tbuckley/cabot-search huggingface dataset:
Abstract 3863: Targeting TACC3 inhibits metastasis in breast cancer with centrosome amplification
Authors: Mustafa Emre Gedik, Ozge Saatci, Kubra Calisir, Metin Cetin, Burge Ulukan Altun, Ozlem Sener Sahin, Rony Hull, Lauren Ball, Elizabeth Hill, Chaemin Lim, Sridhar Vempati, Burcu Caliskan, Erden Banoglu, Ioulia Chatzistamou, Ozgur Sahin
Journal: Cancer Research (2025)

Abstract Centrosome amplification (CA) is highly prevalent in cancer. It is strongly associated with tumor progression and worse prognosis in a variety of different cancers. Preclinical studies have demonstrated that CA can trigger tumor initiation as well as cancer cell invasion. Thus, CA is known to be a promising therapeutic target. We have previously identified Transforming Acidic Coiled-Coil Containing Protein 3 (TACC3) as being overexpressed in tumors with CA. TACC3 forms distinct functional interactomes regulating spindle stability, clustering extra centrosomes and transcription of key tumor suppressors in mitosis and interphase to ensure proliferation and survival of cancer cells with CA. Despite the known mechanisms in tumor growth inhibition, the molecular mechanisms by which TACC3 drives tumor invasion and metastasis in cancers with CA remain underexplored. Here, we aim to test TACC3 targeting as a novel strategy to block invasion and metastasis and to elucidate the underlying mechanisms. We found that higher TACC3 levels are strongly associated with worse metastasis-free survival in breast cancer patients with CA. Using a combination of in vitro assays, transcriptomics, proximity labeling (APEX2-TACC3), and mass spectrometry, we demonstrate that TACC3 promotes cancer cell migration and invasion. In addition, we provide evidence that targeting TACC3 via a small-molecule inhibitor or CRISPR-Cas9-mediated knockout significantly reduces cell migration and invasion. Furthermore, TACC3 inhibition reduces the number of circulating tumor cells and spontaneous metastasis to the lungs in the MMTV-PyMT transgenic mouse model and lung-tropic breast cancer xenografts without any toxicity. Overall, our findings demonstrate the potential for TACC3 as a therapeutic target to inhibit metastasis in breast cancer with CA. This work offers new insights into the molecular underpinnings of TACC3’s role in metastatic breast cancer, particularly in CA-driven tumors and underscores its therapeutic relevance. Citation Format: Mustafa Emre Gedik, Ozge Saatci, Kubra Calisir, Metin Cetin, Burge Ulukan Altun, Ozlem Sener Sahin, Rony Hull, Lauren Ball, Elizabeth Hill, Chaemin Lim, Sridhar Vempati, Burcu Caliskan, Erden Banoglu, Ioulia Chatzistamou, Ozgur Sahin. Targeting TACC3 inhibits metastasis in breast cancer with centrosome amplification [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 3863.
