PURPOSE:Patients with gastric cancer, biliary tract cancer (BTC), and pancreatic ductal adenocarcinoma (PDAC) have poor survival outcomes and limited second- or later-line treatment options. Certain drugs targeting vascular endothelial growth factor (VEGF) or programmed cell death protein 1 (PD-1) signaling pathways are currently used in these cancers in specific circumstances; however, there remains a need for novel treatment combinations. LEAP-005 is a multicohort, open-label, phase II study that evaluated lenvatinib (multitargeted inhibitor of tyrosine kinases, including VEGF) plus pembrolizumab (anti-PD-1 monoclonal antibody) in select previously treated solid tumors. PATIENTS AND METHODS:Participants with previously treated, advanced gastric cancer, BTC, and PDAC were enrolled in cohorts C, F, and G of LEAP-005, respectively, and received lenvatinib 20 mg/day orally plus pembrolizumab 200 mg i.v. every 3 weeks. Primary endpoints were objective response rate (ORR) and safety. RESULTS:Of 99, 102, and 103 total participants enrolled in cohorts C, F, and G, respectively, median times from first dose of study treatment to data cutoff (February 6, 2023) were 23.7, 24.2, and 19.5 months. ORRs (95% confidence interval) by blinded independent central review were 15.2% (8.7%-23.8%) in cohort C, 17.6% (10.8%-26.4%) in cohort F, and 7.8% (3.4%-14.7%) in cohort G. Grade 3 to 5 treatment-related adverse events occurred in 54.5% of participants in cohort C, and grade 3 to 4 (no grade 5) occurred in 60.8% and 59.2% of participants in cohorts F and G, respectively. CONCLUSIONS:Lenvatinib plus pembrolizumab demonstrated modest antitumor activity and a manageable safety profile in previously treated, advanced gastric cancer, BTC, and PDAC. SIGNIFICANCE:In the phase II LEAP-005 study, lenvatinib plus pembrolizumab showed modest antitumor activity and a manageable safety profile in participants with previously treated gastrointestinal-related cancers. Exploratory analyses in participants with BTC indicated higher ORRs in participants with targetable alterations versus those without.

Efficacy results in cohort G, PDAC. A, Time on study treatment and treatment response per RECIST version 1.1 by BICR for participants with an objective response (confirmed CR or PR). B, Best percentage change from baseline in target lesion size per RECIST version 1.1 by BICR among participants with ≥1 postbaseline assessment. C, PFS per RECIST version 1.1 by BICR. D, OS. In B, percentage changes from baseline >100% are presented as 100%.

Current mRNA approaches in immuno-oncology lack specificity for optimal T cell mRNA expression, necessitating tailored mRNA expression systems. In this study, we developed novel mRNA constructs in which the standard α-globin (HBA1) 5' UTR is replaced with sequences derived from genes highly expressed in effector T cells. Using primary human T cells, expression levels of UTR-modified reporter genes were evaluated, revealing significant variability based on the substituted UTR. For instance, interferon gamma (IFN-γ) UTRs facilitated enhanced and sustained protein expression, whereas TNF UTRs showed diminished expression. Unexpectedly, the in silico-predicted RNA stability of the various UTR-modified constructs did not correlate with the altered expression. These UTR-mediated differences in protein expression were unique to T cells, as HEK cells introduced with the same constructs showed distinct expression profiles. CD19-CAR constructs expressed in T cells using various 5' UTRs demonstrated different protein expression and function toward antigen-positive target cells, as well as tonic signaling, manifested by the immune output in the absence of antigen. Specifically, for CD19-CAR, using the TIGIT 5' UTR proved optimal for achieving maximal reactivity while minimizing tonic signaling. These findings provide proof of concept for the pivotal role of T cell-specific UTRs in optimizing CAR-T cell functionality by fine-tuning expression, reducing tonic signaling, and minimizing off-target effects, thus emphasizing their potential in advancing the therapeutic potential of mRNA-based CAR-T cell therapies.

