Cancer letters最新文献

{"title":"CHK1/2 as a potential therapeutic target in Neurofibromatosis type 2 Schwannomas.","authors":"Dorothy Benton, Ramil Khusnutdinov, Mariia Buts, Mariia Dmitrieva, Daniela Araiza-Olivera, Cristina Uribe-Alvarez, Jonathan Chernoff","doi":"10.1016/j.canlet.2026.218886","DOIUrl":"https://doi.org/10.1016/j.canlet.2026.218886","url":null,"abstract":"<p><p>The Merlin protein, encoded by the tumor suppressor gene Neurofibromatosis type II (NF2), serves as a linker between the actin cytoskeleton, the plasma membrane receptors, and other intracellular signaling molecules. While there is a basic understanding of how Merlin regulates oncogenic signaling pathways, current targeted therapies have yet to demonstrate consistent clinical efficacy. Using a library of protein kinase inhibitors, we found that NF2-null Schwann cells (SCs) were uniquely sensitive to prexasertib, a drug that targets the DNA damage response pathway kinases CHK1/2 (Checkpoint Kinase 1 and 2). NF2-null SC proliferation was also sensitive to small molecule inhibitors of CHK1/2 downstream effectors. At baseline, NF2-null SCs have increased RAC1 activity, elevated levels of reactive oxygen species (ROS) production, and higher levels of DNA damage. Exposing NF2-null SCs to DNA damaging agents such as doxorubicin or carboplatin, alone or in combination with prexasertib, further decreased their proliferation. Consistent with this idea, suppressing RAC1 or NOX2 activity with small molecule inhibitors, decreased ROS production and restored resistance to prexasertib in NF2-null hSCs, suggesting that active RAC1 and high ROS render NF2-null hSC uniquely vulnerable to DNA damage. Furthermore, restoring NF2 expression in NF2-null Schwann cells restored their resistance to prexasertib, reduced RAC1 activity, and lowered levels of ROS and DNA damage. The intrinsic elevation of RAC1, ROS, and DNA damage in NF2-null hSCs suggest that inhibiting DNA damage response pathways might be clinically useful in patients with NF2-null schwannomas.</p>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":" ","pages":"218886"},"PeriodicalIF":11.8,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149227333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Next-Generation CAR-Macrophage Therapies: Design Principles and Advances in Cancer Treatment.","authors":"Weihua Wang, Songyue Guo, Qihui Chu, Qian Yu, Mariano Romero, Xiaoya Shi, Shuo Shan, Chao Gao, Shunli Fu, He Ren","doi":"10.1016/j.canlet.2026.218899","DOIUrl":"https://doi.org/10.1016/j.canlet.2026.218899","url":null,"abstract":"<p><p>Macrophages possess intrinsic tumor-homing and tissue-infiltrating abilities, performing various effector functions, including phagocytosis and antigen presentation. These properties make chimeric antigen receptor macrophages (CAR-M) a promising approach to overcoming major barriers in cellular therapy for solid tumors. This review systematically compares and critically evaluates key design variables that determine the therapeutic activity and clinical feasibility of CAR-M, including CAR architecture, macrophage source, gene-delivery method, and manufacturing strategy. We also discuss emerging engineering approaches tailored to macrophage biology, including macrophage-adapted intracellular signaling, regulation of phagocytic checkpoints, metabolic and phenotypic reprogramming, and combinations with immunomodulatory therapies. Their therapeutic potential and translational boundaries are assessed based on current preclinical evidence and early clinical findings. Notably, the major barriers to clinical translation are shifting from focusing solely on antitumor potency to addressing system-level challenges involving cell source and product consistency, in vivo expansion and persistence, phenotypic stability, off-target toxicity, and scalable manufacturing. Therefore, we propose that next-generation CAR-M development should move beyond conventional optimization of the CAR construct to multidimensional engineering centered on macrophage biology. Coordinated optimization of receptor signaling, antigen recognition, cell-state control, delivery, and safety mechanisms will be essential to balance efficacy, persistence, safety, and manufacturability. This review provides an integrated framework for the rational design and clinical evaluation of CAR-M and the development of next-generation CAR-M cellular therapy platforms.