Citations

The temporomandibular joint (TMJ) is an anatomically rich area, and TMJ surgery may be considered both anatomically and technically challenging, particularly when the pathology is complex or poorly visualized on conventional imaging. This case series highlights the role of advanced in-house 3D printing in TMJ surgical planning. The authors present 7 diverse TMJ surgical cases treated over the past decade, where 3D models were instrumental in preoperative planning. Models were fabricated from CT and/or MRI data using different materials for the print and model design, and customized to highlight relevant anatomy or pathology. This case series featured patients with a range of different TMJ conditions, such as condylar resorption, benign tumors, and joint ankylosis. 3D models improved the visualization of pathologic anatomy, enabled surgical simulation, and guided prosthesis design or resection planning. Models facilitated interdisciplinary collaboration and enhanced patient safety by improving anatomic orientation near critical structures. Outcomes included restored mandibular function, successful removal of the pathology, and improved facial symmetry, with follow-up ranging from 1 to 3 years. Advancing technology and capability in 3D printing can be very helpful in identifying the extent of disease, anatomic boundaries, critical regional anatomic risk, predicted joint mechanics, and patient education. Depending on the type of disease, different types of modeling and printing techniques may be warranted to best illustrate to the surgeon and patient how to proceed with treatment.

Objective: To assess the feasibility and clinical impact of sideline telemedicine for real-time injury assessment during high school athletic events in rural communities and to determine its potential effect on emergency department (ED) utilization. Design: Prospective, observational cohort study. Setting: Three rural high schools in southeast Minnesota without on-site athletic trainer or emergency medical services coverage. Participants: High school athletes and attendees injured during school-sponsored athletic events during the 2021 to 2022 school year. Intervention: Sideline telemedicine consults were initiated by school officials using tablets to connect with on-call dual board-certified emergency and sports medicine physicians. Consults included video-based assessment, triage, return-to-play guidance, and follow-up recommendations. Main Outcome Measures: Disposition after consultation (return to play, outpatient follow-up, ED referral), satisfaction scores using the 10-item Telehealth Satisfaction Scale, and patient-reported intent to seek ED care if telemedicine were unavailable. Results: Telemedicine was activated 15 times. Most (53%) injuries were musculoskeletal. Two (13%) patients were referred to the ED, where time-sensitive diagnoses (NSTEMI, testicular torsion) were confirmed. Thirteen patients were treated without ED referral; 6 (46%) reported they would have otherwise visited the ED. All diagnoses were confirmed by outpatient follow-up. Telehealth Satisfaction Scale scores were high: interpersonal communication (mean 4.00), respectfulness (3.96), and technical quality (3.99). Conclusions: Sideline telemedicine is a feasible and well-received model for acute injury evaluation at rural athletic events lacking on-site medical providers. It may reduce unnecessary ED use while preserving care quality and satisfaction, offering scalable support for resource-limited sports settings.

