorium, Hall 9 · lidERA (538RO) and DESTINY-Breast05 (539RO) patient-reported outcomes, Fri 23 Oct 16:15-17:45 · KEYNOTE-905 (4733O) and EV-103 (4740RO) in cisplatin-ineligible urothelial cancer · Dostarlimab real-world data by age (1286P), Mon 26 Oct poster · EONS19: quality of life for older adults with head and neck cancer (Cherith J. Semple), Sun 25 Oct 08:30 · TALENT (LBA23) and NATALEE 6-year OS (LBA25), Fri 23 Oct 13:30-15:00
Madrid local time. Clocks go back overnight on 24-25 October (CEST to CET). Late-breaking abstracts are embargoed until presentation; halls from secondary sources, check the programme app on the day.
@nicolobattisti
Raffaele Colombo @raffcoloPost text
MRG007 (CDH17 ADC) #ESMO26
Nice to see PK...
...but the exposure comment is ridiculous 🤯!
Calculated in ng/mL based on Cmax, but MW are very different (150000 vs 435).
In reality exatecan exposure is high (6% of ADC AUC), especially for a DAR4 ADC!
Here replotted (in nM) 👇 https://t.co/azFyj7vwsA
#ESMO26
MRG007 (ARR-217) PK, 6 mg/kg
MRG007 (ARR-217)
Exatecan
Concentration (nM)
Time post dose (days)
Payload/ADC AUC ratio = 6%
Payload/ADC Cmax ratio = 2.5%
(significant payload exposure)
Raffaele Colombo @raffcoloPost text
Here replotted the PK of MRG007 (#ESMO26) vs. AMT-676 (#ESMOGI26) in the same format.
Enjoy @JacobPlieth https://t.co/LjMYLHKY0J https://t.co/fzZKgqxKGS
#ESMO26
MRG007 (ARR-217) PK, 6 mg/kg
MRG007 (ARR-217)
Exatecan
#ESMOGI26
AMT-676 PK, 6.4 mg/kg
AMT-676
Exatecan
Concentration (nM)
Time post dose (days)
Iovance Biotherapeutics @IovanceBioPost text
Today at #ESMO26, an oral presentation highlighted the first clinical data for #TILtherapy in two difficult-to-treat soft tissue #sarcomas with limited treatment options. 🧬
Learn more: https://t.co/e4MUev02fG https://t.co/cm6JTuM8hh
RAPID ORAL PRESENTATION
#3725RO
Lifileucel in Patients With Undifferentiated Pleomorphic Sarcoma (UPS) or Dedifferentiated Liposarcoma (DDLS)
"The unprecedented efficacy for one-time lifileucel in UPS and DDLPS sets a new bar for response rates with TIL therapy in refractory patients and underscores the powerful potential of our TIL platform across many solid tumor cancers."
Brian Gastman, MD
Executive Vice President, Translational Medicine and Research at Iovance Biotherapeutics
IOVANCE BIOTHERAPEUTICS
TIL, tumor-infiltrating lymphocyte.
ESMO - Eur. Oncology @myESMOPost text
Concomitant publications at #ESMO26: new data moving swiftly from the podium to the peer-reviewed journals.
@Annals_Oncology @ESMO_Open @NEJM @NatureMedicine @TheLancet @TheLancetOncol @Nature @JAMA_current https://t.co/OdlG1FMDYA
MADRID 2026 ESMO congress
48 CONCOMITANT PUBLICATIONS
21 Annals of Oncology
6 The New England Journal of Medicine
6 ESMO Open
5 Nature Medicine
6 The Lancet
2 The Lancet Oncology
1 Nature
1 JAMA
MADRID SPAIN
23-27 OCTOBER 2026
ESMO
OncoAlert @OncoAlertPost text
🇪🇸 #ESMO26 Day 1 in numbers 📊 and it Just got Started
🔥 17.9M impressions
💬 1.1K posts
👥 437 participants
🌍 26 countries
⚡ 18.7 posts/hour
Proud to lead the conversation at #1 💪 Thank you @myESMO and everyone sharing the science from Madrid 🙌
Real-time metrics powered by AcuVox 🎙️ https://t.co/D5QkLIE1kW
@cdanicas @hoperugo @DrChoueiri @TiansterZhang @matteolambe @NiuSanford @stolaney1 @christine_lovly @amerseburger @GlopesMd @tompowles1 @montypal @Icro_Meattini @PGrivasMDPhD @brian_rini @CathyEngMD @apolo_andrea @AndreaNecchi @DrSGraff @BenWestphalen @graokane @to_be_elizabeth @ElisaAgostinett @nataliagandur @UOzkerim @DrMirallas @DrYukselUrun @Lucarecco @mzugman @HHorinouchi @p_ciracimd @DraMartinezLago @DrVilmaPBarcia @GIMedOnc @MarioBalsaMD @scocmem @AmandaNizamMD @GaiaGriguolo @JankovicK @Dr_Oncologista @Erman_Akkus @WeOncologists @niklas_kluemper @Markuseckstein3 @PTarantinoMD @ScottGottliebMD @VivekSubbiah @dr_yakupergun
Same image also posted by @OncoAlert
DAY 1 · SOCIAL PULSE ● LIVE
#ESMO26
Madrid.
23-27 OCTOBER 2026 | IFEMA MADRID
POTENTIAL REACH
17.9M
impressions on day one
1.1K Posts on X - clean, no bots or dupes
437 Participants - voices in the conversation
26 Countries - a global conversation
18.7 Posts / hour - across the meeting day
2.6 Posts / HCP - engagement depth
28% Positive - of scored posts
TOP INFLUENCERS (by reach · day 1)
1 OncoAlert @OncoAlert [X]
2 ESMO - Eur. Oncology @myESMO [X]
3 ESMO esmo_eur_oncology [IG]
4 Scott Gottlieb, MD @ScottGottliebMD [X]
5 Adam Feuerstein @adamfeuerstein [X]
6 Gilberto Lopes @GlopesMd [X]
7 Gil Morgan, MD @weoncologists [X]
8 Toni Choueiri, MD @DrChoueiri [X]
9 Vivek Subbiah, MD @VivekSubbiah [X]
10 Memorial Sloan Kettering @MSKCancerCenter [X]
11 Paolo Tarantino @PTarantinoMD [X]
12 The OncoAlert Netw... Bluesky [BSKY]
13 Yakup Ergün @dr_yakupergun [X]
14 Sumanta K. Pal, MD @montypal [X]
WHERE IT CAME FROM
Europe 363
North America 310
Asia-Pacific 100
Latin America 18
Middle East & Africa 2
TOP COUNTRIES
United States 275 | Spain 98
Switzerland 79 | Japan 63
Turkey 58 | United Kingdom 54
Canada 35 | Italy 25
TOP CITIES
Lugano 57
Boston 47
London 43
Tokyo 40
New York 34
Madrid 31
LANGUAGES
English 92%
Spanish 5%
Japanese · Italian · French 1% each
ACUVOX real-time congress metrics · by OncoBites x OncoAlert
ONCOLOGY INSIGHTS. REAL-TIME IMPACT.
Annals of Oncology @Annals_OncologyPost text
📢 #ESMO26 concomitant paper - Efficacy and safety of risvutatug rezetecan versus gemcitabine plus docetaxel in relapsed/refractory advanced osteosarcoma: Primary results from the ARTEMIS-011 phase 3 trial.
🔗https://t.co/e7Jw27cx6I https://t.co/CVu7K3TSeI
Primary results from the Phase 3 ARTEMIS-011 study
Risvutatug rezetecan (Ris-Rez) demonstrated a statistically significant and clinically meaningful improvement in BICR-assessed PFS versus gemcitabine plus docetaxel in patients with R/R osteosarcoma after failure of least 2 lines of therapy
Phase 3 ARTEMIS-011 Study Design
Key Eligibility Criteria
• Age ≥12 years
• Pathologically confirmed diagnosis of osteosarcoma
• Progression or intolerance to at least two previous lines of therapy
• ≥1 measurable target lesion per RECIST v1.1
• ECOG PS 0–1
R 2:1
Ris-Rez 12.0 mg/kg IV D1, Q3W (n = 80)
Gemcitabine + Docetaxel (n = 42)
Crossover allowed*
Each Q3W cycle Gemcitabine 1000 mg/m2 IV, Days 1 and 8 Docetaxel 75 mg/m2 IV, Day 8
Treatment until PD, toxicity, or withdrawal of consent
* Crossover allowed after objective disease progression if crossover criteria were met
Primary endpoint: BICR-assessed PFS
4-mo rate 65% 33%
PFS (%)
Time since randomization (mo)
Patients at risk (censored), n
Ris-Rez (n = 80) | Gemcitabine + Docetaxel (n = 42)
mPFS (95% CI) 5.5 mo (4.1–7.4) | 1.4 mo (0.8–2.7)
HR (95% CI) 0.33 (0.20–0.55)
P value < 0.0001
Safety
Median treatment duration Ris-Rez: 4.5 mo Gemcitabine: 1.5 mo; Docetaxel: 1.4 mo
TEAEs in ≥20% of patients
WBC count ↓, Anemia, Platelet count ↓, Neutrophil count ↓, Lymphocyte count ↓, Pyrexia, Vomiting, Nausea, Hypoalbuminemia, ALT ↑, Appetite ↓, Asthenia, Infusion-related reaction, AST ↑, Constipation, Epistaxis, Hypokalemia, Weight ↓, Blood LDH ↑, GGT ↑, Rash
[per-AE bar percentages small; not transcribed]
Ris-Rez (n = 80) Grade 1–2 Grade ≥3
Gemcitabine + Docetaxel (n = 42) Grade 1–2 Grade ≥3
Percentage of patients
Ris-Rez is a promising new treatment for patients with previously treated R/R advanced osteosarcoma
Survival table
Endpoint: PFS by BICR (primary endpoint)
Arm | N | Median | Median CI
Ris-Rez | 80 | 5.5 mo | 4.1–7.4
Gemcitabine + Docetaxel | 42 | 1.4 mo | 0.8–2.7
HR: 0.33
HR CI: 95% CI 0.20–0.55
P: <0.0001
4-mo rate: 65% vs 33%
OncoAlert @OncoAlertPost text
OncoAlert 4Sight Abstracts to be Presented at #ESMO26
Risvutatug Rezetecan (Ris-Rez) Versus Gemcitabine and Docetaxel (GD) in Heavily Pretreated Patients With Relapsed or Refractory (R/R) Osteosarcoma: Primary Results From the Phase 3 ARTEMIS-011 Study
🦴 Phase 3 (n=122, China): B7-H3-directed ADC risvutatug rezetecan vs gemcitabine + docetaxel in R/R osteosarcoma after ≥2 prior lines; 25% adolescents. Primary endpoint: PFS by BICR.