BACKGROUND:Metastatic cancer patients receiving systemic chemotherapy face increased risks for venous thromboembolism (VTE). Benefit has been shown for prophylactic anticoagulants in risk-stratified populations. Ovarian cancer (OC) is commonly advanced at diagnosis and treated with chemotherapy. Despite high VTE rates among OC patients, predictors of risk in this population are not well studied, and information on the benefit of oral anticoagulants is lacking. OBJECTIVE:A quality improvement (QI) intervention to improve appropriate anticoagulation in risk-selected OC patients receiving first-line chemotherapy was implemented, prospectively assessing VTE risk reduction. METHODS:Patients receiving first-line chemotherapy for OC at Sheba Medical Center 2020-2025 were included. A QI program (launched 07/2023) included staff education, EMR-incorporated Khorana scoring, integrated apixaban prescriptions and targeted chemo-suite questionnaires. Data was extracted from the EMR using MDClone® software with Natural Language Processing to identify VTE events in imaging reports. Descriptive statistics were used to compare patients treated before and after program implementation. Predictors of VTE were evaluated with logistic regression. RESULTS:Patient characteristics were comparable before and after program implementation. VTE rates were high at 16.9% before, and 12.5% following roll-out. No increase in bleeding events or blood products consumption was appreciated. Program implementation was found to be a significant protective factor on multivariable analysis, adjusting for other risk factors (aOR = 0.39 (0.17-0.81), p = 0.015). CONCLUSION:The implementation of an oral anticoagulation QI program successfully decreased VTE events during first-line chemotherapy for OC with no appreciable increase in risk. Future work will focus on improved risk stratification and selection for thromboprophylaxis.

Abstract Many cancer therapies show strong preclinical activity yet fail clinically due to inadequate experimental models. Conventional 2D cultures lack physiological relevance because they cannot reproduce the complex tumor-stromal-immune interactions or the biomechanical cues that shape tumor behavior and therapeutic response. This limitation is particularly pronounced in aggressive tumors, where patient heterogeneity and dynamic microenvironmental interactions drive treatment outcomes, or in rare tumors, where data on response to available therapies is scarce. To address this translational gap, we developed two patient-derived 3D platforms: (1) 3D tumoroids generated from the dissociated tumor tissues and co-cultured with matched peripheral blood mononuclear cells (PBMC), enabling tumor-immune-stromal interactions, and (2) 3D-bioprinted constructs formed using two bioinks: one incorporating tumor and tumor-microenvironment (TME) cells, and the other containing endothelial cells and pericytes to create perfusable vascular channels flowing PBMC and drugs. We are validating the ability of these high-throughput 3D models to recapitulate patient-specific tumor biology and predict responses to chemotherapy, immunotherapy, and targeted therapies. Their predictive performance is being evaluated in an IRB-approved clinical study (SMC-9417-22) involving 80 patients across seven cancer types. To guide personalized therapy selection, we integrate standard-of-care and investigational drugs with AI-derived treatment matches generated by ENLIGHT-DP (Pangea Biomed), a deep-learning platform that infers gene expression from tumor HandE slides and combines them with proprietary predictive biomarkers to produce individualized drug-response scores. AI-prioritized treatments are reviewed with oncologists and then tested on 3D platforms. Preliminary evidence suggests a correlation between the 3D tumoroid models and clinical outcomes. Notably, in a case of mucosal melanoma, standard therapies failed both clinically and ex vivo, whereas ENLIGHT-DP screening identified regorafenib, which demonstrated potent activity in the 3D model. Compassionate-use treatment led to a durable clinical response lasting nearly 12 months. In another metastatic melanoma case harboring an ALK rearrangement (identified via Tempus sequencing and prioritized by ENLIGHT-DP), lorlatinib demonstrated significant efficacy ex vivo and produced a sustained clinical response in the patient for more than 6 months at the time of this writing, with near-complete responses of visceral and brain metastases. Together, these patient-derived 3D models, integrated with AI-based drug prioritization, provide a robust platform for functional precision oncology, enabling personalized drug screening, reducing ineffective treatments, and bridging the gap between preclinical modeling and clinical response. Citation Format: Anshika Katyal, Anne Krinsky, Opal Avramoff, Yulia Liubomirski, Gal Dinstag, Omer Tirosh, Ranit Aharonov, Tuvik Beker, Iris Barshack, Shaked Lev-Ari, Shirly Grynberg, Ronnie Shapira-Frommer, Ronit Satchi-Fainaro. Patient-derived 3D tumor models integrated with AI-driven treatment matching for target discovery and personalized therapy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 2 (Late-Breaking, Clinical Trial, and Invited Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(8_Suppl):Abstract nr LB334.

