In resected stage III BRAF V600-mutated melanoma, patients are eligible for adjuvant targeted therapy or immune checkpoint inhibitors (ICIs), but no comparative data guide this choice. Understanding factors shaping patient preferences is essential for shared decision-making. To identify factors associated with patient choice between adjuvant ICI or targeted therapy in resected stage III BRAF V600-mutated cutaneous melanoma. This multicenter, prospective, questionnaire-based, cross-sectional study was conducted from November 2024 to July 2025 across oncology centers in France concerning adults with completely resected AJCC8 stage III BRAF V600-mutant melanoma. Patients received standardized information from their oncologist regarding two adjuvant options - anti-PD1 immunotherapy (nivolumab or pembrolizumab) and targeted therapy (dabrafenib plus trametinib) - before making their treatment choice. The primary outcome was treatment selection (ICI vs. targeted therapy). Secondary outcomes consisted of describing determinants of patient decision-making using a structured questionnaire. Among 45 participants, 25 chose ICI and 20 selected targeted therapy. Questionnaire analysis showed that younger, professionally active patients with dependent children were more likely to prefer targeted therapy, valuing autonomy in treatment administration and reduced hospital visits. In contrast, older or nonworking patients more often favored ICI, citing reassurance from regular medical follow-up and the ability to delegate treatment management. Age and employment status were significantly associated with therapeutic choice. Identifying drivers of treatment preference may support more personalized adjuvant strategies. The finding that targeted therapy is favored by younger patients reinforces the relevance of sentinel lymph node biopsy in BRAF-mutated melanoma, despite expanding indications for immunotherapy in earlier stages.

INTRODUCTION:The updated edition of the French intergroup guidelines for the management of patients with gastric and gastroesophageal junction adenocarcinoma is a collaborative work of several national medical societies, and available on the website of the French Society of Gastroenterology (SNFGE) (www.tncd.org). METHODS:The recommendations are graded into three categories (A, B, and C), based on the level of scientific evidence published until January 2026. RESULTS:Initial staging and risk assessment should include physical evaluation, endoscopy and computed tomography-scan of the thorax, abdomen, and pelvis. For resectable disease, endoscopic ultrasonography can be used for T and N staging, while laparoscopic exploration may be performed to exclude occult peritoneal metastases, especially for cT3/cT4 and poorly cohesive tumors. Endoscopic or surgical resection alone is appropriate for very early cT1N0 tumors. For locally advanced disease ≥cT2 and/or cN + , the perioperative FLOT chemotherapy is recommended as the standard of care. Recently, the addition of durvalumab to perioperative FLOT followed by durvalumab for 10 months as maintenance therapy was associated with a significant improvement of survival. For metastatic disease, the first-line chemotherapy is based on platinum-fluoropyrimidine combination. The addition of targeted therapy and/or immunotherapy to doublet chemotherapy depends on the tumor biomarker profile, including HER2 (trastuzumab), claudin18.2 (zolbetuximab), PD-L1 and dMMR/MSI phenotype (anti-PD1 monoclonal antibodies). The addition of docetaxel, based on the triplet TFOX regimen may be considered for selected patients with biomarker-negative tumors. Resection of primary tumor and metastases cannot be recommended but may be considered on an individual basis in highly selected patients with oligometastatic disease who respond to systemic treatment. Various drugs are indicated beyond first-line of treatment, including trastuzumab-deruxtecan for HER2-positive tumors. CONCLUSION:These national guidelines on gastric cancer are intended to facilitate decision-making in daily clinical practice. These recommendations are subject to ongoing review. Each individual case should be discussed within a multidisciplinary team.