➡️ Median PFS 5.5 vs 1.4 mo; HR 0.33; p<0.0001
➡️ OS immature; HR 0.51
➡️ Grade ≥3 TEAEs 92.5% vs 83.3%; treatment-related SAEs 63.8% vs 28.6%
✅ Significant PFS improvement with a favorable OS trend and manageable safety, highlighting potential as a new treatment standard for R/R osteosarcoma.
🎙️ Lu Xie
(4Sight Made from Abstracts publicly available at the ESMO website)
[Slide 2]
Background
Risvutatug Rezetecan vs Gemcitabine + Docetaxel in Relapsed/Refractory Osteosarcoma: ARTEMIS-011
Randomized, open-label phase 3 (China) Risvutatug rezetecan (Ris-Rez), a B7-H3-directed ADC, previously showed promising antitumor activity with manageable toxicity in heavily pretreated R/R sarcomas. ARTEMIS-011 compared Ris-Rez with gemcitabine + docetaxel in Chinese patients with R/R osteosarcoma.
Based on publicly released #ESMO 2026 abstract. Preliminary data, not peer-reviewed. Not medical advice. © original authors/ESMO.
[Slide 3]
Methods
DESIGN
2:1 randomization to Ris-Rez 12.0 mg/kg Q3W (n=80) or gemcitabine + docetaxel Q3W (n=42).
POPULATION
Patients ≥12 years with osteosarcoma that progressed or relapsed after ≥2 prior lines. Median age 21; adolescents (12–18 years) 25.4%.
ENDPOINT
Primary: PFS by BICR.
FOLLOW-UP
DCO Jun 17, 2026; median follow-up 7.1 mo.
Based on publicly released #ESMO 2026 abstract. Preliminary data, not peer-reviewed. Not medical advice. © original authors/ESMO.
[Slide 4]
Results
All comparisons: Ris-Rez vs gemcitabine + docetaxel
PFS (BICR)
Median 5.5 vs 1.4 mo; HR 0.33; p<0.0001.
PFS (INVESTIGATOR) & OS
Investigator-assessed median PFS 5.6 vs 1.0 mo. OS immature; HR 0.51.
SAFETY
Grade ≥3 TEAEs 92.5% vs 83.3%. Treatment-related SAEs 63.8% vs 28.6%, mainly hematologic. Discontinuation due to TRAEs 3.8% vs 2.4%.
ILD & DEATHS
One treatment-related ILD (grade 2, resolved) with Ris-Rez. No treatment-related deaths.
Based on publicly released #ESMO 2026 abstract. Preliminary data, not peer-reviewed. Not medical advice. © original authors/ESMO.
ESMO - Eur. Oncology @myESMOPost text
#ESMO26: Single-cell and spatial profiling can map how the tumour ecosystem shifts under treatment pressure and may help to enhance understanding of treatment response and #resistance on a granular level, as discussed by James Reading
#InsightsbyESMO ➡️ https://t.co/GZLh51zfTm https://t.co/FsV6cqZXOA
MADRID 2026 ESMO congress
"As the field embraces the paradigm shift towards cancer interception, a natural progression of neoadjuvant profiling studies is to explore pre-invasive lesions in patients under surveillance in screening programmes."
James L. Reading
UCL Cancer Institute, University College London,UK
#InsightsbyESMO
ESMO
OncoAlert @OncoAlertPost text
MOIO: Interim Analyses of a Phase III Randomized Non-Inferiority Trial Assessing Reduced Frequency Immune Checkpoint Inhibitors in Responding Patients With Advanced/Metastatic Cancer
@SabatierRenaud
🔬 Academic phase III non-inferiority trial (n=340, France): standard IO vs reduced dose intensity (every 3 months) in patients responding after 6 months of IO for advanced solid tumors.
➡️ PFS HR 1.35 (0.9–2.0); median 21.9 vs 25.0 mo; futility boundary exceeded
➡️ OS HR 2.0 (1.1–3.9) with reduced IO
➡️ Grade 3–4 irAEs 9.5% vs 10.5%
✅ Authors: non-inferiority not achieved, no meaningful safety advantage, and a signal of inferior survival; differential effects argue against uniform de-escalation.
🎙️ Gwenaëlle Gravis
👥 Patricia Marino · Daniel Olive · Frédérique Penault-Llorca · Jean-Pierre Delord · Clotilde Simon · Assia Lamrani-Ghaouti · Renaud Sabatier · Joseph Ciccolini · Jean-Marie Boher
Pinging our faculty
@Lucarecco @Dr_Oncologista @guiandri76 @DrVilmaPBarcia, @Erman_Akkus, @GIMedOnc, @niklas_kluemper @Markuseckstein3 @nataliagandur, @oriolmirallas @ugurozkerim
[Slide 2]
Methods
DESIGN
Randomization to standard IO or reduced dose intensity (same dose, every 3 months); up to 646 patients planned across 36 French centers.
POPULATION
Locally advanced/metastatic solid tumors in partial or complete response after 6 months of standard-dose IO (melanoma in CR excluded). 340 randomized, Mar 2022–Nov 2025.
ENDPOINT
Primary: PFS, with a non-inferiority margin of HR 1.3.
Secondary: OS, response duration and safety.
INTERIM ANALYSES
Futility analyses planned at 25% and 50% of 498 events, with stopping if the one-sided P for HR=1 was <0.0192. Median follow-up 18.6 mo; mITT n=308.
Based on publicly released #ESMO 2026 abstract. Preliminary data, not peer-reviewed. Not medical advice. © original authors/ESMO.
[Slide 3]
Results
Reduced vs standard IO (HR >1 favors standard)
PFS
Median 21.9 (12.1–31.6) vs 25.0 (19.4–NE) mo; HR 1.35 (95% CI 0.9–2.0); p=0.0635, exceeding the prespecified futility boundary.
OS
Reduced IO was associated with a higher risk of death: HR 2.0 (95% CI 1.1–3.9); p=0.0143.
BY TUMOR TYPE & LINE
PFS HR: urothelial 2.9 (1.3–6.7), lung 1.6 (0.8–3.1), renal cell 0.7 (0.3–1.5), head and neck 0.6 (0.1–2.4). Beyond first line: 2.9 (0.9–4.9).
SAFETY
Grade 3–4 immune-related AEs 9.5% vs 10.5%; SAEs 25.0% vs 26.3%.
Based on publicly released #ESMO 2026 abstract. Preliminary data, not peer-reviewed. Not medical advice. © original authors/ESMO.
[Slide 4]
Conclusion
Reduced-frequency IO did not achieve PFS non-inferiority
Reduced dose intensity showed no meaningful safety advantage and was associated with a signal of inferior survival. The authors state that differential effects by tumor type and treatment line argue against a uniform de-escalation strategy, and that biomarker-driven strategies warrant further study.
Based on publicly released #ESMO 2026 abstract. Preliminary data, not peer-reviewed. Not medical advice. © original authors/ESMO.