</p>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":" ","pages":"218899"},"PeriodicalIF":11.8,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149227357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatial Plasticity and Multidirectional Crosstalk of Cancer-Associated Adipocytes in Therapy-Remodeled Niches.","authors":"Jingdong Xie, Tingting Cai, Neng Wang, Wei Zhang, Shaowen Zhong, Hong Qian, Yaxiao Liu, Dingwei Ye, Zhiyu Wang, Hailin Tang","doi":"10.1016/j.canlet.2026.218911","DOIUrl":"https://doi.org/10.1016/j.canlet.2026.218911","url":null,"abstract":"<p><p>Cancer-associated adipocytes (CAAs) are increasingly recognized as active and heterogeneous components of the tumor microenvironment. Initially defined as tumor-adjacent adipocytes characterized by lipid depletion, reduced expression of mature adipocyte markers, and inflammatory activation, CAAs are now understood to encompass a spectrum of context-dependent states. These states are shaped by anatomical location, preexisting adipocyte properties, tumor-derived signals, and therapeutic exposure. Through metabolic exchange, paracrine signaling, direct cell contact, extracellular-vesicle communication, and matrix remodeling, CAAs influence tumor-cell plasticity, metastatic colonization, immune dysfunction, stromal organization, and treatment response. In turn, signals from tumor, immune, and stromal cells continuously reshape adipocyte identity and function, placing CAAs within reciprocal multicellular networks. This review examines the evolving criteria used to identify CAAs, their lineage origins and plasticity, their spatial organization, and their interactions with tumor, immune, and stromal compartments. The contribution of CAAs to therapeutic adaptation is also discussed, together with potential intervention points involving CAA-derived outputs and the metabolic dependencies induced in recipient cells. Finally, major methodological challenges are considered. Adipocyte-resolved profiling, lineage tracing, spatial multiomics, lipid flux analysis, and physiologically relevant models will be needed to distinguish transient remodeling from stable state transitions and to identify context-specific therapeutic vulnerabilities.</p>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":" ","pages":"218911"},"PeriodicalIF":11.8,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149227316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early transcriptional divergence and spatial remodeling toward immune activation and evasion shape lung adenocarcinoma precancer evolution.","authors":"Jian-Rong Li, Bo Zhu, Yuhao Chi, Hong Chen, Pingjun Chen, John V Hemaych, Yanhua Tian, Xin Hu, Kang Qin, Monique B Nilsson, Jianjun Zhang, Chao Cheng","doi":"10.1016/j.canlet.2026.218915","DOIUrl":"https://doi.org/10.1016/j.canlet.2026.218915","url":null,"abstract":"<p><p>Tumor heterogeneity is a universal feature of cancer and may arise as early as precancer stages during lung adenocarcinoma evolution, yet the emergence of aggressive transcriptional programs remains incompletely understood. Here, we integrated spatial transcriptomics with single-cell RNA sequencing to characterize inter- and intratumoral heterogeneity across hyperplasia, adenoma, and invasive adenocarcinoma (IAC) in a genetically engineered mouse model (129S4/Sv Kras^LSL-G12D/+). Disease progression was accompanied by coordinated remodeling of epithelial, stromal, and immune compartments, along with dynamic changes in proliferation, immune response, and metabolic pathways. Notably, lesions of the same histological stage exhibited substantial transcriptional heterogeneity. By quantifying dedifferentiation states, we identified a subset of adenomas that had already diverged toward highly proliferative and metabolically active programs despite lacking invasive features. These lesions were further marked by early chromosome 6 amplification, whose corresponding