Background Doublet chemotherapy plus anti-epidermal growth factor receptor (EGFR) is a standard of care in left-sided, microsatellite stable RAS and BRAF wild-type metastatic colorectal cancer. Guidelines recommend treatment de-escalation after achieving disease control with induction. Maintenance and intermittent strategies were investigated but not directly compared.Methods We performed an individual patient data pooled analysis of 3 randomized phase II trials (PanaMa, Valentino, PRODIGE-28 TIME) focused on toxicity analysis. Only patients with left-sided, nonmicrosatellite instability high RAS and BRAF V600E wild type who started protocol-planned postinduction were included and stratified into 3 treatment groups: 5-fluorouracil and leucovorin plus anti-EGFR maintenance, anti-EGFR alone, or intermittent. Longitudinal toxicity data were collected and analyzed according to literature-based approach (toxicity over time), incorporating dimension of time into adverse event assessment and analyzing individual and groups of adverse events comparing treatment groups.Results Overall, 327 patients were included: 166, 109, and 52 patients received anti-EGFR plus 5-fluorouracil and leucovorin maintenance, anti-EGFR alone, and intermittent strategy, respectively. Mean adverse event grades for chemotherapy-related toxicity showed different longitudinal patterns. Mean grades in intermittent strategy were lower in early cycles and increased later, and higher values were reported for combination maintenance. Considering anti-EGFR-related skin toxicity, the mean adverse event grade was constantly lower for intermittent strategy compared with maintenance groups. Overall, grades 3 and 4 adverse events were more represented in maintenance groups vs intermittent strategy, although the predominant grade was 1 across cycles for all groups.Conclusions In our individual patient data analysis, indirectly comparing 3 clinical trials, intermittent strategy showed lower anti-EGFR skin-related toxicity vs maintenance. Shared decision making, considering patient and tumor features and treatment tolerability, may allow defining optimal de-intensification strategy.+*+9

BACKGROUND AND AIMS:Pretherapeutic evaluation of ampullary carcinomas (ACs) is important to choose the optimal therapeutic strategy. We aimed to assess the ability of EUS and CT to predict the pathologic tumor node metastasis stage of resected AC. METHODS:We analyzed data collected in the Fédération Française de Cancérologie Digestive AC cohort, a French multicentric prospective cohort of patients with resected AC. Our main outcome was the diagnostic performance of EUS to predict pathologic tumor (pT) and pathologic node (pN) and CT to predict pN. RESULTS:Among the 389 patients included in the cohort, data for ultrasound tumor staging, ultrasound node staging, and CT node staging, along with pathology results, were available for 143, 160, and 185 patients, respectively. For pT1 prediction, values for sensitivity (Se), specificity (Sp), positive predictive value (PPV), and negative predictive value (NPV) were 68%, 87%, 53%, and 93%, respectively, for EUS, with an accuracy of 84%. For pT2 prediction, values were 58%, 75%, 56%, and 75%, respectively, with an accuracy of 68%. For pT3-T4 prediction, values were 62%, 79%, 71%, and 71%, respectively, with an accuracy of 71%. For pN0 prediction, values for Se, Sp, PPV, NPV, and accuracy were 88%, 38%, 60%, 75%, and 64%, respectively, for EUS, and 94%, 39%, 63%, 85%, and 68%, respectively, for CT. CONCLUSIONS:Although the overall performance of both modalities was low, we found that both EUS and CT had good NPV for the prediction of pN0, and EUS had a good NPV for predicting pT1.

BACKGROUND:Early-onset pancreatic adenocarcinoma (EOPA), defined as the diagnosis of pancreatic adenocarcinoma before the age of 50, is increasingly reported and may differ molecularly from average-onset pancreatic adenocarcinoma (AOPA). Understanding these differences is essential for precision medicine in this poor-prognosis malignancy. METHODS:A systematic review and meta-analysis were conducted following PRISMA guidelines. Studies published between 2015 and 2025 reporting molecular data on EOPA and/or AOPA were identified. Comparative studies stratified by age group for molecular alterations were included in the meta-analysis. Quality assessment was performed using the JBI checklist. This study aimed at systematically review and meta-analyse existing data comparing the molecular landscape of EOPA and AOPA, and evaluate whether EOPA constitutes a distinct molecular subgroup of pancreatic adenocarcinoma. RESULTS:Thirty-nine articles were included in the systematic review, of which eight met criteria for meta-analysis. KRAS mutations were significantly less frequent in EOPA than in AOPA (OR = 0.61; 95%CI [0.43-0.86], p = 0.005). No significant differences were observed for TP53, CDKN2A, SMAD4, or BRCA1/2 alterations. Sensitivity analyses confirmed the robustness of the KRAS finding. Study heterogeneity was moderate (I2 = 40%). Quality assessment revealed substantial variability in design, molecular methods, and reporting standards. CONCLUSIONS:EOPA is enriched in KRAS wild-type tumours. This profile may offer alternative therapeutic opportunities, including RNA-based fusion detection, inclusion in targeted therapy trials, and suggest alternative oncogenic pathways for a proportion of this subpopulation. Standardised definitions, consistent molecular reporting, and exploration of age-specific risk factors are critical to improve understanding and management of EOPA.