Abstract 3757: Development of potent orally bioavailable inhibitors of nicotinamide N-methyl transferase
Authors: Samarjit Patnaik, Janna Heide, Ke Kong, Mark Eckert, Maria Allega, Min Shen, Hongmao Sun, Jonathan Shrimp, Quinlin Hanson, Ken Cheng, Andrew Flint, William J. Moore, Matthew Hall, Gordon M. Stott, Ernst Lengyel
Journal: Cancer Research (2025)

Abstract Nicotinamide N-methyltransferase (NNMT) has emerged as a cancer therapeutic target as a master metabolic regulator that catalyzes the differentiation of normal fibroblasts to cancer associated fibroblasts (CAFs) in the stromal tissue surrounding various tumors, most notably ovarian carcinomas. NNMT activity depletes S-adenosyl methionine (SAM) reducing histone methylation. This change in the stromal epigenome results in changes to the interstitial tumor space which in turn promotes tumor growth and metastasis We will present the development of novel orally bioavailable selective inhibitors of NNMT. We conducted a high throughput screen (HTS) of over 150, 000 compounds against NNMT, using MTase-Glo™ (Methyltransferase Glo™, Promega), to identify actionable chemical matter for medicinal chemistry. In collaboration with NCI’s Chemical Biology Consortium (CBC), we carried out a structure-based drug discovery campaign with a triazole hit which emerged from the high-throughput screen. To support compound optimization, we developed multiple orthogonal assays, including biochemical methyltransferase counter-assays to assess compound activity and selectivity, a CRISPR-based HiBiT tagged NNMT cell line for CETSA-based cell engagement assays and a cellular functional mass spectrometry-based assay that measures the production of the NNMT enzymatic product 1-methylnicotinamide (1-MNA). Our medicinal chemistry optimization campaign led to the development of inhibitors with low nanomolar cellular potency, oral bioavailability and dose-dependent inhiibtion of NNMT in mice. The lead compound ‘960 is the most potent inhibitor of human NNMT disclosed to date but its potency against mouse NNMT is right shifted (hNNMT IC50 12 nM, mNNMT IC50 240 nM). In MC38 tumor bearing mice, topical treatment with ‘960 significantly reduced tumor growth compared to vehicle. The less active enantiomer ‘961 (hNNMT IC50 1.36 μM, mNNMT IC50 21.5 μM) serves as a chemical negative control in most of our studies. In an EO771-LMB tumor model, ‘960 pre-treatment before IV injection of cancer cells significantly reduced lung metastasis burden. Current efforts are ongoing to generate mice with human NNMT to establish the accurate dose for efficacy in cancer mouse models. Citation Format: Samarjit Patnaik, Janna Heide, Ke Kong, Mark Eckert, Maria Allega, Min Shen, Hongmao Sun, Jonathan Shrimp, Quinlin Hanson, Ken Cheng, Andrew Flint, William J. Moore, Matthew Hall, Gordon M. Stott, Ernst Lengyel. Development of potent orally bioavailable inhibitors of nicotinamide N-methyl transferase [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 3757.
Abstract 6072: Engineering and preclinical development of an anti-TROP2/PD-L1 bispecific antibody drug conjugate (ADC) for enhanced anti-tumor efficacy
Authors: Chuan Chen, Liang Tian, Chenpeng Su, Dandan Liu, Jiyuan Tian, Yujuan Li, Bing Yang, Yongxin Shan, Xiaoqian Chen, Jian Peng, Zhenping Zhu
Journal: Cancer Research (2025)

Abstract Human trophoblast cell surface antigen 2 (TROP2) and programmed death ligand 1 (PD-L1) are often overexpressed in a variety of human cancers. Both anti-PD-L1 antibodies and TROP2-based antibody drug conjugates (ADCs) have shown significant clinical benefit, and a number of these agents, including atezolizumab and durvalumab (both anti-PD-L1 antibodies) and sacituzumab govitecan (an anti-TROP2-SN38 ADC), have been approved by the US FDA for certain cancer indications. The efficacy of these agents is, however, often limited by the unwanted on-target/off-tumor toxicities and the emergence of resistance of tumor cells. In this study, we engineered a humanized bispecific antibody (bsAb) simultaneously targeting both TROP2 and PD-L1 and produced several drug conjugates utilizing various linkers and cytotoxic payloads. The bsAb ADC binds efficiently to tumor cells that express either or co-express both TROP2 and PD-L1, trigger rapid ADC internalization, and induce potent tumor killing activity. Further, the bsAb ADC also effectively blocks PD1/PD-L1 interaction, and in parallel, induce PD-L1 internalization and down-regulation on tumor cell surface, resulting in significantly enhanced T cell activation for tumor cell killing. In multiple xenografted tumor models, the bsAb ADC demonstrated greater tumor inhibitory activity than their respective monospecific parent antibody ADCs. Taken together, our findings support further development of this bsAb ADC for the treatment of multiple TROP2- and/or PD-L1-expressing cancers, and of those patients who are refractory and/or resistant to TROP2 or PD-L1 single target-based therapies. Citation Format: Chuan Chen, Liang Tian, Chenpeng Su, Dandan Liu, Jiyuan Tian, Yujuan Li, Bing Yang, Yongxin Shan, Xiaoqian Chen, Jian Peng, Zhenping Zhu. Engineering and preclinical development of an anti-TROP2/PD-L1 bispecific antibody drug conjugate (ADC) for enhanced anti-tumor efficacy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 6072.