human ortholog signature recapitulated aggressive proliferation-associated programs in early-stage human lung adenocarcinoma. Spatial analyses further revealed pronounced intratumoral heterogeneity within IAC, with tumor core regions showing increased proliferation and metabolism but reduced immune signaling compared to peripheral regions. In addition, immune checkpoint gene expression in T cells was transiently elevated at the hyperplasia stage, suggesting early immune modulation prior to overt malignancy. Together, these findings indicate that aggressive transcriptional divergence can emerge early during lung adenocarcinoma evolution and that spatial organization critically shapes tumor and immune programs before and after invasion.</p>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":" ","pages":"218915"},"PeriodicalIF":11.8,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149227354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Four clinical lenses for interpreting the Chinese guideline for pediatric craniopharyngioma.","authors":"Yi Lin, Zhixiong Lin","doi":"10.1016/j.canlet.2026.218903","DOIUrl":"https://doi.org/10.1016/j.canlet.2026.218903","url":null,"abstract":"","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":" ","pages":"218903"},"PeriodicalIF":11.8,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149227306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LRH-1 is a novel regulator of neutrophil-driven immune responses within the tumor microenvironment.","authors":"Yu Wang, Bryan Duong, Sam Keeley, Natalia Krawczynska, Shruti V Bendre, Claire P Schane, Dhanya Pradeep, Desirée Rodríguez-Casiano, Erin Weisser, Nadia Cobo Vuilleumier, Sabrina Akter, Lara Kockaya, Yifan Fei, Anasuya Das Gupta, Hashni Epa Vidana Gamage, Adam T Nelczyk, Sisi He, Hannah Kim, Jin Young Yoo, Jenny Drnevich, Aiman Soliman, Zeynep Madak-Erdogan, Benoit R Gauthier, Erik R Nelson","doi":"10.1016/j.canlet.2026.218910","DOIUrl":"https://doi.org/10.1016/j.canlet.2026.218910","url":null,"abstract":"<p><p>Plasma cholesterol is correlated with worse outcomes in breast and ovarian cancer. Prior work indicates that myeloid immune cells are highly responsive to cholesterol metabolism. Interestingly, Liver Receptor Homolog-1 (LRH-1, or NR5A2), a key transcriptional regulator of cholesterol homeostasis is highly expressed in neutrophils and is associated with increased survival time. However, the roles of LRH-1 within neutrophils remain unclear. We therefore focused on how LRH-1 influences neutrophil behaviors relevant to cancer. Small molecule ligands for LRH-1 regulated neutrophil migration towards cancer cells. Phagocytosis was also regulated by LRH-1 ligands, the extent being dependent on type of bait (e. coli vs. cancer cells). In T cell co-cultures, neutrophils pretreated with an LRH-1 agonist promoted greater T cell expansion, particularly in CD4⁺ cells, while LRH-1 inhibition suppressed this response. NETosis is a known trigger of recurrence from dormancy and subsequent tumor growth. Importantly LRH-1 activation reduced NETosis, while treatment with an antagonist or inverse agonist enhanced NETosis, likely through altered reactive oxygen species. Treatment of mice with an inverse agonist of LRH-1 increased the growth of mammary tumors in a NET-dependent manner. Mice harboring dormant D2.0R mammary cancer lesions treated with an LRH-1 inverse agonist exhibited earlier tumor recurrence and enhanced metastatic progression. In contrast, treatment with BL001, a small chemical LRH-1 agonist, delayed recurrence in D2.0R-grafted mice. These findings reveal that LRH-1 is a novel regulator of neutrophil-driven immune responses within the tumor microenvironment. LRH-1 is thus a promising therapeutic target to suppress the progression of breast and ovarian cancer.