Anorexia, malnutrition, and cachexia are common in patients with cancer, yet evidence-based pharmacological guidance remains limited. Olanzapine is an antipsychotic that can increase appetite and cause weight gain. This systematic review evaluated the effects of olanzapine on appetite and body weight in patients with cancer. This systematic review included randomized controlled trials (RCTs) and observational studies assessing the effects of olanzapine on appetite and/or body weight in patients with cancer. The search strategy was conducted in Medline (PubMed), Embase, and the Cochrane Library. Risk of bias was assessed using Cochrane RoB2 for RCTs and the ROBINS-I for observational studies. Of 1,733 records identified, 79 reports underwent full-text review. Fourteen RCTs, one prospective observational study, and three retrospective studies met the inclusion criteria. Most studies were not designed primarily to evaluate olanzapine as an orexigenic intervention; instead, olanzapine was typically studied for other indications (e.g. chemotherapy-induced nausea and vomiting control), with appetite and/or weight reported as secondary outcomes. Weight gain with olanzapine was reported in two RCTs using 2.5-5 mg/day for 8–12 weeks in adults. Increased appetite was reported in 10 of 14 studies in which olanzapine (2.5–10 mg/day) was administered for 3 days to 12 weeks. However, only three studies prospectively assessed appetite as a primary outcome, and only two prespecified body weight change as an endpoint, indicating that most evidence derives from secondary analyses. Most RCTs raised some concerns or were at high risk of bias, and observational studies generally had serious or critical risk of bias for outcomes of interest. Only 2 RCTs were judged to be at low risk of bias, underscoring substantial methodological limitations and heterogeneity in populations, indications, dosing regimens, and outcome definitions. Available evidence suggests that olanzapine may have orexigenic effects in patients with cancer, with increased appetite reported in several studies and body weight gain observed with long-term use. These findings should be interpreted cautiously given the heterogeneity in study designs and the generally limited methodological quality of the evidence. Further research is needed to confirm these effects and to define the optimal dose and treatment duration for improving appetite and body weight in patients with cancer.

PURPOSE:We investigated whether circulating tumor DNA (ctDNA) changes may be useful to assess clinical outcomes in patients with metastatic colorectal cancer (mCRC) randomized in the TIME-PRODIGE-28 trial comparing biweekly maintenance with cetuximab alone with observation after 4-month fluorouracil, folinic acid, and irinotecan (FOLFIRI) plus cetuximab induction chemotherapy. EXPERIMENTAL DESIGN:ctDNA samples were collected at four time points from baseline until disease progression during the first chemotherapy-free interval and analyzed using next-generation sequencing and methylation marker approaches. Progression-free survival (PFS) and overall survival (OS) from randomization were analyzed according to ctDNA kinetics and EGFR-MAPK pathway alterations. RESULTS:Among 139 randomized patients, 104 (74.8%) had paired samples available. Patients with negative baseline ctDNA remaining negative after 4-month induction chemotherapy had significantly longer PFS from randomization (9.6 months) as compared with patients with a ctDNA decrease of ≥80% (3.4 months) or a ctDNA decrease of <80% (2.1 months; P = 0.013). Patients with EGFR-MAPK pathway alterations identified either in tissue or baseline ctDNA had worse PFS and OS from randomization. Acquired alterations found in 17 of 63 (26.9%) patients at disease progression during the first chemotherapy-free interval were associated with worse OS from reintroduction of the full induction chemotherapy (14.9 vs. 19.4 months; P = 0.025). CONCLUSIONS:Our findings show the prognostic impact of both ctDNA kinetics and EGFR-MAPK pathway alteration dynamics following induction chemotherapy with FOLFIRI-cetuximab in patients with mCRC. Prospective studies evaluating ctDNA-guided treatment strategies are needed to validate the clinical utility of ctDNA monitoring to improve patient selection for first-line treatment de-escalation and anti-EGFR-based maintenance regimens, including treatment adaptation over time.