Abstract 6095: T-PureTM: A bispecific antibody cocktail for T cell isolation from human blood, enabling simple and affordable point-of-care CAR-T manufacturing
Authors: Ying Xiong, Yanping Xie, Ann Wang, Victor Bass, Matt Addington-hall, Oxana Slessareva, Yang Liu, Tony Luo, Ibeawuchi Oparaocha, Kathy Schonely, Kara Anlauf, Megan Forrest, Jacqueline Schaeffer, Shashi Koduru, Andrew Worden, Mike Kadan, Boro Dropulic, Zhongyu Zhu
Journal: Cancer Research (2025)

Abstract Adoptive immunotherapy with engineered T cells, especially chimeric antigen receptor (CAR) T cells, has revolutionized the treatment of leukemia, lymphoma, and multiple myeloma. However, the high production costs of CAR-T therapy severely limit patient access. To address this challenge, we developed T-pureTM, a proprietary bispecific antibody cocktail for isolating T cells from human blood through negative selection. The Bi-specific antibody cocktail selectively links red blood cells (RBCs) to key marker antigens on non-target cells, such as B cell, NK cell, Monocytes, and granulocytes, allowing easy and cost-effective separation using Ficoll density gradient centrifugation. By isolating T cells without engaging their surface receptors, this approach avoids inadvertent activation of isolated T cells, while also preserving cell types like γδ T cells, which show promise for their anti-tumor potential. Additionally, the depletion process efficiently removes CD19-positive cancer cells and can be tailored to eliminate T cell subpopulations like T regulatory (T-reg) cells that could compromise CAR-T efficacy in clinical application. This versatile antibody cocktail can also be adapted to isolate other cell types, such as NK cells, B cells, and monocytes for various biomedical applications. Designed for cost-effective clinical manufacturing, our GMP grade T-pure reagents are commercially available to academic and industry partners for preclinical and clinical applications. This work highlights the ongoing innovation in CAR-T manufacturing and the potential for optimizing cell selection protocols to enhance efficacy and lower the cost of cell therapies. Citation Format: Ying Xiong, Yanping Xie, Ann Wang, Victor Bass, Matt Addington-hall, Oxana Slessareva, Yang Liu, Tony Luo, Ibeawuchi Oparaocha, Kathy Schonely, Kara Anlauf, Megan Forrest, Jacqueline Schaeffer, Shashi Koduru, Andrew Worden, Mike Kadan, Boro Dropulic, Zhongyu Zhu. T-PureTM: A bispecific antibody cocktail for T cell isolation from human blood, enabling simple and affordable point-of-care CAR-T manufacturing [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 6095.