9512 Background: Treatment of BRAF -mutant (mut) melanoma has been transformed by targeted inhibition of MEK and BRAF kinases. However, duration of clinical benefit has been limited by de novo and acquired resistance through RAF-kinases signaling as dimers, poor activity in brain metastases (BMs), and paradoxical activation adverse events (AEs) negatively impacting tolerability. PF-07799544 is an oral, brain-penetrant, reversible MEK inhibitor (MEKi). PF-07799933 is an oral, brain-penetrant, selective BRAF dimer inhibitor (BRAFi) with activity against BRAF V600 and non-V600 muts. We report initial results of this next-generation BRAFi/MEKi combination from ongoing phase 1 study. Methods: This platform study (NCT05538130) is evaluating PF-07799544 as monotherapy or combined with other targeted therapy for BRAF -mut melanoma and other solid tumors. Substudy B is an open-label, multicenter study assessing safety, tolerability, pharmacokinetics (PK), pharmacodynamics, and clinical activity of PF-07799544 + PF-07799933. Dose escalation (DE) enrolled into 4 dose levels patients (pts) with BRAF -mut advanced melanoma who had progressed on standard therapy, including pts with BMs. Randomized dose optimization (DO) enrolled pts with BRAF V600 -mut advanced melanoma previously treated with 1-2 immunotherapy (IO) lines and ≤1 BRAFi ± MEKi line; pts with BMs were eligible if asymptomatic. We report pooled baseline characteristics and safety and separate efficacy. Results: As of Nov 12, 2025, 60 pts received ≥1 dose of study treatment. At baseline: median age, 54.5 years; female, 50%; White, 95%; ECOG PS of 0, 63%; adrenal insufficiency, 25%; BMs, 53%; and BRAF V600 mutation, 95%; 77% received ≥3 prior systemic anticancer therapies, 100% received prior IO, 100% of pts with BRAF V600 mutation received prior BRAFi ± MEKi, and 73% received BRAFi ± MEKi <6 months before beginning study treatment. Any-grade treatment-emergent AEs (TEAEs) occurred in 95%; most common (≥20%) were rash (40%), fatigue (37%), diarrhea (32%), and peripheral edema (22%). Grade ≥3 TEAEs occurred in 67%; most common (≥5%) were rash (7%), disease progression (7%), anemia (5%), and fall (5%). Dose modifications due to TEAEs (any-causality, treatment-related) included reductions (13%, 13%), interruptions (53%, 33%), and discontinuations (10%, 3%). Objective response rate (ORR; including unconfirmed) by investigator was 27% in 41 DE pts and 32% in 19 DO pts. In pts with baseline BMs, intracranial (IC) ORR was 30% in 23 DE pts and 22% in 9 DO pts. PK showed BRAFi/MEKi exposures consistent with preclinical exposures which showed antitumor activity supporting selected DO doses. Conclusions: PF-07799544 + PF-07799933 showed manageable safety and promising systemic and IC antitumor activity in heavily pretreated BRAF -mut advanced melanoma. Evaluation of dose expansion cohorts is ongoing. Clinical trial information: NCT05538130 .

PFS and OS by KRAS in participants with biliary tract cancer (cohort F)

OBJECTIVES:To evaluate the utility of CD19-directed chimeric antigen receptor T cell (CAR-T) therapy in patients with persistent inflammatory refractory RA (PIRRA), who failed ≥5 biologic/targeted synthetic DMARDs classes. METHODS:Three women with long-standing, seropositive PIRRA received autologous anti-CD19 CAR-T therapy with CD 28 co-stimulation. After lymphodepletion with fludarabine and cyclophosphamide, an infusion of 0.6-1 × 106 CAR-T cells/kg was administered. Clinical, laboratory, imaging and histological outcomes were assessed up to 18 months. RESULTS:Median age was 54 years (range 39-68), and median disease duration was 14 ± 3.1 years. All developed grade 3 cytokine release syndrome (CRS), and one developed grade 4 ICANS. No long-term toxicities were observed, except for hypogammaglobulinemia, that has not required replacement therapy. Within 3 months, two patients achieved remission, and one had low disease activity. At the last follow-up, two remained in drug-free remission, and one attained low disease activity with abatacept and MTX. HAQ-DI scores improved from severe disability to near-normal. RF and ACPA titres markedly declined. Furthermore, imaging demonstrated resolution of synovitis and clearance of CD19+B cells from the synovium establishing histological remission. CONCLUSION:CD19 CAR-T therapy induced profound, durable responses in extremely severe patients with seropositive PIRRA. Despite significant acute toxicities, recovery was complete and long-term safety was favourable. These findings suggest that CAR-T may provide a transformative benefit in severe RA, warranting controlled clinical trials.