Abstract Background: High-dose interleukin-2 (IL-2) is administered after tumor-infiltrating lymphocyte (TIL) infusion to promote in-vivo expansion and persistence, yet optimal dosing and the clinical significance of out-of-specification (OOS) TIL products remain unclear. We investigated the impact of number of infused IL-2 doses and manufacturing OOS status on outcomes in metastatic melanoma treated with commercial TIL therapy. Methods: We retrospectively analyzed 31 patients treated across three Mayo Clinic sites. Planned IL-2 was 600,000 IU/kg every 12 hours for ≤6 doses; actual dosing varied based on clinical tolerance. Patients were grouped as low (0-2) vs high (≥3) IL-2 doses. TIL products were classified as within-specification or OOS per commercial release criteria. Survival associations were evaluated using Kaplan-Meier and multivariable Cox regression. Results: In our 31-patient cohort, the median age was 59 years (range 17-77), 58% were male, and 84% had ECOG 0. At TIL infusion, M-stage distribution was M1a 6%, M1b 10%, M1c 61%, and M1d 23%. LDH was elevated above the upper limit of normal in 42%. The median number of IL-2 infusions was 4 (range 0-6); 58% of patients received ≥3 doses, while 2 patients (6%) received none. Out-of-specification (OOS) TIL products occurred in 6 patients (19%). Best responses included complete response (26%) and partial response (23%), for an overall response rate of 48% and a disease-control rate of 61% (CR + PR + SD). Among responders, the median duration of response was 84 days (95% CI 73-95). At data cutoff, the median follow-up was 253 days (95% CI 137-370). The most common grade 3/4 toxicities occurring >14 days after TIL infusion were lymphopenia (39%), anemia (16%), and thrombocytopenia (10%). Median progression-free survival (PFS) was 99 days (95% CI 73-125) with 20 progression events, and median overall survival (OS) was 193 days (95% CI 32-354) with 13 deaths. Number of infused IL-2 doses was dependent on patients tolerability. Receiving ≥3 IL-2 doses was associated with improved overall survival (394 vs 101 days; p < 0.001) and a trend toward longer progression-free survival (110 vs 59 days; p = 0.055). OOS products predicted inferior PFS (30 vs 110 days; p = 0.003) and showed a trend toward worse OS (120 vs 394 days; p = 0.079). In multivariate analysis, ≥3 IL-2 doses independently improved PFS (HR 0.20, 95% CI 0.06-0.69; p = 0.011) and OS (HR 0.09, 0.02-0.36; p = 0.001), while OOS status increased risk of progression (HR 8.10, 2.24-29.25; p = 0.001) and death (HR 6.16, 1.35-28.20; p = 0.019). Conclusions: Higher number of infused doses IL-2 and meeting commercial TIL release criteria were independently associated with improved outcomes. Citation Format: Mohamed A. Aboelatta, Jeffrey E. Johnson, Jabra G. Zarka, Matyáš Benada, James W. Jakub, Roxana S. Dronca, Ruqin Chen, Mahesh Seetharam, Deepti Behl, Svetomir N. Markovic, Lisa A. Kottschade, Heather N. Montane, Matthew S. Block, Anastasios Dimou, Robert R. McWilliams, Paula Gill, Yi Lin, Arkadiusz Z. Dudek. Impact of number of IL-2 infusions and product out of specification status on outcomes of tumor infiltrating lymphocyte therapy for melanoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 3706.

Abstract Multiple Myeloma is the second most common hematologic malignancy among US adults and remains incurable. Immunotherapies, including bispecific T cell engagers (BiTEs) targeting BCMA, have greatly improved outcomes. However, a significant fraction of patients still fail to respond, or develop resistant disease. Conventional models of T cell cytotoxicity focus on delivery of perforin- and granzyme-containing granules following antigen recognition and T cell activation, an inefficient mode of killing that requires effector-to-target cell contact. Activated T cells, however, also secrete cytokines capable of diffusing and acting on distant targets. This raises the possibility of paracrine killing, in which these cytokines induce tumor cell death independently of cell-cell contact.Tumor necrosis factor (TNF) is a key cytokine released during T cell activation and is unique in that it can drive either cell survival or cell death. Although most cells default to cell survival and NFkB-mediated inflammation, several modulators can shift this survival signaling toward cell death. We therefore hypothesized that sensitizing Myeloma cells to TNF could enable T cell paracrine killing and enhance the efficacy of anti-Myeloma T cell immunotherapies.To test this, we first established an in vitro model of clinical response to Teclistamab, a BCMA-directed BiTE, using Multiple Myeloma cell lines that displayed sensitive, intermediate, or resistant responses to T cell killing. Combining these data with assays of cytokine sensitivity and receptor expression, we found that susceptibility to TNF-mediated cell death was a major determinant of Teclistamab sensitivity. This correlation was further supported by reduction or complete abrogation of Teclistamab T cell killing of sensitive Myeloma cell lines when soluble TNF was neutralized from these co-cultures using monoclonal antibodies. Pharmacologic inhibition and CRISPR-mediated deletion of known regulators of TNF survival-signaling further sensitized Myeloma cells to both TNF and T cell killing. In the absence of these regulators, BCMA-negative myeloma targets retained sensitivity to Teclistamab, supporting the idea that the main mechanism of cell death was indeed paracrine killing.Together, these findings establish a direct link between TNF sensitivity and T cell-mediated killing of Myeloma cells, and support TNF-driven paracrine killing as a dominant mechanism of response to Teclistamab. Enhancing this TNF-mediated death signaling may therefore represent a strategy to overcome resistance and improve clinical efficacy of T cell-based immunotherapies in Multiple Myeloma. Citation Format: Allison Carr, Elise Sintim-Aboagye, Adrian Ting, . TNF-driven paracrine killing determines the cytotoxic efficacy of Teclistamab in Myeloma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 1636.