Abstract 3746: Genomic landscape in metaplastic breast cancer: Results from the AACR GENIE Database
Authors: Blessie Elizabeth Nelson, Jacqueline Nkrumah, Mohammed Gouda, Jordi Rodon, Sarina Piha-Paul, Bora Lim
Journal: Cancer Research (2025)

Abstract Background: Metaplastic breast cancer (MPBC) is a rare, heterogeneous invasive subtype of breast cancer with predominant triple negative receptor status. MPBC typically has limited treatment options and portends to a poorer prognosis. Here, we focus on understanding the genomic landscape that may aid in discovering effective targeted therapies for MPBC. Methods: Using the data from the American Association for Cancer Research Project Genomics Evidence Neoplasia Information Exchange (AACR GENIE) Cohort v16.1 database, we cataloged genetic alterations in metaplastic breast cancer. ​​ Results: We identified 258 cases from 267 samples of metaplastic breast cancer. The median age known at the time of sequencing was 59 (range 25-87). Gender analysis suggested a predominantly female distribution (96.5%, n=249) compared to male (1.6%, n=4). Race/ethnicity included 62% (n=160) White, Others 25% (n=64), 6.6% (n=17) Asian, 5.8% (n=15) African American, 5.0% (n=13) Hispanic, and Native American 0.8% (n=2). Most frequent genomic alterations in the overall cohort were found in TP53 (57%, 152) with 30.3%; 81 missense and 11.2%; 30 nonsense mutations and 9%; 24 frameshift deletions; PIK3CA (34%, 90) with 30%; 80 missense mutations and 3%; 8 in frame deletions; KMT2C (17.1%, 37); KMT2D (10.8%, 31); FAT1 (13%; 29); TERT (12%; 28); KMT2D (10.5%; 25); PTEN (9.4%; 25); SPEN (10%; 22); PIK3R1 (8.3%; 20); RB1 (6.7%; 18); NF1 (7.1%; 17) genes. The most TP53 frequent mutations were seen in R248Q (14.5%; 9), R175H (8.1%; 5), Q192* (4.8%; 3), H193R (4.8%; 3), and R273C (4.8%; 3). The most frequent PIK3CA mutations were seen in H1047R (55.1%; 49), followed by E545K (14.6%; 13), Q546R (4.5%; 4), E542K (2.2%; 2), and C420R (1.1%; 1). The average mutation count was 5.0. TP53 and PIK3CA aberrations were mutually exclusive (p=0.043). Most frequent copy number alterations (deletions 66%; 181 and amplifications 34%; 93) were seen in AGO2 (22.9%, 16) RAD21 (20.4%, 19); RECQL4 (19.8%, 20); MYC (19.4%, 21); EXT1 (19%; 3); CDKN2A (14%; 15) and CDKN2B (13%; 14) genes. Conclusion: Our analysis provides valuable insights into the genetic landscape of this aggressive and rare cancer subtype. Overall, these findings support further investigation into targeted therapies for MPBC that address its unique genetic landscape, potentially improving outcomes for patients facing limited treatment options and poor prognosis. Citation Format: Blessie Elizabeth Nelson, Jacqueline Nkrumah, Mohammed Gouda, Jordi Rodon, Sarina Piha-Paul, Bora Lim. Genomic landscape in metaplastic breast cancer: Results from the AACR GENIE Database [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 3746.
Abstract 7065: Desmocollin3 and tumor immune infiltrate: A bioinformatics evaluation
Authors: Bakulesh M. Khamar, Sanjay V. Malhotra
Journal: Cancer Research (2025)

Abstract Introduction: Desmocollin-3 (DSC3), a transmembrane glycoprotein is expressed in various cancers like squamous lung, head &amp; neck, Cervical, Melanoma, bladder cancer etc. DSC3 is also a predictive biomarker for efficacy of Mycobacterium w (Mw) vaccine, a heat-killed suspension of a non-pathogenic mycobacterium. It induces a DSC3-specific cell-mediated (CD8+ T cells) immune response and considered to be a barrier for immune infiltrate. Efficacy of anti-PD1/PDl1 therapy depends on tumor infiltrating immune cells. Present study focuses on the key immune genes and their relationship with DSC3 gene. Materials and Methods: DSC3 and other genes encoding various immune functions (Table) were evaluated across 17 cancers using cBioPortal TCGA PAN CANCER data set. For correlation between DSC3 and other immune genes, samples with a positive Z score for DSC3 or upper quartile DSC3 (lower of two) were used. Results: DSC3 expression in Squamous lung cancer, Cancer cervix, head &amp; neck, melanoma, colorectal