LARVOL @LarvolSANOVOKEYNOTE-671PANKU-Lung01ASTRIDEDeLLphi-304TroFuse-005MOIOKEYNOTE-C93SWITCHDESTINY-Breast09OptiTROP-Breast01BRIDGETINCB161734 (zecdarasib) + chemoLEAP-012PANKU-Breast01
Post text
@myESMO 2026: Day 4 Preview
Explore #ESMO26 insights here: https://t.co/JBaV2QEuxu
#LARVOL #ESMO2026 #CancerResearch #CancerData #Oncology #OncologyInsights #MedicalOncology #ClinicalTrials #LungCancer #LCSM #SCLC #NSCLC #GICancer #GastrointestinalCancer #GICSM #ColorectalCancer #GastricCancer #LiverCancer #PancreaticCancer #ThymicCancer #BreastCancer #BCSM #GynecologicOncology #GYMSM | @ErikaHamilton9 | @DrSGraff | @DrJNaidoo | @HHorinouchi | @Erman_Akkus | @ilyassahinMD | @ShannonWestin | @DrKatyMoore
ESMO 2026 KEY TRIALS | DAY 4 PREVIEW | 26 OCT
Alicante Auditorium - Hall 6 08:30-08:40 | Lung Cancer | SANOVO Savo + Osi Abs: LBA69 | Savolitinib or placebo combined with osimertinib in treatment-naïve advanced NSCLC with EGFR mutation and MET overexpression: Results from the phase 3 SANOVO study | Yi-Long Wu
Alicante Auditorium - Hall 6 09:14-09:24 | Lung Cancer | PANKU-Lung01 Iza-bren Abs: LBA71 | PANKU-Lung01: Randomized phase III study of izalontamab brengitecan (iza-bren) in EGFR-mutant non-squamous non-small cell lung cancer (NSCLC) after progression on a third-generation EGFR TKI | Li Zhang
Alicante Auditorium - Hall 6 10:15-10:20 | Breast Cancer | OptiTROP-Breast01 Sac-TMT vs Chemo Abs: 4639RO | Final OS analysis of sacituzumab tirumotecan versus chemotherapy in previously treated locally recurrent or metastatic triple-negative breast cancer: Phase III OptiTROP-Breast01 | Man Li
Alicante Auditorium - Hall 6 10:20-10:25 | Breast Cancer | SWITCH Target/payload switching Abs: 4RO | Target switching with conserved-payload novel ADCs in patients with metastatic breast cancer following prior ADC therapy (SWITCH): A prospective, open-label, phase 2 platform trial | Lei Fan
Alicante Auditorium - Hall 6 10:30-10:35 | Breast Cancer | NCT06492005 BFv Abs: 4640RO | Bulumtatug fuvedotin (BFv, 9MW2821), a nectin-4-directed antibody-drug conjugate (ADC), in patients with locally advanced or metastatic triple negative breast cancer (la/mTNBC) previously treated with topoisomerase I inhibitor (TopI)-based ADCs: Results from a phase 2 study | Yanchun Meng
Alicante Auditorium - Hall 6 10:50-10:55 | Breast Cancer | BRIDGET Tucatinib + Tras/Pertu or T-DM1 Abs: 1767RO | BRIDGET: A phase II trial of tucatinib added to trastuzumab/pertuzumab or ado-trastuzumab emtansine after isolated intracranial progression in patients with advanced HER2-positive breast cancer | Sarah Sammons
Alicante Auditorium - Hall 6 11:00-11:05 | Breast Cancer | DESTINY-Breast09 T-DXd + Pertu Abs: LBA49 | A DESTINY-Breast09 (DB-09) analysis of trastuzumab deruxtecan (T-DXd) + pertuzumab (P) vs taxane + trastuzumab + pertuzumab (THP) for patients (pts) with HER2+ advanced/metastatic breast cancer (a/mBC) and baseline (BL) brain metastases (BMs) | Cristina Saura Manich
Burgos Auditorium - Hall 3 11:07-11:12 | Thymic Cancer | iTHYM Ivo + Chemo Abs: 4156RO | Ivonescimab plus chemotherapy as first-line treatment in recurrent/metastatic thymic carcinoma: Results from the iTHYM phase II study | Xue Hou
Alicante Auditorium - Hall 6 14:45-14:55 | Lung Cancer | DeLLphi-304 Tarla Abs: 3808O | Tarlatamab in previously treated SCLC: Extended follow-up of overall survival from the phase 3 DeLLphi-304 trial | Charles M. Rudin
Alicante Auditorium - Hall 6 14:55-15:05 | Lung Cancer | ASTRIDE Serplu + Chemo vs Atezo + Chemo Abs: 3809O | Randomized trial of serplulimab or atezolizumab plus chemotherapy in USA patients with extensive-stage small cell lung cancer (ASTRIDE) | David R. Gandara
Alicante Auditorium - Hall 6 15:33-15:43 | Lung Cancer | KEYNOTE-671 Pembro + Chemo Abs: 2519O | Association of biomarkers with efficacy in the phase 3 KEYNOTE-671 study of perioperative pembrolizumab (Pembro) plus neoadjuvant chemotherapy (Chemo) in early-stage non-small-cell lung cancer (NSCLC) | Marina C. Garassino
Barcelona Auditorium - Hall 9 14:50-14:55 | GI Cancer | NCT06179160 INCB161734 + Chemo Abs: 3137RO | Safety and efficacy of INCB161734, a novel oral KRAS G12D inhibitor, in combination with chemotherapy in patients (pts) with advanced/metastatic pancreatic ductal adenocarcinoma (PDAC) | Antoine Hollebecque
Barcelona Auditorium - Hall 9 15:07-15:12 | GI Cancer | LEAP-012 Lenva + Pembro + TACE Abs: 1678RO | Phase 3 LEAP-012 study of lenvatinib + pembrolizumab vs dual placebo with transarterial chemoembolization (TACE) for unresectable non-metastatic hepatocellular carcinoma: Long-term OS results | Josep M. Llovet
Alicante Auditorium - Hall 6 16:54-17:06 | Metastatic Cancer | MOIO Reduced dose intensity of IO Abs: LBA10 | MOIO: Interim analyses of a phase III randomized non inferiority trial assessing reduced frequency immune checkpoint inhibitors in responding patients with advanced/metastatic cancer | Gwenaëlle Gravis
Alicante Auditorium - Hall 6 17:18-17:30 | GYN Cancer | TroFuse-005 Sac-TMT Abs: LBA11 | Sacituzumab tirumotecan in previously treated advanced or recurrent endometrial cancer: Results from the phase 3 TroFuse-005/ENGOT-en23/GOG-3095 study | Domenica Lorusso
Alicante Auditorium - Hall 6 17:42-17:54 | GYN Cancer | KEYNOTE-C93 Pembro vs Chemo Abs: LBA12 | KEYNOTE-C93/GOG-3064/ENGOT-en15: Phase 3, randomized, open-label study of first-line (1L) pembrolizumab (pembro) vs carboplatin (C) + paclitaxel (P) in mismatch repair-deficient (dMMR) advanced or recurrent endometrial carcinoma (a/rEC) | Brian M. Slomovitz
LARVOL
LARVOL @LarvolPost text
POD1UM-303: Updated data from @myESMO 2026 in 1L mAnal SCC landscape from Dr. Erman Akkus (@Erman_Akkus) 👉 https://t.co/VmpUZHFAT4
Updated landscape 👉 https://t.co/GZQOHuWAt0
Explore #ESMO26 insights here: https://t.co/JBaV2QEuxu
#LARVOL #ESMO2026 #CancerResearch #CancerData #Oncology #OncologyInsights #MedicalOncology #ClinicalTrials #AnalCancer #SquamousCellCarcinoma | @pashtoonkasi | @DrChoueiri | @DrYukselUrun | @tompowles1 | @AndreaNecchi
Updated POD1UM-303 Data in 1L mAnal SCC - ESMO 2026
Trials | InterAACT P2 (N=80) The ROYAL MARSDEN NHS Foundation Trust | SCARCE P2 (N=99) GERCOR | POD1UM-303 P3 (N=308) Incyte
Status | Unknown Status | Active, Not Recruiting | Active, Not Recruiting
Intervention | Carboplatin + Paclitaxel (N=45) | Docetaxel + Cisplatin + 5-FU + Atezolizumab (N=64) | Carboplatin + Paclitaxel + Retifanlimab (N=154)
Control | 5FU + Cisplatin (N=46) | Docetaxel + Cisplatin + 5-FU (N=33) | Carboplatin + Paclitaxel (N=154)
mOS | 20.0 vs 12.3 | 24.8 vs NR | 32.8 vs 22.2
mPFS | 8.1 vs 5.7 | 9.4 vs 8.7 | 9.3 vs 7.4
ORR% | 59 vs 57 | 75 vs 78 | 56.5 vs 44.8
Adapted from a post by Dr. Erman Akkus, originally published on X on Sep 29, 2024.
LARVOL
EORTC @EORTCPost text
At today’s #ESMO2026 Policy session, Iryna Shakhnenko presented findings from an EORTC study on patient partner reviews of informed consent forms across 49 clinical trials.
👏 Congratulations to Iryna on presenting this work.
See the key highlights below. 👇 @myESMO https://t.co/D3LHK5HN9j
ESMO Rapid Oral session presented by:
Iryna Shakhnenko (Brussels, Belgium)
EORTC European Organisation for Research and Treatment of Cancer
Key messages
The challenge is not the amount of information, but how it is organised and presented
• Patients' understanding comes first
• Practical information matters
• Transparency builds trust
• Information should support participation, not just consent
Next: Survey → Focus groups → Recommendations → New EORTC PISIC template
ESMO
LARVOL @LarvolPost text
The Key Biomarkers Linked to Clinical Trials from @myESMO 2026 abstracts.