PURPOSE:Perioperative chemotherapy with FLOT is a standard of care for patients with resectable gastric or gastroesophageal junction (GEJ) adenocarcinoma. This trial evaluated the anti-PD-1 monoclonal antibody spartalizumab combined with FLOT as perioperative treatment for resectable patients. PATIENTS AND METHODS:GASPAR is a multicenter, single-arm, Simon two-stage phase 2 trial. Patients with untreated localized gastric or GEJ adenocarcinoma considered resectable (≥ cT2 or cN+) received 4 pre- and post-operative cycles of FLOT and 2 pre- and post-operative cycles of spartalizumab. The main endpoint was the rate of pathological complete regression (pCR) according to the Becker criteria, requiring 67 patients (H0/H1 =10/23 %, α=5 %, β=20 %). RESULTS:Overall, 68 patients were included: men (78 %), median age 63 years [range 31-79], cT3 51 %, GEJ 60 %, cN+ 58 %. Treatment was started in 67 patients. Delayed FLOT administration for toxicity and dose reduction concerned 14 (21 %) and 28 (42 %) patients, respectively. Surgery was R0 in 62 (95 %) of the patients operated on. Among 64 patients assessable for efficacy, pCR was observed in 20 patients (31 %), and major pathological response in 12 patients (19 %), meaning a major response rate of 50 %. Five patients developed grade 3 immune-mediated adverse events. One death related to pneumocystis occurred. Severe post-surgery complications occurred in 15 patients (23 %). After a median follow-up of 30 months [range 4-42], OS and DFS at 2 years were 86 % [77.8-94.9] and 77.5 % [68.1-88.2], respectively. CONCLUSIONS:Spartalizumab combined with FLOT shows high efficacy as perioperative treatment in patients with resectable gastric cancer, and an acceptable safety profile. TRIAL REGISTRATION:ClinicalTrials.gov Identifier: NCT04736485.

Prognostic performance of mitotic index, DL score, and MJ risk models in cohorts C1 to C3.

Kaplan-Meier curves for recurrence-free survival (RFS) and overall survival (OS) in the subgroup of C2 and C3 patients with high risk score according to pathological Miettienen-Joensuu scoring system and Imatinib sensitive mutations depending on the deep Miettinen-Joensuu models. Kaplan-Meier curves for RFS (A) and OS (B) depending on the deep Miettinen-Joensuu model employing the C2 DL Score in this subgroup of the C2 subcohort. Kaplan-Meier curves for RFS (C) and OS (D) depending on the deep Miettinen-Joensuu model employing the C3 DL Score in this subgroup of the C3 subcohort. *: p < 0.05; ***: p < 0.001. Tests are log-rank tests.

To evaluate the clinical applicability of previously established transcriptomic signatures (molecular subtypes, components and GemPred status) in metastatic pancreatic cancer, we conducted a retrospective pooled analysis of 178 patients from three phase 2 trials (PRODIGE35/37, AFUGEM; 2013-2016) testing first-line regimens (FOLFIRINOX, GemNab, FuNab, FOLFIRI3). RNA sequencing was performed on primary/metastatic tumors across French centers, with blinded assessment of subtypes (immune classical, pure basal-like, stroma-activated), quantitative components, and GemPred status. Primary endpoint: progression-free survival (PFS). Immune classical subtype showed superior median PFS (9.03 months) and OS (11.27 months) versus basal-like and stroma-activated subtypes (PFS: p = 0.015; OS: p = 0.010). Higher classical component correlated with improved OS (HR = 0.737, p = 0.005) but not PFS (HR = 0.90, p = 0.339). Inactive stroma predicted better PFS (HR = 0.66, p = 0.003) and OS (HR = 0.697, p = 0.013). GemPred-negative patients treated with FOLFIRINOX versus GemNab had higher ORR (46.9% vs. 19.1%, p = 0.046), longer PFS (8.2 vs. 2.3 months; HR = 2.28, p = 0.008), and OS (11.6 vs. 5.0 months; HR = 2.04, p = 0.021). No differences occurred in GemPred-positive patients. In a formal treatment-by-GemPred interaction analysis (FOLFIRINOX vs. GemNab), the interaction was significant for OS (adjusted p-interaction = 0.050) but not for PFS (adjusted p-interaction = 0.51). Transcriptomic signatures retain prognostic and predictive utility in metastatic pancreatic cancer, with GemPred representing a hypothesis-generating predictive signal for OS (e.g., a FOLFIRINOX OS benefit in GemPred-negative). Prospective validation is warranted for clinical implementation.