cancer, mesothelioma and adenocarcinoma stomach were found to have major impact with negative Z score for majority of CD8, M1, Th1, T exhaust, M2 and Th2 genes suggesting lower infiltration of immunosuppressive and immunostimulant immune cells. Following genes had negative Z scores in all seven cancers:1. CD8 group: CD8A, CD8B, GZMA, GZMB, GZMK, GZMM, PRF1, TBX12. M1 group: CCL15, CCL20, CCR7, CXCL10, FCGR1BP, CYBB, Il15, 1l15RA3. Th1 group: CXCR3, IL274. Texhast; BTLA, LAG3, PDCD1, SLAMF6, TIGIT 5. Th2: BATF, CXCR6, SOCS1 6. M2: CD163Similar finding of lower magnitude were also seen in bladder cancer, ovarian cancer, thyroid cancer, pancreatic cancer, adenocarcinoma lung, uterine cancer, testicular germ cell cancer, renal cancer, sarcoma, hepatocellular cancer. Conclusion: DSC3 expressing tumours are likely to have lower TIL (immunostimulant as well immunosuppressive) and may not be ideal candidate for check point inhibitors. Citation Format: Bakulesh M. Khamar, Sanjay V. Malhotra. Desmocollin3 and tumor immune infiltrate: A bioinformatics evaluation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 7065.
Abstract 5916: Investigating the antiproliferative effects of green synthesized silver and gold unfunctionalized nanoparticles on cervical cancer cell lines
Authors: Nrateng Tsotetsi, Lesetja Motadi, Mpho Choene
Journal: Cancer Research (2025)

Abstract Background: Across the globe cervical cancer is the 4th most common cancers affecting women; however, the burden of CC is greater in Sub-Saharan Africa as it ranks 2nd common cancer and number one cause of deaths. Although cervical cancer can be successfully treated if diagnosed early, many women are diagnosed in advanced stages, rendering current treatments ineffective. Metal nanoparticles which are commonly used in optic imaging of tumours have shown potential as anti-tumour agents when either used alone or in combination with other chemotherapy drugs. Therefore, this study investigated the anti-proliferative potential of Cannabis Sativa synthesized Ag and Au NPs using Me-180 and HeLa human cell lines. Methods: Metallic Ag and Au nanoparticles were synthesized biologically using Cannabis sativa plant. The cell viability was assessed following treatment with Au and Ag NP of 0-200µg/ml in some cases in combination with Hexaxim (DTaP-IPV-HB-Hib) vaccine using alamar blue assayall subsequent assays in combination with. Following treatment, ATP levels, pyruvate kinase activity, effector caspase 3/7 and mitochondrial toxicity were evaluated, to further investigate induction of apoptosis, annexin V staining, Hoechst staining, and deoxyribonucleic acid (DNA) fragmentation analysis by agarose gel electrophoresis were performed. Through siRNA, P53, MDM2 and RBBP6 genes were silenced, and the amplification of pro-apoptotic and cell cycle genes were assed using qPCR. Results: The Me-180 IC50 values of 24.17 ug/m 28, 35ug/ml and 37.31 ug/ml for AgNP, AuNP and C. Sativa respectively. The IC50 of HeLa were 35.43, 39.02 and 41.45 ug/ml for AgNP, AuNP and C. Sativa respectively. The increased mitochondrial toxicity was consistent with the decrease in ATP levels, pyruvate kinase activity and the decrease in effector caspase 3/7 in NPs treatments. With C. sativa caspase 3/7 activity and ATP levels slightly increased with decreased mitochondrial toxicity. Hoechst staining and DNA fragmentation analysis showed apoptotic bodies in Me-180. In all silenced C. sativa treatments, the expression of P53 remained unchanged with increase expressions of Bax and Bak-1 in Me-180 cell lines whereas in HeLa all were decreased. Conclusion: Me-180 cell lines that expresses wild-type P53 was more sensitive to apoptosis induction by C. sativa. The increased Bax/Bax expression suggest intrinsic pathway of apoptosis supported by decreased ATP and mitochondrial activity. Citation Format: Nrateng Tsotetsi, Lesetja Motadi, Mpho Choene. Investigating the antiproliferative effects of green synthesized silver and gold unfunctionalized nanoparticles on cervical cancer cell lines [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 5916.