BACKGROUND:Current treatments for patients with previously treated metastatic colorectal cancer (CRC) have poor outcomes. LEAP-005 (ClinicalTrials.gov, NCT03797326) was a multicohort, open-label phase II study evaluating the efficacy and safety of lenvatinib plus pembrolizumab in participants with previously treated selected solid tumors. We report findings from the LEAP-005 CRC cohort. PATIENTS AND METHODS:Participants aged ≥ 18 years with advanced (metastatic and/or unresectable) CRC with 2 prior lines of systemic therapy were eligible for the CRC cohort of LEAP-005. Participants received oral lenvatinib (20 mg/day) plus intravenous pembrolizumab (200 mg Q3W) combination therapy (Arm 1) or lenvatinib (24 mg/day) monotherapy (Arm 2). Dual primary endpoints were objective response rate (ORR) per RECIST version 1.1 and safety. Secondary endpoints were duration of response (DOR), progression-free survival (PFS), and overall survival (OS). RESULTS:135 participants were enrolled in the CRC cohort (Arm 1, n = 105; Arm 2, n = 35). In Arm 1, ORR was 14% (95% CI, 8-23), median PFS was 3.4 (95% CI, 2.1-4.1) months, and OS was 8.7 (95% CI, 7.0-10.0) months. In Arm 2, ORR was 7% (95% CI, 1-22), median PFS was 3.4 (95% CI, 2.1-4.2) months, and OS was 7.7 (95% CI, 5.6-14.8) months. Treatment-related AEs occurred in 96% of participants (grade 3/4, 63%) in Arm 1 and 97% (grade 3/4, 63%) in Arm 2. One participant in Arm 1 died due to treatment-related intestinal perforation. CONCLUSION:Lenvatinib plus pembrolizumab demonstrated antitumor activity in participants with advanced CRC with 2 prior lines of treatment. No new safety signals were identified.

Oncoprint from central WES in participants with biliary tract cancer (cohort F)

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PFS and OS by baseline PD-L1 status in participants with biliary tract cancer (cohort F)

Melanoma cells secrete melanosomes, large extracellular vesicles that reinforce tumor growth and survival signaling. To determine whether these vesicles elicit functional humoral immunity, we immunized mice with melanoma-derived melanosomes and analyzed the resulting antibody responses. This approach induced B cell expansion and generated antibodies directed against heat shock protein 70 (HSP70) present on the surface of melanosomes. Functionally, anti-HSP70 monoclonal antibodies inhibited growth in murine B16 and human MNT-1 melanoma cells independently of immune effector cells while suppressing key transcriptional programs involved in proliferation. In vivo, passive administration of anti-HSP70 antibodies delayed tumor onset and improved survival in a prophylactic B16 model. Moreover, in patients with metastatic melanoma treated with immune checkpoint blockade, higher serum anti-HSP70 immunoglobulin G (IgG) levels were associated with complete response compared with progressive disease. Together, these findings identify an extracellular vesicle-antibody axis that constrains melanoma survival signaling and has biomarker and therapeutic implications.

Antitumor activity per RECIST version 1.1 by BICR.