Explore #ESMO26 insights here: https://t.co/JBaV2QEuxu
#LARVOL #ESMO2026 #CancerResearch #CancerData #Oncology #OncologyInsights #MedicalOncology #ClinicalTrials | @tompowles1 | @HHorinouchi | @TiansterZhang | @Erman_Akkus
Key Biomarkers Linked to Clinical Trials – ESMO 2026 Abstracts
HER-2
PD-L1
EGFR
KRAS
CD8
BRAF
TP53
BRCA2
ER
BRCA1
0 50 100 150 200 250
LARVOL
LARVOL @LarvolPost text
The Key Diagnostic Companies Linked to Clinical Trials from @myESMO 2026 abstracts.
Explore #ESMO26 insights here: https://t.co/JBaV2QEuxu
#LARVOL #ESMO2026 #CancerResearch #CancerData #Oncology #OncologyInsights #MedicalOncology #ClinicalTrials | @DrYukselUrun | @zklaassen_md | @Erman_Akkus | @PTarantinoMD | @StephenVLiu
Key Diagnostic Companies Linked to Clinical Trials – ESMO 2026 Abstracts
Natera
Roche
Guardant Health
Illumina
Agilent Tech
Veracyte
Exact Sciences Corp
0 2 4 6 8 10
LARVOL
Oncobites.tv @OncobitesTvDeLLphi-305INTerpath-001TroFuse-005IROCASARTEMIS-011KEYNOTE-866KRASCENDO-1DeLLphi-304LITESPARK-012KEYNOTE-B49KEYNOTE-C93
Post text
📊 #ESMO26 Cierre | Radiografía final del congreso en ACUVOX
Junto a @OncoAlert analizamos las cifras definitivas de la conversación médica tras clausurar el programa oficial:
🔹 Alcance global: 98.6M impresiones potenciales con 5.9K posts cualificados (sin bots ni duplicados).
🔹 Comunidad médica: 952 participantes de 33 países, con 6.2 posts por profesional.
🔹 Sentimiento: 45% de posts puntuados con sentimiento positivo.
🔹 Buzzing últimas 24 h: TroFuse-005 (23), ARTEMIS-011 (21), MOIO (18) y DeLLphi-305 (17).
🟢 Warmly received: INTerpath-001 (+62), DeLLphi-305 (+61) y SAFFRON (+60).
🔴 Coolly received: SWITCH (-80) e IROCAS (-79).
⚖️ Most divisive: ET-FES (50% split) y DB09 (50% split).
Consulta todos los datos y el análisis de los 502 estudios monitorizados 👉 https://t.co/t3AUlKuWNm
#ESMO26 #ACUVOX #OncoAlert #OncoBites #Oncologia
ACUVOX by OncoBites x OncoAlert
Congresses
Impressions 98.6M potential reach
Posts on X 5.9K clean, no bots/dupes
Participants 952 33 countries
Posts / hour 46.1 across the meeting days
Posts / HCP 6.2 engagement depth
Positive 45% of scored posts
On stage
The programme has closed.
14:08 · 27 Oct · Madrid time
Buzzing · last 24 h
1 TroFuse-005 23
2 ARTEMIS-011 21
3 MOIO 18
4 DeLLphi-305 17
5 DeLLphi-304 15
6 KEYNOTE-C93 14
Studies decoded
502 studies · by how the congress received them on X
All 502 studies
Warmly received
DeLLphi-305 +61
VOLGA +49
KRASCENDO-1 +56
SAFFRON +60
INTerpath-001 +62
Coolly received
KEYNOTE-866 -42
LITESPARK-012 -60
IROCAS -79
SWITCH -80
KEYNOTE-B49 -25
Most divisive
ET-FES 50% split
DB09 50% split
COSMIC-313 40% split
OPTIMUM 33% split
NIAGARA 30% split
MitoAI @Vox_MitoAIDeLLphi-305INTerpath-001DASL-HiCaPKEYNOTE-B49ACTICCA-1VOLGADUO-EZW191BEHOLD-1 → BEHOLD-Ovarian01VIKTORIA-1TANGENTPROTEUSTROPION-Breast02FINER (CCTG MA.40)PACE-LUNGPOP-DURVACheckMate 8HWPRABITASBEATccKEYNOTE-B21
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🔥 #ESMO2026 late-breakers 24 Oct scored 1–10 for SoC impact
🚀 9/10: VOLGA, DeLLphi-305, INTerpath-001
✅ 7–8: DASL-HiCaP, CheckMate 8HW, PRABITAS, BEATcc, DUO-E, PROTEUS, TANGENT
⏸️ No shift: FINER, KEYNOTE-B49, ACTICCA-1
Preliminary, pending full data. What moves practice most?
[Slide 1]
ESMO 2026 · SATURDAY 24 OCTOBER · LATE-BREAKING ABSTRACTS · PAGE 1 OF 2
HOT OFF THE PRESS
Late-Breaking Abstracts: Perspective
28 readouts scored for their impact on standard of care (1–10)
PRELIMINARY Abstract-level assessment, pending full data presentations. Scores may change.
28 LBAs released today and scored
DISTRIBUTION BY IMPACT TIER: 3 | 7 | 9 | 6 | 3
9–10 Paradigm-shifting | 7–8 Practice-changing | 5–6 Practice-informing | 3–4 Hypothesis-generating | 1–2 No shift / negative
LBAs BY TUMOR AREA: Breast 8 | Gynecologic 5 | Colorectal 3 | GU (prostate, bladder) 3 | Lung 3 | Hepatobiliary 2 | Pan-tumor 2 | Melanoma 1 | Sarcoma (TGCT) 1
9–10 Paradigm-shifting · Practice-defining — Phase 3 survival endpoints met in major unmet-need settings · 3 LBAs
LBA1 · MELANOMA 9/10 INTerpath-001 — Intismeran autogene + pembrolizumab · Resected stage IIB–IV — RFS HR 0.58 · DMFS HR 0.62 — First Phase 3 win for an individualized mRNA neoantigen therapy over anti-PD-1 alone. WNTB: Personalized manufacturing and supply chains scale to adjuvant time windows without treatment delays.
LBA2 · BLADDER 9/10 VOLGA — Perioperative durvalumab + EV · Cisplatin-ineligible MIBC — EFS HR 0.51 · OS HR 0.58 — First perioperative regimen to beat cystectomy on both EFS and OS in cisplatin-ineligible MIBC. WNTB: EV + IO skin and neuropathy toxicity stays acceptable in frail, elderly surgical candidates in community practice.
LBA3 · ES-SCLC 9/10 DeLLphi-305 — Tarlatamab + durvalumab · 1L maintenance — OS HR 0.42 · 21.1 vs 12.7 mo — Near-doubling of median OS sets a new benchmark for ES-SCLC maintenance. WNTB: Centers manage step-up dosing and CRS (49.6% any grade) in fragile outpatients without early mortality.
7–8 Practice-changing · Regimen-altering — Phase 3 superiority, smarter schedules, or OS confirmation · 7 LBAs
LBA4 · PROSTATE 8/10 DASL-HiCaP — Darolutamide + RT + ADT · Localized very high-risk / salvage — MFS-CI HR 0.42 — 4-yr 95% vs 88%; p = 0.0001. Supports ARPI intensification with curative RT. WNTB: MFS gain converts to OS without long-term cardiometabolic QoL cost.
LBA31 · COLORECTAL 8/10 PRABITAS — Biweekly FTD/TPI + bevacizumab · Refractory mCRC — OS HR 0.93 non-inferior — Severe neutropenia 13% vs 39% compared with standard 28-day dosing. WNTB: Guidelines and community practice pivot to biweekly dosing, cutting G-CSF use.
LBA32 · COLORECTAL 8/10 CheckMate 8HW — Nivolumab + ipilimumab · MSI-H/dMMR mCRC — OS HR 0.61 vs nivo — All lines (296 vs 286): 95% CI 0.46–0.82; p = 0.0009; medians NR. 1L vs chemo (171 vs 84): OS HR 0.37 (0.24–0.57), p < 0.0001; mOS NR vs 50.1 mo. WNTB: Long-term survival gain justifies higher immune toxicity vs single-agent PD-1.
LBA38 · CERVICAL 8/10 BEATcc — Atezolizumab + chemo + bevacizumab · 1L persistent/recurrent/metastatic — OS HR 0.69 — Mature mOS 31.9 vs 22.7 mo; p = 0.003; benefit regardless of PD-L1. WNTB: Atezolizumab used alongside pembrolizumab, notably in PD-L1 low/negative disease.
LBA37 · ENDOMETRIAL 7/10 DUO-E — Durvalumab + CP → durvalumab ± olaparib · 1L advanced/recurrent — OS HR 0.77 ITT — p = 0.037 for chemo + IO + PARPi; pMMR trend HR 0.85. WNTB: Added PARPi OS benefit in pMMR/HRD warrants dual-maintenance toxicity and cost.
LBA53 · PROSTATE 7/10 PROTEUS substudy — Apalutamide + ADT + RP · High-risk localized / locally advanced — EFS HR 0.38 — mEFS NR vs 19.1 mo; p < 0.0001; less salvage therapy. WNTB: Surgery + ARPI yields MFS/OS gains beyond RT + long-term ARPI.
LBA89 · TGCT 7/10 TANGENT — Emactuzumab (CSF-1R mAb) · Symptomatic advanced TGCT — ORR 29.7% RECIST — TVS ORR 53.8%; better physical function, stiffness and pain. WNTB: A 5-dose fixed course replaces chronic daily oral CSF-1R inhibitors.