Abstract Background: Pancreatic ductal adenocarcinoma (PDAC) is driven predominantly by oncogenic KRAS signaling and characterized by an immunosuppressive, fibrotic tumor microenvironment that limits therapeutic responses. RMC-6236, a pan-KRAS inhibitor, and ONIOYID, an investigational anti-tumor agent, each demonstrate partial activity in KRAS-mutant cancers. However, their combined therapeutic potential in PDAC remains unexplored. Here, we evaluated the anti-tumor efficacy, survival benefit, and immunomodulatory effects of RMC-6236, ONIOYID and irinotecan alone and dual combinations multiple in vitro and in vivo PDAC models. Methods: In vitro cytotoxicity assays were performed using KPC, PANC-1, AsPC-1, and PANC-02 cell lines. In vivo therapeutic studies were conducted in orthotopic KPC and PANC-1 tumor models. RMC-6236 was administered orally at 10 mg/kg; ONIOYID and irinotecan was administered intravenously at 5 mg/kg. Tumor growth inhibition, survival, collagen deposition, and immune cell infiltration were analyzed. Tumor microenvironment remodeling was quantified via immunohistochemistry for CD8, CD4, collagen I, and fibronectin. Results: The combination of RMC-6236 and ONIOYID elicited potent anti-tumor effects across all evaluated PDAC cell lines, achieving greater than 90% growth inhibition in vitro. In vivo, co-treatment resulted in more than 90% tumor regression in both KPC and PANC-1 xenograft models, markedly surpassing the efficacy of individual monotherapies and other dual-agent controls. Combination therapy significantly extended overall survival and produced sustained suppression of tumor progression. Mechanistic analyses revealed a substantial reduction in collagen and fibronectin deposition within the tumor microenvironment, consistent with attenuation of desmoplasia. Immune profiling demonstrated a robust enhancement of intratumoral CD8+ and CD4+ T-cell infiltration, along with a pronounced decrease in survivin expression. Importantly, no observable systemic toxicity was detected in treated animals. Conclusions: RMC-6236 combined with ONIOYID yields synergistic anti-tumor effects, remodels the fibrotic PDAC microenvironment, enhances T-cell infiltration, and significantly improves survival in aggressive pancreatic tumor models. These findings provide strong rationale for clinical evaluation of RMC-6236-based combination therapies for KRAS driven PDAC. Citation Format: Hari Krishnareddy Rachamala, Fang Wei, Debabrata Mukhopadhyay, Hani M. Babiker. Combined KRAS pathway inhibition and ONIOYID treatment enhances tumor regression, attenuates desmoplasia, and augments T cell infiltration in pancreatic ductal adenocarcinoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 5842.