</p>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":" ","pages":"218910"},"PeriodicalIF":11.8,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149227362","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"AMPK signaling in cancer: Molecular insights and therapeutic opportunities.","authors":"Weiwei Jiang, Peiqiang Yan, Jingchao Wang, Xutong Xue, Daoyuan Huang, Li Chen, Yuelin Yang, Hiroyuki Inuzuka, Wenyi Wei","doi":"10.1016/j.canlet.2026.218912","DOIUrl":"https://doi.org/10.1016/j.canlet.2026.218912","url":null,"abstract":"<p><p>AMP-activated protein kinase (AMPK) is a highly conserved serine/threonine kinase regarded as an indispensable energy sensor during metabolic stress, coordinating diverse biological processes, including glycolysis, the tricarboxylic acid (TCA) cycle, mitochondrial dynamics, and multiple stress-responsive signaling pathways. Growing evidence shows that dysregulated AMPK signaling plays closely linked roles in tumorigenesis. Depending on the context, AMPK signaling can suppress or promote tumor growth. Mechanistically, dysregulated AMPK kinase activity contributes to metabolic reprogramming, mitochondrial dysfunction, and epigenetic alterations, all recognized hallmarks of cancer. Consequently, targeting AMPK signaling has emerged as a promising strategy for cancer therapy. In this review, we summarize the molecular mechanisms regulating AMPK signaling, discuss its dual functions in tumor biology, highlight recent advances in AMPK-targeted therapeutic strategies, and address current challenges and future perspectives for the clinical translation of AMPK-targeted cancer therapy.</p>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":" ","pages":"218912"},"PeriodicalIF":11.8,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149227367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting CDC7 Overcomes Gemcitabine Resistance in Cholangiocarcinoma by Inducing Cellular Senescence.","authors":"Rong Xiao, Jing Han Hong, Peili Wang, Yi Zhong, Zhiwei Ye, Ziyu Hao, JiuPing Gao, Yu Jiang, Yu Peng, Siyu Chen, Jiaxin Yin, Lizhen Liu, Qiqing Xiong, Yaojun Zhang, Mei Li, Jianfeng Chen, Jing Tan","doi":"10.1016/j.canlet.2026.218902","DOIUrl":"https://doi.org/10.1016/j.canlet.2026.218902","url":null,"abstract":"<p><p>Advanced-stage cholangiocarcinoma (CCA) frequently develops resistance to chemotherapy, highlighting an urgent unmet need for novel therapeutic strategies. Here, we analyzed 16 pairs of CCA and adjacent non-tumor tissues, and demonstrated that dysregulation of the cell cycle machinery is a hallmark of CCA, closely associated with chemoresistance and poor prognosis. Targeting aberrant cell cycle regulation therefore represents a promising approach to improve current treatment outcomes. We identify the CDC7 inhibitor XL413 as an effective agent capable of re-sensitizing gemcitabine-resistant tumors across multiple preclinical models of CCA. Mechanistic analyses, including transcriptomic profiling, reveal that combination therapy activates senescence-associated pathways, with therapeutic efficacy is mediated via a ROS-DNA damage-senescence cascade. Notably, synergistic induction of cellular senescence is observed in CCA cells upon co-treatment with a CDC7 inhibitor and gemcitabine. Collectively, these findings provide robust preclinical evidence supporting the combination of gemcitabine and CDC7 inhibitors as a viable therapeutic strategy to enhance the clinical management of CCA.</p>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":" ","pages":"218902"},"PeriodicalIF":11.8,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149227284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"UBL3 Modification Reduces Nuclear POLE Levels to Potentiate Antitumor Immunity in Aero-upper Digestive Squamous Cell Carcinomas.","authors":"Zhonglan Dong, Wenbai Huang, Lei Zhang, Qianru Guo, Xiaobei Zhang, Yang Yang, Xudong Wang, Zhihua Liu, Yiqing Yin, Gang Ma","doi":"10.1016/j.canlet.2026.218905","DOIUrl":"https://doi.org/10.1016/j.canlet.2026.218905","url":null,"abstract":"<p><p>While immune checkpoint inhibitors (ICIs) have revolutionized treatment of the patients with aero-upper digestive squamous cell carcinomas (SCCs), including esophageal squamous cell carcinoma (ESCC) and lung squamous cell carcinoma (LUSC), only a subset of patients benefit from ICIs, therefore entailing exploration of the mechanisms to regulate treatment responsiveness. POLE, as a subunit of DNA polymerase ε, possesses 3'-5' proofreading activity, and its mutations have been