Background:Gastrointestinal stromal tumor (GIST) is the most common gastrointestinal mesenchymal tumor, driven by tyrosine-protein kinase KIT and platelet-derived growth factor receptor A (PDGFRA) mutations. Specific variants, such as KIT exon 11 deletions, carry prognostic and therapeutic implications, whereas wild-type (WT) variants derive limited benefit from tyrosine kinase inhibitors (TKIs). Given the limited reproducibility of established clinicopathological risk models, deep learning (DL) applied to whole-slide images (WSIs) emerged as a promising tool for molecular classification and prognostic assessment. Patients and methods:We analyzed 8398 GIST cases from 21 centers in 7 countries, including 7238 with molecular data and 2638 with clinical follow-up. DL models were trained on WSIs to predict mutations, treatment sensitivity, and recurrence-free survival (RFS). Results:DL predicted mutational status in GIST from WSIs, with area under the curve (AUC) of 0.87 for KIT, 0.96 for PDGFRA. High performance was observed for subtypes, including KIT exon 11 del-inss 557-558 (0.67) and PDGFRA exon 18 D842V (0.93). For therapeutic categories, performance reached 0.84 for avapritinib sensitivity, 0.81 for imatinib sensitivity. DL models predicted RFS, with hazard-ratios (HR) of 8.44 (95%CI 6.14-11.61) in the overall cohort and 4.74 (95%CI 3.34-6.74) in patients receiving adjuvant therapy. Prognostic performance was comparable to pathology-based scores, with highest discrimination in the overall cohort and in patients without adjuvant therapy (9.44, 95%CI (5.87-15.20)). Conclusion:DL applied to WSIs enables prediction of molecular alterations, treatment sensitivity, and RFS in GIST, performing comparably to established risk scores across international cohorts, providing a baseline for future multimodal predictors.

DL predicts treatment sensitivity and supports clinical decision-making in GIST. A, Standard clinical workflow from initial diagnosis to treatment selection in patients with GIST. B, Proposed integration of the DL model into the diagnostic–therapeutic pathway, enabling early triage of patients for further molecular analysis or tailored treatment selection. C, AUC with 95% CI for DL-based prediction of treatment sensitivity, reported for the internal validation cohort (pink), external validation cohort (green), and an external biopsy-only validation cohort (light green). D, Confusion matrices for avapritinib and imatinib sensitivity, shown at the optimal threshold by Youden’s index (green) and at the threshold yielding the highest F1 score (pink).

e16441 Background: Pancreatic ductal adenocarcinoma is one of the most lethal malignancies with a 5-year survival rate under 5%. Locally advanced pancreatic ductal adenocarcinoma (LAP) represents 30-40% of cases at the diagnosis, with an overall survival around 15 months. Optimizing chemotherapy in LAP is still a huge challenge. A concomitant inhibition of epithelial mesenchymal transition (EMT) process may potentiate chemotherapy efficacy and decrease the development of resistances. Netrin-1 is upregulated in many metastatic cancers including 60% of pancreatic cancer and promotes tumor invasiveness and metastases development through EMT induction. NP137, a first-in-class anti-Netrin-1 monoclonal antibody, has shown in phase I study the ability to inhibit EMT, potentially overcoming resistance (Cassier et al., Nature, 2023). The goal of LAP-NET1 (NCT05546853) is to evaluate the safety and efficacy of the combination of modified FOLFIRINOX with anti-Netrin-1 targeting (NP137). Methods: LAP-NET1 is a phase 1b multicentric trial studying the combination of modified FOLFIRINOX with NP-137 every 2 weeks for 12 cycles in patients naive of systemic treatment with LAP according to National Comprehensive Cancer Network criteria. A safety lead-in phase will initially enroll 3-12 patients to confirm the recommended dose of NP137 (14 or 9 mg/kg) according to a 3+3 de-escalation protocol, followed by an expansion phase of 40 patients. The primary endpoint is the proportion of patients experiencing adverse events (AEs) of any grade and grade 3/4 AEs (CTCAE v 5.0) related to the experimental treatment at 6 months. Secondary endpoints are best overall objective response according to RECIST 1.1, 12-month progression-free survival (PFS-12m), 12-month overall survival (OS-12m), surgical resection rate, quality of life (EORTC QLQ-C30), time to deterioration and ancillary outcomes based on spatial transcriptomic and classic bulk RNA sequencing. Clinical trial information: NCT05546853 .