Abstract Background: Up to 50% of patients with breast cancer experience chemotherapy-inducednausea (CIN) and 95% experience fatigue. A comprehensive understanding of biological mechanisms remains elusive. Herein, we evaluated the association of CIN and fatigue with clinical and multi-omics features, including serum and stool metabolites before (T1) to after chemotherapy (T2). Methods: Patients with breast cancer (n=36) who were to receive chemotherapy, provided symptom assessment using the Memorial Symptom Assessment Scale, stool and blood samples at T1 and T2. Patients provided dietary intake data using a Dietary Screener Questionnaire at T1. Descriptive and univariate analyses evaluated associations of co-occurringsymptoms and diet with CIN and fatigue at T2. Gut microbiome was sequenced using shotgun metagenomics. Targeted metabolomics was performed on stool and serum. Shift in the abundance of taxonomic groups and metabolite levels from T1 to T2 were evaluated in association with CIN and fatigue. Results: Approximately 64% of the patients experienced CIN and 94% experienced fatigue atT2. Three gastrointestinal symptoms co-occurred with CIN and fatigue. Higher daily average intake of calcium (p=0.013) and dairy (p=0.035) were associated with CIN. Levels of hexosylceramides, ceramide, phosphatidylcholine and sphingomyelins were significantly perturbed in association with CIN and fatigue (p<0.05). Conclusion: CIN and fatigue are associated with perturbation in the sphingolipid turnover pathway, which negatively impacts functions in the gut-liver axis that include apoptosis activity and change in bile acid levels. Confirmatory studies are warranted to support the development of interventions to alleviate CIN and fatigue in patients with breast cancer receiving chemotherapy.Keywords: breast cancer; chemotherapy-induced nausea; fatigue; metabolites; sphingolipids Citation Format: Komal Preet Singh, Brenda J. Ernst, Jun Chen, Surendra Dasari, Felipe Batalini, Cindy Tofthagen, Kathryn J. Ruddy, Keenan Pituch, Linda Chlan. Perturbations in gut liver axis functions are associated with chemotherapy induced nausea and fatigue in patients with breast cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 6309.

Background Immune exclusion inhibits antitumor immunity and response to immunotherapy, but its mechanisms remain poorly defined. In triple-negative breast cancer (TNBC), an aggressive and generally immune-rich subtype, an immune-cold microenvironment predicts poor prognosis due to a limited response to chemotherapy and immune checkpoint inhibitors. This study aimed to identify mechanisms regulating immune infiltration in TNBC. Methods We performed spatial transcriptomic analysis comparing immune-enriched versus immune-cold treatment-naïve TNBCs. Functional analyses, including loss-of-function and reconstitution experiments, were conducted to investigate the role of trophoblast cell-surface antigen 2 (TROP2), a key target of anticancer antibody drug conjugates (ADCs), in promoting TNBC progression. A humanized TROP2 syngeneic TNBC model was used to assess the effects of TROP2-targeting in combination with anti-programmed cell death protein 1 (PD-1) therapy. Additionally, data from patients treated with immune checkpoint blockade were used to test hypotheses from the preclinical findings. Results We reveal that TROP2 controls barrier-mediated immune exclusion in TNBC through claudin 7 association and tight junction regulation. TROP2 expression is inversely correlated with T-cell infiltration and predicts poor outcomes in TNBC. We demonstrate that TROP2 is sufficient to drive tumor progression in vivo in a CD8 T cell-dependent manner, while its loss deregulates expression and localization of multiple tight junction proteins, enabling T-cell infiltration. We show that TROP2 targeting via hRS7, the antibody component of the ADC sacituzumab govitecan, enhances the anti-PD-1 response and improves T-cell accessibility and effector function. Correspondingly, TROP2 expression is highly associated with lack of response to anti-PD-1 therapy in human breast cancer. Conclusions This study defines a new mechanism of barrier-mediated immune exclusion in cancer controlled by TROP2-dependent tight junctions. This mechanism drives tumor progression but can be targeted via TROP2-directed therapy to activate antitumor immunity and enhance immunotherapy response.