associated with favourable response to ICIs in several solid tumors. However, post-translational modification (PTM) of POLE and its impact on the therapeutic efficacy of ICIs are unknown. Here, this study demonstrates that ubiquitin-like protein 3 (Ubl3), whose expression is markedly downregulated in SCCs, covalently binds to Pole, reduces nuclear Pole levels, triggers DNA damage, and activates cGAS-STING signaling pathway. Notably, Ubl3 modification of Pole significantly primes the local immune microenvironment to mitigate the growth of murine aero-upper digestive SCC cells and boost the efficacy of αPD-1 treatment in vivo. Single-cell RNA sequencing (scRNA-seq) analysis further revealed that UBL3 expression is positively correlated with better clinical outcomes in a cohort of ESCC patients receiving neoadjuvant chemotherapy combined with αPD-1. Together, our findings unravel UBL3 modification as a novel PTM mechanism governing subcellular location of POLE and its influence on immunotherapy responsiveness, thus making UBL3 modification as a promising immunomodulatory approach to enhance immunotherapy efficacy in patients with aero-upper digestive SCCs.</p>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":" ","pages":"218905"},"PeriodicalIF":11.8,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149227343","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CDK9 Degradation Suppresses Gastroesophageal Cancer Growth and Overcomes Radiation Resistance through Chromatin Remodeling and YAP1/TEAD Downregulation.","authors":"Yan-Ting Yann Zhang, Mikel Ghelfi, Yu Xue, Haiying Chen, Gennaro Calendo, Generosa Grana, Yuan Li, Dipti Athavale, Curt Balch, Xiaodan Yao, Woonbok Chung, Zhenning Wang, Vladimir Khazak, Francis Spitz, Jean-Pierre Issa, Jia Zhou, Shumei Song","doi":"10.1016/j.canlet.2026.218916","DOIUrl":"https://doi.org/10.1016/j.canlet.2026.218916","url":null,"abstract":"<p><p>Gastroesophageal adenocarcinoma (GEAC) remains a highly aggressive malignancy with limited effective targeted therapies. Cyclin-dependent kinase 9 (CDK9), a key regulator of transcriptional elongation, has been implicated in oncogenic processes across multiple cancer types; however, its functional role and therapeutic potential in GEAC remain poorly defined. In this study, we systematically investigated CDK9 expression, function, and therapeutic targeting in GEAC, with particular emphasis on its interaction with the YAP/TEAD signaling axis. Immunohistochemical analysis of primary GEAC tumors and patient-derived xenografts revealed elevated CDK9 expression, which correlated with poor patient survival. Mechanistic studies using immunofluorescence and co-immunoprecipitation demonstrated a reciprocal regulatory interaction between CDK9 and YAP1, promoting transcriptional programs associated with tumor progression and radiation resistance. We developed novel CDK9-targeting proteolysis-targeting chimeras (PROTACs) and identified YX0597 as a potent CDK9 degrader. YX0597 effectively suppressed RNAP II Ser2 phosphorylation (RNAP II P-S2) and downregulated oncogenic drivers, including MCL-1. Functionally, CDK9 degradation markedly inhibited GEAC cell proliferation, invasion, and tumor sphere formation, with enhanced efficacy in radiation-resistant cells. Integrated RNA sequencing and ATAC sequencing revealed that CDK9 degradation increased chromatin accessibility, reactivated epigenetically silenced genes, and profoundly suppressed YAP/TEAD transcriptional activity. These coordinated transcriptional and epigenetic alterations disrupted oncogenic homeostasis, resulting in broad cytotoxicity. Importantly, co-targeting CDK9 and YAP/TEAD signaling produced strong synergistic antitumor effects in vitro and in vivo. Collectively, our findings identify CDK9 as a critical oncogenic driver in GEAC and highlight CDK9 degradation, particularly in combination with YAP/TEAD inhibition, as a promising therapeutic strategy for refractory GEAC.</p>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":" ","pages":"218916"},"PeriodicalIF":11.8,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149227375","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}