TODAY'S THEMES: Novel modalities lead: mRNA neoantigen therapy, a bispecific T-cell engager and perioperative ADC + IO top the board. GU is the busiest curative-intent arena, with ARPI intensification around both RT and surgery. Breast is the most represented area (8 LBAs) but has no readout above 6/10.
HOW TO READ THIS · SCORING KEY
9–10 Paradigm-shifting. Phase 3 OS/EFS wins in major unmet need; new modality or new standard.
7–8 Practice-changing. Phase 3 superiority vs active standards, less-toxic schedules, or OS confirmation.
5–6 Practice-informing. Positive in narrow subsets, secondary endpoints, or PFS without OS.
3–4 Hypothesis-generating. Early-phase, feasibility, or AI tools needing prospective validation.
1–2 No shift. Failed primary endpoint or no survival benefit.
Continued on page 2 → 5–6 Practice-informing · 3–4 Hypothesis-generating · 1–2 No shift
WNTB = What You Need to Believe. Preliminary perspective on abstracts released 24 October 2026. Not medical advice.
[Slide 2]
ESMO 2026 · SATURDAY 24 OCTOBER · LATE-BREAKING ABSTRACTS · PAGE 2 OF 2
HOT OFF THE PRESS
Late-Breaking Abstracts: Perspective
Scores 1–6: practice-informing, hypothesis-generating and no-shift readouts
PRELIMINARY Pending full data
5–6 Practice-informing · Subgroup-specific — Narrow subsets, secondary endpoints, or PFS without OS · 9 LBAs
LBA15 · BREAST 6/10 KN026/HB1801 — Anbenitamab + docetaxel · HER2+ ABC, 1L — PFS HR 0.46 — Bispecific beat THP; ORR 87.6%; p < 0.0001. PFS only, OS not yet shown. WNTB: A bispecific doublet displaces the CLEOPATRA dual-mAb standard beyond regional registration.
LBA16 · BREAST 6/10 VIKTORIA-1 — Gedatolisib + palbociclib + fulvestrant · PIK3CA-mut HR+/HER2– ABC — PFS HR 0.52 visceral mets — Superior to alpelisib + fulvestrant, without the hyperglycemia signal. OS not yet reported. WNTB: The triplet shows OS benefit without cumulative stomatitis or diarrhea.
LBA48 · HCC 6/10 EMERALD-3 — STRIDE ± lenvatinib + TACE · Embolisation-eligible — mOS 44.6 vs 39.2 ALBI 1 — Liver function preserved; OS by ALBI grade is exploratory, not yet formally tested. WNTB: Upfront dual IO + TACE does not accelerate hepatic decompensation.
LBA96 · BREAST 6/10 TROPION-Breast02 — Dato-DXd · 1L mTNBC, brain metastases cohort — PFS HR 0.37 · OS HR 0.55 — mPFS 7.7 vs 3.5 mo; mOS 13.5 vs 10.7 mo. Subgroup of the main trial. WNTB: CNS penetration is sufficient to defer upfront cranial irradiation.
LBA20 · BREAST 6/10 Digital MammaPrint — AI digital pathology on H&E · Early HR+/HER2– — r = 0.954 vs RNA assay — Independent 10-year prognostic validation, HR 0.12. WNTB: Regulators accept image-based AI as a substitute for genomic RNA testing.
LBA36 · ENDOMETRIAL 6/10 KEYNOTE-B21 ctDNA — Adjuvant pembrolizumab · Resected high-risk dMMR — DFS HR 0.34 · DDFS 0.25 — ctDNA clearance strongly tracks outcomes. WNTB: Post-op ctDNA is standardized across labs to steer adjuvant IO.
LBA74 · LUNG 6/10 DESTINY-Lung04 PROs — T-DXd vs chemo-IO · 1L HER2-mutant NSCLC — Cough HR 0.66 — Delayed cough deterioration; physical functioning maintained. WNTB: The QoL edge cements T-DXd as preferred 1L over platinum chemo-IO.
LBA17 · BREAST 5/10 PREDICT-HER — HER2-PET imaging · T-DXd-treated ABC — NPV 88.2% — 100% NPV in HER2-low/zero; flags T-DXd non-responders. WNTB: PET tracer and nuclear medicine capacity can integrate into T-DXd pathways.
LBA73 · LUNG 5/10 PACE-LUNG — ctDNA-guided chemo escalation · EGFRm, ctDNA+ at wk 3 of osimertinib — mPFS 16.3 mo · OS 29.2 — Feasibility of 4-cycle chemo escalation in non-clearers. WNTB: Early ctDNA-triggered escalation can replace upfront FLAURA2 triplet.
3–4 Hypothesis-generating · Early validation — Early-phase signals and digital/AI tools awaiting outcome data · 6 LBAs
LBA41 · OVARIAN 4/10 BEHOLD-1 — Mocertatug rezetecan (B7-H4 ADC) · Platinum-resistant — ORR 62% — DoR 12.2 mo; mPFS 11.1 mo. Early-phase, single-arm. WNTB: Activity replicates in Phase 3, independent of FRα status.
LBA40 · OVARIAN 4/10 ZW191-101 — ZW191 (FRα ADC) · Platinum-resistant, non-clear cell — ORR 48% · DCR 96% — Phase 1, heavily pretreated disease, across dose levels. WNTB: Activity holds in Phase 3 at lower FRα than mirvetuximab requires.
LBA26 · BREAST 4/10 UNLOCK 14 (POP-DURVA) — Preoperative durvalumab · Stage I TNBC, TILs ≥ 5% — Downstaging 41.3% — Immune remodeling seen, but monotherapy pCR only 1.4%. WNTB: Short IO remodeling supports later chemo de-escalation safely.
LBA52 · PAN-TUMOR 4/10 iNATURE — PPVax neoantigen vaccine + CLERT · Advanced refractory solid tumors — PFS HR 0.29 — mPFS 10.3 vs 3.1 mo; p = 0.007. WNTB: Focal ablation + vaccines give systemic, abscopal-like control across tumors.
LBA18 · CRC · AI 3/10 BEAGLE-MDT — Multi-agent AI platform · Tumor board workflow — 73–100% concordance — Case summaries vs experts; trial matching 67–93%. WNTB: MDTs adopt LLM recommendations without prospective outcome endpoints.
LBA19 · SUPPORTIVE · AI 3/10 ALLIANCE — LLM-assisted side-effect management · Breast & CRC — 5.4 vs 2.8 toxicities logged — No change in dose modifications or quality of life. WNTB: Better symptom logging alone justifies adoption without linked interventions.
1–2 No shift · Practice-affirming negative — Missed primary endpoint or no survival benefit · 3 LBAs
LBA14 · BREAST 2/10 MA.40/FINER — Fulvestrant + ipatasertib · HR+/HER2– ABC post-CDK4/6i — OS HR 0.97 ITT — PFS benefit (HR 0.61, ASCO 2025) did not carry to OS; AKT-altered OS HR 1.14. Takeaway: No role for ipatasertib; capivasertib and oral SERDs remain preferred.
LBA51 · BREAST 2/10 KEYNOTE-B49 — Pembrolizumab + chemo · HR+/HER2– ABC, CPS ≥ 1 — OS HR 1.04 — PFS HR 0.74, but mOS 21.0 vs 22.2 mo; p = 0.6185. Takeaway: PFS gain without OS can't justify adding PD-1 given available ADCs.
LBA21 · BILIARY 2/10 ACTICCA-1 — Gem-cis vs capecitabine · Resected cholangio/gallbladder — DFS p = 0.097 missed — Primary log-rank not met; RMST shows a modest +2.6 mo DFS. Takeaway: Adjuvant capecitabine remains the standard; the RMST signal is hypothesis-generating.
WNTB = What You Need to Believe for the readout to change practice. Preliminary perspective based on late-breaking abstracts released 24 October 2026; scores will be revisited once full data are presented. Not medical advice. Scoring key on page 1.
ESMO 2026 · Page 2 of 2
OncoDaily @oncodailyPost text
🧬 OrigAMI-4 at ESMO 2026: 77% Response Rate With Amivantamab, Pembrolizumab, and Carboplatin in Head and Neck Cancer
Could combining EGFR-MET bispecific targeting with immunotherapy and chemotherapy improve first-line treatment outcomes in recurrent or metastatic head and neck cancer?
At ESMO Congress 2026, Paul Swiecicki presented results from the phase Ib/II OrigAMI-4 trial, evaluating amivantamab plus pembrolizumab and carboplatin in recurrent or metastatic head and neck squamous cell carcinoma (HNSCC).
🔬 Key Findings:
🔹 HPV-unrelated disease: Confirmed ORR of 77% (17/22), including three complete responses.
🔹 Response durability: 65% of confirmed responses in HPV-unrelated disease remained ongoing at the data cutoff.
🔹 HPV-positive oropharyngeal cancer: ORR of 29% (2/7).
🔹 Safety: The most common adverse events included anemia, hypoalbuminemia, thrombocytopenia, stomatitis, and hypomagnesemia.
🔹 Administration-related reactions: Reported in 13% of patients, with no grade ≥3 events.
Clinical Takeaway: OrigAMI-4 demonstrated encouraging preliminary activity, particularly in HPV-unrelated HNSCC. While the small cohort and short follow-up limit conclusions, these findings have supported the phase III OrigAMI-5 trial comparing this combination with standard first-line treatment.