Abstract Introduction: Early relapse limits durable remissions in multiple myeloma (MM). Cell-free DNA (cfDNA) fragment patterns capture tumor burden and nucleosome positioning. We tested whether a fragmentomics signature trained at MRD time points stratifies progression-free survival (PFS) when applied to pretreatment plasma. Methods: We performed 30-40× whole-genome sequencing of plasma cfDNA from 43 newly diagnosed MM patients, with 65 additional MRD timepoint samples from 41 of those patients (post-ASCT n=30; 1-year maintenance n=30; other maintenance n=5) across eight Canadian sites (TFRIM4 and IMMAGINE studies) and one U.S. site (Mayo SPORE). MRD testing used multiparameter flow cytometry for all follow-up samples (n=65) and clonoSEQ in a subset (n=31). Logistic and elastic-net models were trained at MRD timepoints on fragmentomics features (short-fragment burden; a combined model integrating fragment-length distributions with inferred nucleosome positioning at MM-specific chromatin accessibility regions [Ordoñez et al., Genome Res. 2020]). A decision threshold was fixed by the Youden index during training and applied unchanged to diagnosis samples. PFS was analyzed by Kaplan-Meier, log-rank, and Cox models. Results: After a median follow-up of 49.1 months, 16 of 43 patients (37%) progressed. Using the prespecified locked threshold, patients classified as MRD+ by the proportion-of-short-fragments model had significantly shorter PFS than MRD- patients (HR = 5.12; 95% CI 1.16-22.57; log-rank p = 0.016), with median PFS of 49.2 months for MRD+ cases versus not reached for the MRD- group. Fixed-horizon PFS favored MRD- samples at 24/36/48 months (100/94/87% vs 85/81/53% for MRD+). A combined model integrating weighted fragment lengths with inferred nucleosome positioning also separated outcomes (log-rank p=0.054); the Cox HR was not estimable because no MRD- patients relapsed. At 24, 36, and 48 months, baseline MRD positivity by the short-fragment model identified 100%, 83%, and 86% of patients who relapsed within those intervals (specificity 44%, 43%, and 52%), while the combined model detected all early relapses across the same horizons (specificity 15-21%), indicating consistently high sensitivity but modest specificity for predicting early progression. Conclusions: A cfDNA fragmentomics signature trained at MRD time points stratified PFS when applied to diagnostic plasma, identifying patients at risk of early relapse. Short-fragment burden was most discriminative, and a combined model with nucleosome positioning recapitulated it with higher sensitivity, albeit lower specificity. These data support cfDNA fragmentomics as a practical liquid-biopsy risk biomarker in MM and suggest higher signals may proxy aggressive disease with greater tumor shedding and chromatin disorganization. Future work will validate findings in larger cohorts and integrate cytogenetic and immune features. Citation Format: Dor David Abelman, Jenna Eagles, Aimee Wong, Saumil Shah, Jeffrey Bruce, Stephanie Pedersen, David S. Scott, Cecilia Bonolo de Campos, Signy Chow, Darrell White, Irwindeed Sandhu, Kevin Song, Esteban Braggio, Shaji Kunnathu Kumar, Alli Murugesan, Tony Reiman, A. Keith Stewart, Suzanne Trudel, Trevor J. Pugh. Baseline cfDNA fragmentomics identifies multiple myeloma patients at risk of early progression [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 2597.

Abstract Chimeric antigen receptor (CAR)-T cell therapy has revolutionized the treatment of B-cell malignancies. Despite the clinical success of CD19-targeted approaches, relapsed/refractory (R/R) disease—often driven by antigen loss or immune escape—remains a major challenge. To overcome this, we developed a novel CAR-T cell therapy targeting BAFF-R, a receptor consistently expressed in chronic lymphocytic leukemia (CLL) and other B-cell malignancies. We developed a new anti-BAFF-R monoclonal antibody and engineered the MC10029 CAR construct using its scFv. Antigen-specific cytotoxicity was validated in both in vitro and in vivo models, including Nalm-6 (leukemia) and Z138 (lymphoma), and CD19-knockout tumor cells to model (R/R) disease. MC10029 CAR-T cells were generated from healthy donors and CLL patients, and their cytotoxicity was evaluated against MEC-1, a CLL cell line, as well as autologous CLL patient tumor samples. These studies demonstrated potent and specific antitumor efficacy. We transitioned to clinical-grade production, using GMP-compliant lentivirus to manufacture MC10029 CAR-T cells under regulatory guidelines. With FDA IND approval, we initiated a Phase 1 clinical trial to evaluate safety and dosing. Our first patient, treated with a low-dose, single infusion, achieved a complete metabolic response within 2 months. The therapy is well tolerated, with no severe advent events such as cytokine release syndrome or neurotoxicity, supporting both the safety and efficacy of the therapy. Conclusion: This study represents Mayo Clinic’s first homegrown CAR-T cell therapy, developed entirely in-house—from antibody discovery and CAR design to GMP manufacturing and clinical trial—marking a significant step toward personalized, next-generation immunotherapy for B-cell malignancies. Citation Format: Yan Luo, Shaohua Guo, Yaqing Qie, Martha E. Gadd, Tanya Hundal, Hemant S. Murthy, Mohamed A. Kharfan-Dabaja, Hong Qin. From gene to bedside: Mayo Clinic’s first-in-house BAFF-R CAR-T [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 3719.