Cell-free DNA (cfDNA) analysis is an emerging tool for diagnosis, prognosis, and monitoring in cancer. This ancillary study of the REGIRI-PRODIGE 58 trial (NCT03722108) evaluated cfDNA dynamics in patients with metastatic gastroesophageal adenocarcinoma (mGA) treated with regorafenib plus irinotecan. Plasma samples from 34 patients in the experimental arm were analyzed (239 samples at baseline, post-treatment initiation [days 2, 8, 15 of Cycle 1; days 1, 8, 15 of Cycle 2]). cfDNA was extracted, quantified by fluorimetry, and characterized by fragment analysis. Baseline concentrations were dichotomized into "low" and "high" subgroups using a 2.07 ng/µL threshold. Changes from baseline to the final timepoint defined four dynamic subgroups (low-low, low-high, high-low, high-high). At baseline, 27 patients (79.4%) had low cfDNA concentrations and 7 (20.5%) high ctDNA. Progression-free survival (PFS) was longer in the low group (median 4.51 months) versus the high group (median 1.60 months; p = 0.0084). Longitudinally, the low-low subgroup had longer PFS than the high-high subgroup (3.61 vs 1.45 months; p = 0.0004). Baseline and dynamic cfDNA concentrations were significantly associated with PFS in patients with mGA treated with regorafenib plus irinotecan, supporting cfDNA as a potential prognostic biomarker for validation in larger cohorts.

Predictive performance of the DL models for selected molecular mutations in GIST.

4197 Background: Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy characterized by aggressive tumor dissemination and resistance to therapy; processes significantly driven by the epithelial-to-mesenchymal transition (EMT). Netrin-1 is a key regulator for EMT. NP137, an anti-netrin-1 antibody, has shown to inhibit EMT in preclinical models and in a phase 1 monotherapy trial. Methods: LAPNET-01 (NCT06203821) is a single arm phase Ib clinical study to assess the combination of NP137 with mFOLFIRINOX in naive locally advanced unresectable PDAC. A safety lead-in (3–12 pts, 3+3 design, NP137 14 vs 9 mg/kg) was followed by a 40-patient expansion. Treatment consisted of NP137 + mFOLFIRINOX every 2 weeks, up to 12 cycles. The primary endpoint was safety at 6 months (all-grade and grade 3/4 adverse events [AEs], CTCAE v5.0). Secondary endpoints included objective response rate (ORR), progression-free survival (PFS) and overall survival (OS), surgical conversion rate and exploratory transcriptomic analyses. Laser capture microdissection was performed on 22 pre-treatment and 6 surgery samples to allow microbulk RNA sequencing. Immunohistochemistry was also performed on pre-treatment samples. Results: A total of 43 patients were enrolled in this trial. NP137 was well tolerated. AE occurred in 100% of patients (58% grade ≥ 3). ORR and disease control rate were 29% and 95%. Median PFS was 10.9 months (95% CI, 10.0 – 15.6) and median OS was 16.4 months (95% CI, 12.8 – NR) with 21 patients still alive at time of the data cut-off. Surgery was made possible in 23% of patients. Microbulk RNA sequencing revealed that the main pathway downregulated with the combination mFOLFIRINOX+NP137 is EMT, bringing a clinical validation of the main mechanism of action of NP137. Moreover, patients with tumors expressing high levels of the netrin-1 receptor neogenin (high-NEO1) at baseline (both at the RNA and proteic level (IHC)) demonstrated an improved outcomes compared to the low-NEO1 subgroup including longer median PFS (15.7 vs 10.2 months, p = 0.01) and longer median OS (not reached vs 16.5, p = 0.024). These results are consistent with experimental data demonstrating the implication of NEO1 in PDAC EMT and its progression. Conclusions: NP137 in combination with mFOLFIRINOX demonstrates a favorable safety profile, promising clinical activity and a mechanistically distinct mode of action supported by translational analyses. These results warrant further investigation of netrin-1 blockade in randomized trials and provide a rationale for biomarker-driven development of NP137 in PDAC. Further work is ongoing to better characterize the distribution of NEO1 in first-line unresectable PDAC. Clinical trial information: NCT06203821 .