Abstract 5110: Solid stress reduces synaptic density and neuronal activity via hypoxia-induced reactive gene expression programs in glioblastoma
Authors: Maksym Zarodniuk, Anna Wenninger, Jihaeng Lee, Julian Najera, Jack Markillie, Bianca Batista, Christopher Patzke, Meenal Datta
Journal: Cancer Research (2025)

Abstract Mass effect in central nervous system pathologies poses a significant clinical challenge. This phenomenon, characterized by the compression and deformation of neural tissue from space-occupying lesions, can lead to debilitating neurological symptoms. In glioblastoma, we have shown previously that compressive solid stresses from the growing tumor are correlated with significantly worse neurological performance and survival in patients. While edema is often measured as a prognostic biomarker, it fails to consistently predict neurological deficits; conversely, solid stress correlates with functional impairments and reduced cerebral blood flow. In this study, we explored the direct effects of solid stress on human induced pluripotent stem cell (hiPSC)-derived neurons using an in vitro compression system. Our results reveal that solid stress decreases synaptic puncta and neuronal excitability by activating hypoxia response and pro-apoptotic programs in neurons. We further show that compression upregulates reactive gene expression programs in astrocytes and microglia, contributing to neuroinflammation. These findings illuminate the critical role of solid stress in glioblastoma, offering new insights into its potential contribution to neurodegeneration. Citation Format: Maksym Zarodniuk, Anna Wenninger, Jihaeng Lee, Julian Najera, Jack Markillie, Bianca Batista, Christopher Patzke, Meenal Datta. Solid stress reduces synaptic density and neuronal activity via hypoxia-induced reactive gene expression programs in glioblastoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 5110.
Abstract 5644: Identification of alexidine as a novel small molecule inhibitor of TAZ-TEAD interaction in breast cancer cell migration
Authors: Anni Ge, Yawei Hao, Kody Klupt, Zongchao Jia, Yuhong Du, Haian Fu, Xiaolong Yang
Journal: Cancer Research (2025)

Abstract Breast cancer (BC) is the most commonly diagnosed malignancy in women, with a risk of distant metastases after a primary tumor has developed. Despite concerns about the aggressive pathology of metastatic BC (MBC), current medical interventions inadequately address the clinical needs of MBC patients, resulting in worse outcomes compared to other BC cases. This highlights the critical requirement for more effective therapies for MBC patients. The Hippo pathway is often dysregulated during tumorigenesis, and one of the Hippo signaling transducers, Transcriptional co-activator with PDZ-binding motif (TAZ), is involved in multiple stages of BC development. Since TAZ mostly interacts with TEAD to facilitates its function, targeting TAZ-TEAD interaction may be a treatment approach for MBC patients. To identify small molecules that inhibit TAZ-TEAD interaction, we established a highly sensitive NanoLuc and TR-FRET applicable biosensor for quantifying protein-protein interaction of TAZ and TEAD. Using this biosensor, we performed an ultra-high throughput screen (uHTS) and identified alexidine as a novel TAZ-TEAD binding inhibitor capable of suppressing TAZ-induced migration and invasion in BC cells. In conclusion, we describe a robust method for screening inhibitors of TAZ-TEAD interaction, contributing to the development of effective cancer treatments. Citation Format: Anni Ge, Yawei Hao, Kody Klupt, Zongchao Jia, Yuhong Du, Haian Fu, Xiaolong Yang. Identification of alexidine as a novel small molecule inhibitor of TAZ-TEAD interaction in breast cancer cell migration [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 5644.