🔗 Read the full OncoDaily coverage:
https://t.co/SSLFVoTdMB
#ESMO26 #ESMO2026 #OrigAMI4 #OncoDaily
ESMO 2026 Congress
OncoDaily
OrigAMI-4
Amivantamab Plus Pembrolizumab and Carboplatin Shows 77% Response Rate in Head and Neck Cancer
Henlius @HenliusBiotechPost text
New #HLX43 phase 2 data at #ESMO26! 🔬
In advanced G/GEJ adenocarcinoma, our HLX43 achieved 50% cORR, 90% DCR & 5.6-month mPFS at 3.0 mg/kg.
Grade ≥3 drug-related TEAEs: 29% overall, no related deaths.
Another step toward broader antitumor potential!
🔗: https://t.co/beA9vFbVrL https://t.co/9dajAhpMu7
Henlius
ESMO 2026
G/GEJ Adenocarcinoma: Initial Phase II Data
HLX43
Consistent Early Proof-of-Concept Across Multiple Solid Tumors
Pan-tumor Activity Reinforced: New Efficacy and Safety Data in GI Tumors
Promising preliminary efficacy
cORR: 50.0% (3.0 mg/kg)
DCR: 90.0% (3.0 mg/kg)
PFS: 5.6 m (3.0 mg/kg)
Among 10 efficacy-evaluable patients: 1 (10.0%) achieved CR, 4 (40.0%) achieved PR, and 4 (40.0%) had SD
Favorable safety profile
HLX43-related ≥Grade 3 TEAEs: 29.0%
1 patient discontinued treatment due to TEAE
no treatment-related deaths reported
Most common TEAE: hematologic toxicity
Most common ≥Grade 3 TEAE: decreased lymphocyte count (19.4%)
Pulmonary-related adverse events were rare
AESI: 48.4%
most common being decreased neutrophil count (45.2%)
Data cutoff: August 31, 2026
Combining the MoAs of ADC and IO
Pan-tumor Activity Across
NSCLC TSCC Gynecologic Cancers ESCC HNSCC
NPC mCRC G/GEJ adenocarcinoma BC ...
Note: Potential indications under evaluation; POC studies ongoing.
ESMO 2026 | Madrid, Spain
Poster Session: October 25, 12:00–12:45
Lead PI: Professor Lin Shen, Director of the Department of Gastrointestinal Oncology, Peking University Cancer Hospital
ESMO 2026 BREAKTHROUGH
Jose Fernando Moura, PhD @FernandoOncoPost text
Beyond ICI at @myESMO #esmo26
Tcell engagers, TILS, TCR, intratumoral and others https://t.co/RACv5Q732L
[Slide 1]
IMMUNOTHERAPY • BEYOND CHECKPOINTS 1/4
Side effects are not all the same
CAR-T, TCR-T, TILs and T-cell engagers can cause different toxicities.
CRS: fever, hypotension and hypoxia
ICANS: confusion, aphasia and seizures
On-target / off-tumor toxicity may occur.
T CELL (CD3) | T-CELL ENGAGER (e.g., BiTE®, DART®, TRiTAC®) | TUMOR CELL (TARGET ANTIGEN)
Key message: each platform has its own risks and requires specific monitoring.
Session: Toxicities of immunotherapies beyond immune checkpoints
Speaker: Victor Moreno Garcia
Based on ESMO 2026 presentations. @drjosefernandomoura
[Slide 2]
IMMUNOTHERAPY • BEYOND CHECKPOINTS 3/4
Many solid-tumor therapies engage CD3
Different targets, same principle: bring T cells close to tumor cells.
DLL3: tarlatamab, obrixtamig, gocatamig
MUC16: ubamatamab
STEAP1 / KLK2 / PSMA: xalurtamig, pasritamig, JANX007
PRAME / GUCY2C: brenetafusp, PF-07062119
Key message: the same CD3 platform can lead to different toxicity patterns.
Session: Toxicities of immunotherapies beyond immune checkpoints
Speaker: Victor Moreno Garcia
Based on ESMO 2026 presentations. @drjosefernandomoura
[Slide 3]
IMMUNOTHERAPY • BEYOND CHECKPOINTS 2/4
In practice, risk varies by platform
The data highlight 3 key points:
CRS can be frequent — but often low grade
Step-up dosing helps reduce toxicity
Target choice influences where toxicity appears
Example: tebentafusp → CRS ~89% | grade ≥3 ~1%
Key message: monitoring and therapy design matter as much as efficacy.
Session: Toxicities of immunotherapies beyond immune checkpoints
Speaker: Victor Moreno Garcia
Based on ESMO 2026 presentations. @drjosefernandomoura
[Slide 4]
IMMUNOTHERAPY • BEYOND CHECKPOINTS 4/4
CRS can affect multiple organs
Cytokine release syndrome is not just fever.
Systemic: fever, chills, fatigue
Cardiovascular: hypotension, tachycardia
Lungs: hypoxia
CNS: confusion, seizures
GI / liver: nausea, diarrhea, abdominal pain, ↑ transaminases
Muscle / kidney: myalgia, weakness, AKI
Key message: early recognition and supportive care are essential.
Session: Toxicities of immunotherapies beyond immune checkpoints
Speaker: Emanuela Romano
Based on ESMO 2026 presentations. @drjosefernandomoura
MitoAI @Vox_MitoAICLARITY-Gastric01KRASCENDO-1HARMONi-GI1AZUR-1IROCASOPTIMASAFFRONOptiTROP-Lung04DeLLphi-305SigVie-002OptiTROP-Lung06EMT2PE-PEROSETTA Lung-107QoLATI-DAHANCA34
Post text
🔥 #ESMO2026 Day 3/25 Oct: Late-breakers scored 1–10 for SoC impact
🚀 9/10: HARMONi-GI1, CLARITY-Gastric 01
✅ 7–8: Krascendo 1, SAFFRON, OptiTROP-Lung04, LBA44, C-POST, OPTIMA, AZUR-1
⏸️ No shift: SigVie-002, ADMEC-O, RADIAN, IROCAS https://t.co/Htunf2uRPi
[Slide 1]
ESMO 2026 · SUNDAY 25 OCTOBER · LATE-BREAKING ABSTRACTS · PAGE 1 OF 2
HOT OFF THE PRESS
Late-Breaking Abstracts: Perspective
27 readouts scored for their impact on standard of care (1–10)
PRELIMINARY Abstract-level assessment, pending full data presentations. Scores may change.
27 LBAs released today and scored
DISTRIBUTION BY IMPACT TIER: 9–10 Paradigm-shifting 2 | 7–8 Practice-changing 7 | 5–6 Practice-informing 6 | 3–4 Hypothesis-generating 8 | 1–2 No shift / negative 4
LBAs BY TUMOR AREA: Lung 7 | Head & neck 6 | Colorectal 4 | Pan-tumor / other 4 | Skin 3 | Gastric & biliary 2 | Breast 1
9–10 Paradigm-shifting · Practice-defining (Phase 3 OS wins for first-in-class assets · 2 LBAs)
LBA8 · BILIARY TRACT 9/10 HARMONi-GI1: Ivonescimab + GemCis vs durvalumab + GemCis · Phase 3, n = 682. OS HR 0.75 · 14.9 vs 12.1 mo. PD-1 × VEGF-A bispecific beats the durvalumab-chemo standard on OS (p = 0.0031). PFS HR 0.61 (8.4 vs 5.8 mo); ORR 53.8% vs 32.5%. CAVEAT: A 2.8-month median OS gain in a likely mostly Asian population; ivonescimab's global NSCLC trial (HARMONi) did not reach significance on OS. Global replication is the open question. WNTB: The dual PD-1/VEGF-A advantage replicates across non-Asian etiologies.
LBA7 · GASTRIC 9/10 CLARITY-Gastric 01: Sonesitatug vedotin (CLDN18.2 ADC) vs investigator's choice chemo · Phase 3, n = 594. OS HR 0.47 · 10.0 vs 5.0 mo, 3L+. Median OS doubled in 3L+ (p < 0.001). ITT 2L+: OS HR 0.58, 10.6 vs 6.4 mo; PFS 4.2 vs 3.8 mo. CAVEAT: OS doubles while PFS barely moves (4.2 vs 3.8 mo). Post-progression therapy or a weak 3L+ chemo comparator may contribute; the full data need to explain the gap. WNTB: CLDN18.2 expression stays stable and actionable across later lines after fluoropyrimidine/platinum.
7–8 Practice-changing · Regimen-altering (Head-to-head wins, OS confirmation, de-escalation · 7 LBAs)
LBA5 · LUNG 8/10 Krascendo 1: Divarasib vs sotorasib or adagrasib · KRAS G12C NSCLC. PFS HR 0.58 · OS HR 0.56. PFS 9.8 vs 5.7 mo; OS 17.7 vs 12.0 mo (p = 0.0005); ORR 58.4% vs 32.3%. WNTB: Potency and safety edge make divarasib the preferred G12C inhibitor globally.
LBA6 · LUNG 8/10 SAFFRON: Savolitinib + osimertinib vs platinum-pemetrexed · EGFRm, MET-driven, post-osimertinib. PFS HR 0.55 · OS HR 0.68. BICR PFS 7.6 vs 5.4 mo; OS 17.8 vs 12.9 mo (p = 0.010); DoR 9.7 vs 5.7 mo. WNTB: High MET overexpression/amplification marks true bypass dependence after osimertinib.