Background In Study 309/KEYNOTE-775 (NCT03517449), lenvatinib+pembrolizumab versus chemotherapy significantly improved progression-free survival (PFS), overall survival (OS), and objective response rate (ORR) in advanced endometrial cancer (EC). We report 5-year follow-up results.Methods Participants had advanced/recurrent/metastatic EC with progressive disease after one prior platinum-based chemotherapy regimen, measurable disease per Response Evaluation Criteria in Solid Tumors version 1.1 (RECIST v1.1), and no prior receipt of anti-programmed cell death protein 1 or anti-programmed cell death ligand 1 agents. Participants were randomized 1:1 to lenvatinib 20 mg orally once daily plus pembrolizumab 200 mg intravenously every 3 weeks or chemotherapy (doxorubicin or paclitaxel). Pembrolizumab was given for ≤35 cycles. Primary endpoints were OS and PFS per RECIST v1.1 by blinded independent central review (BICR). Secondary endpoints included ORR per RECIST v1.1 by BICR and safety. Efficacy endpoints were analyzed using Cox regression, Kaplan-Meier, and Miettinen and Nurminen methodology.Results 827 participants were randomized. At data cut-off (February 26, 2025), overall median follow-up was 68.8 months; 139 participants were alive (lenvatinib+pembrolizumab, n=86; chemotherapy, n=53), and all had ended their treatment in this study. Five-year OS rate was 16.7% with lenvatinib+pembrolizumab versus 7.3% with chemotherapy in mismatch repair-proficient EC, 36.5% versus 9.8% in mismatch repair-deficient EC, and 19.9% versus 7.7% in all-comers. Five-year PFS rates were 6.3% versus 2.1%, 26.4% versus 10.8%, and 9.8% versus 3.2%, respectively. In all-comers, treatment-related adverse events led to any treatment discontinuation in 32.3% versus 5.9%. Subsequent systemic anticancer therapy was used by 44.8% versus 51.2% (lenvatinib+pembrolizumab by 2.4% vs 10.1%).Conclusions Results were consistent with the primary analysis despite increased use of subsequent systemic anticancer therapy and crossover to lenvatinib+pembrolizumab in the chemotherapy group. The continued durable benefit, including OS, with lenvatinib+pembrolizumab and no new safety signals lend further support for this regimen as a standard of care therapy for EC.

OBJECTIVE:Vulvar and vaginal melanoma are rare gynecologic malignancies with aggressive clinical behavior and poor prognosis. Due to their low incidence and exclusion from most clinical trials, treatment decisions are often extrapolated from cutaneous melanoma data. This study aims to provide real-world insights into the clinical course and outcomes of vulvar and vaginal melanoma in the context of modern systemic therapy. METHODS:We retrospectively analyzed 39 patients with vulvar or vaginal melanoma treated at a single tertiary cancer center between 2011 and 2023. Clinical and pathologic data, including tumor site, stage, treatment modalities, and outcomes, were collected. Systemic therapy regimens included anti-PD-1 antibody monotherapy (either pembrolizumab or nivolumab), anti-PD-1 + anti-CTLA4 combination therapy (ipilimumab and nivolumab), and chemotherapy combined with interleukin-2. Progression-free survival and overall survival were evaluated. RESULTS:Patients frequently presented with locally advanced disease. High rates of multifocality, positive margins, and repeated local recurrence were observed, particularly in vulvar primaries. Among those treated for advanced disease (n = 28), combination immunotherapy yielded the most durable responses. Vulvar melanoma was associated with longer progression-free survival and overall survival compared with vaginal melanoma (median progression-free survival: 33 vs. 5 mo, HR = 3.8; median overall survival: 42 vs. 10 mo, HR = 7.8). CONCLUSIONS:Vulvar and vaginal melanoma present unique diagnostic and therapeutic challenges in gynecologic oncology. Site-specific prognosis and distinct response patterns to immunotherapy underscore the importance of individualized management strategies and multidisciplinary coordination in this rare population.