Abstract Specialized immune niches located in the stroma-tumor junction promote interactions between tumor-resident antigen-presenting cells and effector lymphocytes that are required for immunotherapy efficacy. We have hypothesized that this stromal-based immune crosstalk may be regulated by provisional extracellular matrix signals, analogous to the early-stages of wound healing where provisional matrix hosts robust immune activity. A cardinal provisional matrix remodeling event, the regulated proteolysis of the large proteoglycan versican (VCAN) generates an immunomodulatory fragment (matrikine), versikine, that engages adaptive immunity. We have previously shown that VCAN proteolysis correlates with T-cell infiltration across multiple solid and liquid cancers with the most immune-evasive cancers showing low to negligible rates of VCAN proteolysis (e.g., 0% in pancreatic adenocarcinoma). A recent clinical trial generated informative prospective data linking VCAN proteolysis with immunotherapy outcomes: patients whose metastatic colorectal tumors categorized as VCAN proteolysis-weak (VPW, 60% of cases) demonstrated inferior responses to checkpoint inhibition (CPI, pembrolizumab) and worse outcomes compared to VCAN proteolysis-predominant (VPP, 40%) cases. Leveraging these prospective trial data, we hypothesized that versikine therapy may rationally reverse the immunosuppression associated with the prevalent VPW phenotype. To tailor versikine therapy to specific human biomarker-stratified tumor phenotypes, we studied experimental models replicating partially T-permissive VPW-VCANlo human cancers and poor-prognosis, immune-exclusionary VPW-VCANhi cancers. Across VPW-like tumors, versikine promoted the stromal accumulation of CD40lghiIcoshiFoxp3neg Tfh-like CD4+ T cells that engaged dendritic cells (DC) and CD8+ T cells in “immune triads” even at baseline (prior to CPI), concurrently with the intratumoral expansion of activated CD8+ T cells expressing cytolytic molecules (granzymes, perforin). In VPW-VCANlo tumors, versikine delivered as LNP-mRNA or recombinant protein demonstrated monotherapy activity, dependent on Batf3-lineage DC and CD8+ T cells. When combined with single-agent CPI, versikine cured most VPW-VCANlo tumors with memory to tumor re-challenge. In VPW-VCANhi tumors, versikine synergized with combination immunotherapy modulating “mature DCs enriched in immunoregulatory molecules” (mregDC). Our data provide mechanistic rationale for the biomarker-stratified, therapeutic restoration of a provisional matrix-regulated immune signaling network to reverse resistance to CPI. Moreover, the data highlight the need to reevaluate prior approaches to globally disrupt tumor stroma in favor of biomarker-driven, pathway-focused harnessing of stromal signals that modulate anti-tumor immunity. Citation Format: Daniel J. Lagal, Duncan Hong, Athanasios Papadas, Emma Geatches, George Yacu, Surabhi Naik, Alicia Gibbons, Alexander Cicala, Kersi Pestonjamasp, Peter Toth, Kristina Matkowskyj, Dustin A. Deming, Fotis Asimakopoulos. Biomarker-driven restoration of tumor provisional matrix signaling network reverses resistance to checkpoint inhibition immunotherapy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 6746.