LBA44 · HEAD & NECK 8/10 Metronomic induction: Paclitaxel-carboplatin + metronomic oral chemo vs TPF · Phase 3, n = 475. OS HR 0.826 non-inferior. 13.31 vs 13.99 mo (NI p = 0.0002); resection 57.3% vs 33.9%; grade >3 toxicity 43.2% vs 86.4%. WNTB: Oral metronomic chemo prevents repopulation without lethal induction toxicity.
LBA67 · LUNG 8/10 OptiTROP-Lung04: Sacituzumab tirumotecan vs chemo · EGFRm NSCLC post-TKI. OS HR 0.69 final. 25.9 vs 17.4 mo (p = 0.0021); crossover-adjusted HR 0.57. PFS met at prior readout. WNTB: A TROP2 ADC overcomes varied post-TKI resistance without a predictive biomarker.
LBA59 · SKIN (CSCC) 7/10 C-POST: Adjuvant cemiplimab vs placebo · Resected, irradiated high-risk CSCC. DFS HR 0.46. 95% CI 0.31–0.67; p < 0.001. OS HR 0.63 (0.36–1.11); benefit in ctDNA+ and ctDNA−. WNTB: A >50% DFS gain justifies a year of adjuvant immunotherapy.
LBA86 · BREAST 7/10 OPTIMA: Prosigna-guided chemo decisions · Economic evaluation of Phase 3, n = 3,425. Chemo omitted in 68%. −£654 direct cost; +0.05 QALY; 100% probability of cost-effectiveness at NHS thresholds. WNTB: Omitting chemo at ROR ≤ 60 in postmenopausal node+ disease doesn't cost 10-year survival.
LBA87 · RECTAL 7/10 AZUR-1: Dostarlimab monotherapy, 9 cycles · Registrational Phase 2, n = 154. 12-mo cCR 68%. cCR12 + pCR 76%; 93% avoided radical surgery under non-operative management. WNTB: Sustained 12-month cCR translates into long-term cure without late pelvic recurrence.
TODAY'S THEMES: Both 9/10s are first-in-class GI wins: a PD-1 × VEGF bispecific and a CLDN18.2 ADC. Lung leads (7 LBAs), with three OS-positive Phase 3s in oncogene-driven NSCLC. Head & neck (6 LBAs) is about de-escalation: gentler induction, RT omission, surgery vs RT.
HOW TO READ THIS · SCORING KEY: 9–10 Paradigm-shifting. Phase 3 OS/EFS wins in major unmet need; new modality or new standard. 7–8 Practice-changing. Phase 3 superiority vs active standards, less-toxic schedules, or OS confirmation. 5–6 Practice-informing. Positive in narrow subsets, secondary endpoints, or PFS without OS. 3–4 Hypothesis-generating. Early-phase, feasibility, or AI tools needing prospective validation. 1–2 No shift. Failed primary endpoint or no survival benefit.
Continued on page 2 → 5–6 Practice-informing · 3–4 Hypothesis-generating · 1–2 No shift
WNTB = What You Need to Believe. Preliminary perspective on abstracts released 25 October 2026. Not medical advice.
[Slide 2]
ESMO 2026 · SUNDAY 25 OCTOBER · LATE-BREAKING ABSTRACTS · PAGE 2 OF 2
HOT OFF THE PRESS
Late-Breaking Abstracts: Perspective
Scores 1-6: practice-informing, hypothesis-generating and no-shift readouts
PRELIMINARY Pending full data
5–6 Practice-informing · Subgroup-specific (PFS/ORR without mature OS, positive secondaries, Phase 2 de-escalation · 6 LBAs)
LBA43 · NASOPHARYNX 6/10 TAISHAN-301: Tambotatug pelitecan (B7-H3 ADC) vs chemo · Refractory NPC, n = 431. ORR 50.8% vs 25.8%. OR 2.9; p < 0.0001; DoR 7.9 vs 6.4 mo. OS immature (5.2 mo follow-up). WNTB: The response-rate gain converts into a significant OS benefit.
LBA66 · LUNG 6/10 OptiTROP-Lung06: Sac-TMT + pembrolizumab vs chemo + pembrolizumab · Phase 3, n = 455. PFS HR 0.49. BICR 15.0 vs 5.7 mo; p < 0.0001; DoR 13.6 vs 6.8 mo. Immature OS HR 0.58 (0.38–0.88). WNTB: The large PFS gain and early OS signal convert to definitive OS superiority.
LBA30 · COLORECTAL 5/10 EMT2: Adjuvant EPA 4 g/day vs placebo · Resected colorectal liver metastases. 5-yr OS 62.0% vs 45.1%. Secondary OS HR 0.68 (p = 0.030). Primary PFS negative: 13.5 vs 12.9 mo, HR 0.89 (p = 0.33). WNTB: EPA has a systemic survival effect independent of radiographic PFS.
LBA45 · HEAD & NECK 5/10 QoLATI / DAHANCA34: Primary TORS + neck dissection vs definitive IMRT · Phase 2, n = 136. MDADI +5.1 pts p = 0.04. Swallowing QoL favored TORS but missed the clinical-relevance margin; equal locoregional control; 10% motor nerve injury. WNTB: Modest swallowing gains outweigh surgical morbidity and adjuvant-RT redirection.
LBA47 · HEAD & NECK 5/10 OPTIMAL: Neoadjuvant tislelizumab + chemo vs upfront surgery · Phase 2, n = 116. pCR 45.5% · MPR 65.5%. 2-yr EFS criteria met; ORR 81.0%. RT omitted in major responders: 2 EFS events vs 19 in standard arm. WNTB: Major pathological response reliably identifies tumors safe for RT omission.
LBA88 · OLIGOMETASTATIC 5/10 PE-PE: Perioperative pembrolizumab + MDT vs MDT alone · Phase 2, n = 85. RFS HR 0.47. 25.4 vs 11.0 mo; 95% CI 0.24–0.92; p = 0.024. OS immature; grade 3 AEs 7% vs 3%. WNTB: Intercepting oligometastatic recurrence with IO beats deferred therapy long term.
3–4 Hypothesis-generating · Early validation (Early-phase signals, feasibility and liquid-biopsy platforms · 8 LBAs)
LBA35 · LUNG SCREENING 4/10 LUCAS & MICA: cfDNA fragmentomics + serum proteomics classifier. AUC 0.91. 95% CI 0.86–0.96; discovery n = 718, validated in MICA n = 400. WNTB: It cuts false positives in CT screening.
LBA42 · HEAD & NECK 4/10 HexAgon-HN: Ordastobart (OX40) + pembro vs pembro · Phase 2, n = 68. ORR 48.3% vs 26.5%. HPV+ ORR 80.0% vs 33.3%; grade ≥3 AEs 58.1% vs 47.1%. WNTB: OX40 costimulation overcomes PD-(L)1 resistance in HPV+ disease.
LBA61 · SKIN (EMPD) 4/10 Formula-10: Disitamab vedotin · HER2+ extramammary Paget, n = 27. ORR 88.0%. DCR 100%; mPFS 14.23 mo; DoR 10.90 mo; grade ≥3 TRAEs 29.6%. WNTB: Single-arm responses justify targeted therapy over empiric chemo.
LBA94 · NSCLC & CRC 4/10 TRACERx: Error-corrected plasma WGS for MRD · n = 73 NSCLC, 50 CRC. ctDNA to 2.1 ppm. NSCLC landmark MRD+ predicted RFS (HR 9.81) and OS (HR 5.04). WNTB: Detection comes early enough to guide curative intervention.
LBA33 · PAN-TUMOR 3/10 GFH276: Oral pan-RAS(ON) inhibitor · Phase 1, n = 98. ORR 36%. 29/80; pancreatic 38%, NSCLC 38%; G12A/D/R/V and Q61H; grade 3 TRAEs 27.5%. WNTB: Responses last without dose-limiting wild-type toxicity.
LBA34 · COLORECTAL 3/10 MRG007-001: MRG007 (CDH17 exatecan ADC) · Phase 1. ORR 44.8% at RP2D. 13/29; DCR 93.1%; RAS-mut 42.1%, RAS-wt 50.0%; no ILD reported. WNTB: CDH17 is restricted enough to allow repeated payload delivery.
LBA76 · LUNG 3/10 ROSETTA Lung-107: Pumitamig (PD-L1 × VEGF-A) + docetaxel · Post chemo-IO, n = 50. ORR 36.7%. 11/30 evaluable; DCR 90.0%; mPFS 6.9 mo; grade ≥3 related TRAEs 18.0%. WNTB: Dual blockade restores taxane sensitivity after chemo-IO.
LBA93 · SUPPORTIVE 3/10 FORX: 30-plant weekly diet during checkpoint therapy · Phase 1, n = 54. Fiber +8.5 g/day. Feasibility met (p < 0.001); grade ≥3 irAEs in 3.7%. WNTB: Microbiome diversity causally reduces immune toxicity.