Background Current treatments for patients with previously treated metastatic colorectal cancer (CRC) have poor outcomes. LEAP-005 (ClinicalTrials.gov, NCT03797326) was a multicohort, open-label phase 2 study evaluating the efficacy and safety of lenvatinib plus pembrolizumab in participants with previously treated selected solid tumors. We report findings from the LEAP-005 CRC cohort. Patients and Methods Participants aged ≥18 years, with advanced (metastatic and/or unresectable) CRC with 2 prior lines of systemic therapy were eligible for the CRC cohort of LEAP-005. Participants received oral lenvatinib (20 mg/day) plus intravenous pembrolizumab (200 mg Q3W) combination therapy (Arm 1) or lenvatinib (24 mg/day) monotherapy (Arm 2). Dual primary endpoints were objective response rate (ORR) per RECIST version 1.1 and safety. Secondary endpoints were duration of response (DOR), progression-free survival (PFS), and overall survival (OS). Results 135 participants were enrolled in the CRC cohort (Arm 1, n=105; Arm 2, n=35). In Arm 1, ORR was 14% (95% CI, 8‒23), median PFS was 3.4 (95% CI, 2.1‒4.1) months, and OS was 8.7 (95% CI, 7.0‒10.0) months. In Arm 2, ORR was 7% (95% CI, 1‒22), median PFS was 3.4 (95% CI, 2.1‒4.2) months, and OS was 7.7 (95% CI, 5.6‒14.8) months. Treatment-related AEs occurred in 96% of participants (grade 3/4, 63%) in Arm 1 and 97% (grade 3/4, 63%) in Arm 2. One participant in Arm 1 died due to treatment-related intestinal perforation. Conclusion Lenvatinib plus pembrolizumab demonstrated antitumor activity in participants with advanced CRC with 2 prior lines of treatment. No new safety signals were identified. MICROABSTRACT The colorectal cancer (CRC) cohort of the phase 2 LEAP-005 study evaluated the combination of lenvatinib plus pembrolizumab in participants with advanced CRC that had progressed on 2 prior lines of systemic therapy. The objective response rate with lenvatinib plus pembrolizumab was 14%, with median duration of response of 8.3 months and estimated 6-month overall survival rate of 67%. These findings contribute to ongoing research on chemotherapy-free immunotherapy combination treatment approaches for patients with previously treated advanced CRC. Trial registration ClinicalTrials.gov, NCT03797326

Abstract Background: Central nervous system (CNS) tumors, whether primary or secondary, present significant therapeutic challenges, partly due to the unique environment of the brain, which is both highly immunosuppressive and difficult to penetrate due to the blood-brain barrier (BBB). Glioblastoma (GB) is the most lethal and common CNS cancer, exhibiting a highly invasive and aggressive nature. Within the brain microenvironment, microglia have been shown to facilitate GB invasion and immunosuppression. However, the reciprocal mechanisms by which GB cells alter microglia behavior are not fully understood. We previously demonstrated that P-selectin mediates microglia-enhanced GB proliferation and invasion by modulating microglial activation states. We demonstrated this phenomenon in several models, by neutralizing antibody (Ab), pharmacological (small molecule), and molecular inhibition (shRNA) of P-selectin, which led to reduced tumor growth and increased survival in GB mouse models. Moreover, P-selectin inhibition led to increased infiltration and activation of CD8 cytotoxic T cells, as well as reduced infiltration of T regulatory cells. This suggests that P-selectin inhibition may enhance the susceptibility of GB tumors to existing immunotherapies, thereby sensitizing these non-responsive tumors to become immune checkpoint therapy (ICT)-responsive. Our work sheds light on the function of tumor-associated microglia and the mechanisms by which GB cells suppress the immune system and invade the brain, paving the way to exploit P-selectin as a therapeutic target in GB patients. Methods: NCT05909618 is a single-center, open-label, 3-arm, non-randomized phase I/II study to evaluate the efficacy, safety, and tolerability of an anti-P-selectin antibody, crizanlizumab, alone (cohort 2) or in combination with nivolumab (cohorts 1 and 3) in patients with GB and melanoma brain metastases. Herein, we report preliminary information on Cohort 2, which enrolls patients with newly diagnosed MGMT-unmethylated GB to receive crizanlizumab maintenance therapy following completion of primary radiation therapy. Clinical Trial Registry Number: NCT05909618 Enrollment Status: The trial opened in August 2023 with a planned sample size of 33 subjects (11 patients to cohort 2). As of the time of submission, approximately 50% of the target accrual has been enrolled across the cohorts. The study remains open, and recruitment is ongoing. Citation Format: Anne Krinsky, Anshika Katyal, Opal Avramoff, Yulia Liubomirski, Ranit Aharonov, Tuvik Beker, Gal Dinstag, Omer Tirosh, Alisa Talianski, Ronnie Frommer-Shapira, Ronit Satchi-Fainaro. Phase I/II study of the anti-P-selectin antibody crizanlizumab for newly-diagnosed unmethylated glioblastoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 2 (Late-Breaking, Clinical Trial, and Invited Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(8_Suppl):Abstract nr CT071.