1–2 No shift · Practice-affirming negative (Missed primary endpoint; current standards hold · 4 LBAs)
LBA46 · HEAD & NECK 2/10 RADIAN: Niraparib + dostarlimab + RT · Phase 1b/2, n = 34. 1y DFS 61% vs 55% hist. Cisplatin-unfit cohort missed (p = 0.19); 100% grade >3 TRAEs, 2 toxic deaths. Cohort A 1y DFS 88.2%. Takeaway: PARP + PD-1 radiosensitization is too toxic in frail patients.
LBA60 · SKIN (MCC) 2/10 ADMEC-O: Adjuvant nivolumab vs observation · Resected Merkel cell, n = 179. DFS HR 0.70 NS. 95% CI 0.38–1.26; mature OS HR 0.98 (0.43–2.27). TLS a possible predictive marker. Takeaway: No survival gain from unselected adjuvant anti-PD-1.
LBA68 · LUNG 2/10 SigVie-002: Sigvotatug vedotin vs docetaxel · Pretreated NSCLC, n = 762. OS HR 0.929 p = 0.226. 11.9 vs 11.5 mo; 2L subgroup HR 0.831; grade ≥3 TRAEs 33% vs 36%. Takeaway: Docetaxel holds; the 2L signal is likely confounding.
LBA29 · COLON 1/10 IROCAS: Adjuvant mFOLFIRINOX vs mFOLFOX6 · Stage III colon, n = 792. 3-yr DFS HR 1.07. 65.6% vs 66.3% (p = 0.61); 3-yr OS HR 0.85 (p = 0.37); grade ≥3 diarrhea 15.6% vs 3.8%. Takeaway: Oxaliplatin doublets remain the adjuvant standard.
WNTB = What You Need to Believe for the readout to change practice. Preliminary perspective based on late-breaking abstracts released 25 October 2026; scores will be revisited once full data are presented. Not medical advice. Scoring key on page 1.
ESMO 2026 · Page 2 of 2
OncoDaily @oncodailyPost text
🧬 SMART-KEY at ESMO 2026: 65.1% Laryngectomy-Free Survival With Pembrolizumab-Based Treatment in Advanced Laryngeal Cancer
Can immunotherapy help preserve the larynx while reducing the need for cisplatin-based chemoradiotherapy?
At ESMO Congress 2026, Thiago B. Oliveira presented results from the phase II SMART-KEY (LACOG 0720) trial, evaluating a pembrolizumab-based, cisplatin-free organ preservation strategy in patients with locally advanced laryngeal cancer.
🔬 Key Findings:
🔹 2-year laryngectomy-free survival: 65.1%.
🔹 Larynx preservation: 86% at two years.
🔹 Laryngeal dysfunction-free survival: 83.7%.
🔹 Overall survival: 74.4% at two years.
🔹 Disease recurrence: Locoregional recurrence occurred in 18.8% and distant recurrence in 7.4% at two years.
🔹 Safety: Grade ≥3 treatment-related adverse events occurred in 41.9% of patients, including one treatment-related death.
Clinical Takeaway: SMART-KEY demonstrated encouraging organ preservation and survival outcomes without concurrent cisplatin-based chemotherapy.
However, its single-arm design and historical comparisons mean further randomized studies are needed to establish whether this approach can safely replace standard chemoradiotherapy.
🔗 Read the full OncoDaily coverage:
https://t.co/DiHlRz1nZv
#ESMO26 #ESMO2026 #SMARTKEY #OncoDaily
ESMO 2026
Congress
OncoDaily
SMART-KEY
Pembrolizumab-Based Strategy Achieves 65.1% Laryngectomy-Free Survival in Advanced Laryngeal Cancer
Jose Fernando Moura, PhD @FernandoOncoPost text
Cancer care goes beyond medications. Our patients need more than treatments. They need compassion, connection, and care for the whole person. Science is reminding us why.
Because treating cancer matters. But caring for the person matters just as much. #ESMO2026 @myESMO https://t.co/7kfbMEf0SO
BREAKING NEWS
Spiritual Interventions in Cancer Care [Systematic Review]
Effects on biological and physiological markers in cancer patients
@FernandoOnco
ONCOLOGIA BASEADA EM EVIDÊNCIAS PARA UMA PRÁTICA MELHOR
82 studies included
Adults with cancer
Prayer, meditation, mindfulness
6760 records identified
Methods
JBI methodology, PRISMA and PICO framework
Databases: PubMed, MEDLINE, CINAHL, Scopus, Web of Science, Cochrane Library, SciELO
Search through January 2026
Outcomes assessed
Cortisol, cytokines, CRP
Immune cell counts
Cardiovascular measures
RESULTS Spiritual interventions were associated with favorable changes in multiple biological and physiological markers in patients with cancer.
Stress response [down arrow] Reduced cortisol levels
Inflammation [down arrow] Decreased pro-inflammatory cytokines: IL-1β, IL-6, IL-8, TNF-α
Immune function [up arrow] Enhanced NK cell activity and interferon-γ production
Autonomic regulation [up arrow] Higher heart rate variability and lower resting heart rate
Other signals Possible inhibition of inflammatory pathways (e.g., NF-κB), effects on oxidative stress and markers of cellular aging
KEY TAKEAWAY
Spiritual interventions were associated with favorable changes in multiple biomarkers and physiologic indicators, suggesting potential benefits through stress modulation, immune regulation, and attenuation of inflammatory responses.
CONCLUSIONS
• Evidence supports beneficial biologic and physiologic effects.
• Findings are promising for integrative oncology care.
• Most evidence was synthesized narratively.
Clinical question
Should spiritual care be more intentionally integrated into comprehensive cancer care?
What's your take?
@FernandoOnco | Discussing today. Improving tomorrow. #IntegrativeOncology #CancerCare #SpiritualCare
Dr. Robert F. Siegmund, MBA @robertfsiegmundPost text
.@myESMO conference has started today in Madrid.
#ESMO2026 Top Companies
Source: @Larvol CLIN database
#cancer #oncology #data https://t.co/iCT9kWfiuj
Top Companies by X Posts
Merck (MSD)
AstraZeneca
Novartis
BMS
Sichuan Biokin Pharma
Amgen
Roche
Pfizer
Sichuan Kelun Pharma
Sino Biopharm
X Posts (x-axis 0–350) [stacked sentiment bars; company logos]
CancerTherapyAdvisor @CancerTherAdvsrPost text
Phase 1b/2 RADIAN study data, presented by Marc Oliva, MD, PhD, from @ICO_oncologia, evaluated niraparib + dostarlimab combined with CRT/RT in locally advanced HNSCC.
Presented this weekend at @myESMO Congress 2026 #ESMO26
See the data here!
🔗 https://t.co/huC4w9bbA8 https://t.co/qxgymxeh82
ESMO Oct 23-27
Dostarlimab + niraparib showed promising efficacy in patients both fit and unfit for cisplatin with high disease burden, but with substantial treatment-related toxicity in the maintenance phase, resulting in treatment discontinuation according to the RADIAN study.
Cancer Therapy ADVISOR
FAQ
About this page
What is on the ESMO 2026 Heme & Other slides page?
The 214 Heme & Other slide photos, abstract screenshots and data graphics plus 54 KOL-made infographics that oncologists, societies, media and companies posted on X from the ESMO 2026 embargo lift (October 22) through the congress in Madrid (October 23–27), compiled by KOL Pulse. Each card links to the original post and keeps the author's full text. It is one tumor-type page of the ESMO 2026 slide library: https://kolpulse.com/kol-pulse-esmo26-slides
Which Heme & Other trials are covered?
Trials with their own slide groups, by number of slide posts: MOIO (14), ARTEMIS-011 (12), IMA203CD8 (PRAME TCR-T) (3), TANGENT (1), QoLATI-DAHANCA34 (1). Slides that compare several trials sit in a Cross-trial group, and slides not tied to a tracked trial come last. Physician posts come first in every group.
How do I filter by trial or KOL?
Use the trial chips in each section, the Trial menu (which also finds cross-trial slides that name that trial) and the KOL menu or the Built by avatars. Filters combine; counts only offer combinations that have results, and Clear filters or the Escape key resets. Every state has a shareable link, for example #tag=moio.
What are the OCR text and the source notes?
View OCR Text opens a verbatim transcription of the slide image; survival curves are captured as the printed numbers only, never read off the curve. Where it helps, a short context note gives the figures printed on the presented slide or abstract (for example, a different data cut or analysis). The author's caption is never edited.
Where are the other tumor types and the pre-congress archive?
Breast Cancer: https://kolpulse.com/kol-pulse-esmo26-slides-breast; Lung Cancer: https://kolpulse.com/kol-pulse-esmo26-slides-lung; GU Cancer: https://kolpulse.com/kol-pulse-esmo26-slides-gu; GI Cancer: https://kolpulse.com/kol-pulse-esmo26-slides-gi; Melanoma: https://kolpulse.com/kol-pulse-esmo26-slides-melanoma; Gyn Cancer: https://kolpulse.com/kol-pulse-esmo26-slides-gyn. Pre-congress previews, watchlists and top-10 lists: https://kolpulse.com/kol-pulse-esmo26-slides-archive
Can I use this page with my own AI assistant (NotebookLM, Perplexity, Claude, ChatGPT)?
Yes. Paste the page URL, or a filtered link, into your assistant and ask questions against it. Example prompt: "From the slide transcriptions on this page, list each trial's primary endpoint result with the hazard ratio and data cut exactly as printed on the slide, and the physician who posted it."