Cancer letters最新文献

{"title":"Intersection between lung cancer and neuroscience: Opportunities and challenges","authors":"Xiang Xiao ,&nbsp;Lingli Huang ,&nbsp;Ming Li ,&nbsp;Quanli Zhang","doi":"10.1016/j.canlet.2025.217701","DOIUrl":"10.1016/j.canlet.2025.217701","url":null,"abstract":"<div><div>Lung cancer, which has the highest morbidity and mortality rates worldwide, involves intricate interactions with the nervous system. Research indicates that the nervous system not only plays a role in the origin of lung cancer, but also engages in complex interactions with cancer cells through neurons, neurotransmitters, and various neuroactive molecules during tumor proliferation, invasion, and metastasis, especially in brain metastases. Cancer and its therapies can remodel the nervous system. Despite advancements in immunotherapy and targeted therapies in recent years, drug resistance of lung cancer cells after treatment limits improvements in patient survival and prognosis. The emergence of neuroscience has created new opportunities for the treatment of lung cancer. However, it also presents challenges. This review emphasizes that a deeper understanding of the interactions between the nervous system and lung cancer, along with the identification of new therapeutic targets, may lead to significant advancements or even a revolution in treatment strategies for patients with lung cancer.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"621 ","pages":"Article 217701"},"PeriodicalIF":9.1,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143802606","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":"KAP1 promotes gastric adenocarcinoma progression by activating Hippo/YAP1 signaling via binding to HNRNPAB","authors":"Shumei Song ,&nbsp;Yibo Fan ,&nbsp;Gengyi Zou ,&nbsp;Longfei Huo ,&nbsp;Janani Kumar ,&nbsp;Yuan Li ,&nbsp;Ruiping Wang ,&nbsp;Enyu Dai ,&nbsp;Jiankang Jin ,&nbsp;Ailing W. Scott ,&nbsp;Shan Shao ,&nbsp;Melissa Pool Pizzi ,&nbsp;Jody V. Vykoukal ,&nbsp;Hiryuki Katayama ,&nbsp;Samir Hanash ,&nbsp;George A. Calin ,&nbsp;Xing Zhang ,&nbsp;Min Gyu Lee ,&nbsp;Zhenning Wang ,&nbsp;Yuan-Hung Lo ,&nbsp;Shilpa S. Dhar","doi":"10.1016/j.canlet.2025.217695","DOIUrl":"10.1016/j.canlet.2025.217695","url":null,"abstract":"<div><div>Gastric adenocarcinoma (GAC) remains a significant global health challenge, with over a million new cases annually. Peritoneal carcinomatosis (PC), detected in ∼20% of cases at diagnosis and ∼45% later, is uniformly fatal, with limited treatment options. This study investigated the role of KAP1 in GAC progression, focusing on its interaction with YAP1 and cancer stemness traits. Analysis of over 596 primary GACs and 72 PC samples revealed that high nuclear KAP1 expression correlates with poor prognosis. <em>KAP1</em> knockdown reduced oncogenic activity and stemness traits in GAC cells. Mechanistically, KAP1 positively regulates YAP1 transcription by binding to its promoter and reducing H3K27ac levels. Mass spectrometry identified an interaction between KAP1 and HNRNPAB, further modulating YAP1 signaling. Expression of the KRAB domain of ZFP568 without its DNA-binding zinc fingers inhibited both KAP1 and YAP1 expression, significantly reducing colony formation and tumor growth in vivo. Additionally, emerging antisense oligonucleotides (ASOs) targeting KAP1 or YAP1 effectively suppressed mouse tumor progression. These findings establish KAP1 as a critical driver of tumor progression in GAC through YAP1 regulation and HNRNPAB interaction, highlighting its potential therapeutic target. This study advances our understanding and offers a preclinical framework to improve outcomes for GAC.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"621 ","pages":"Article 217695"},"PeriodicalIF":9.1,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143794524","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":"Ferroptosis meets inflammation: A new frontier in cancer therapy","authors":"Hu Liu ,&nbsp;Hui Xue ,&nbsp;Qian Guo ,&nbsp;Xutong Xue ,&nbsp;Lixue Yang ,&nbsp;Kaijun Zhao ,&nbsp;Yu'e Liu","doi":"10.1016/j.canlet.2025.217696","DOIUrl":"10.1016/j.canlet.2025.217696","url":null,"abstract":"<div><div>Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has emerged as a critical player in cancer pathogenesis. Concurrently, inflammation, a key biological response to tissue injury or infection, significantly influences cancer development and progression. The interplay between ferroptosis and inflammation represents a promising yet underexplored area of research. This review synthesizes recent advances in understanding the molecular mechanisms governing their interaction, emphasizing how ferroptosis triggers inflammatory responses and how inflammatory mediators, such as TNF-α, regulate ferroptosis through iron metabolism and lipid peroxidation pathways. Key molecular targets within the ferroptosis-inflammation axis, including GPX4, ACSL4, and the NF-κB signaling pathway, offer therapeutic potential for cancer treatment. By modulating these targets, it may be possible to enhance ferroptosis and fine-tune inflammatory responses, thereby improving therapeutic outcomes. Additionally, this review explores the broader implications of targeting the ferroptosis-inflammation interplay in disease treatment, highlighting opportunities for developing innovative strategies to combat cancer. By bridging the gap in current knowledge, this review provides a comprehensive resource for researchers and clinicians, offering insights into the therapeutic potential of this intricate biological relationship.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"620 ","pages":"Article 217696"},"PeriodicalIF":9.1,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143791327","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":"Gap-App: A sex-distinct AI-based predictor for pancreatic ductal adenocarcinoma survival as a web application open to patients and physicians","authors":"Anuj Ojha ,&nbsp;Shu-Jun Zhao ,&nbsp;Basil Akpunonu ,&nbsp;Jian-Ting Zhang ,&nbsp;Kerri A. Simo ,&nbsp;Jing-Yuan Liu","doi":"10.1016/j.canlet.2025.217689","DOIUrl":"10.1016/j.canlet.2025.217689","url":null,"abstract":"<div><div>In this study, using RNA-Seq gene expression data and advanced machine learning techniques, we identified distinct gene expression profiles between male and female pancreatic ductal adenocarcinoma (PDAC) patients. Building on this insight, we developed sex-specific 3-year survival predictive models alongside a single comprehensive model. Despite smaller sample sizes, the sex-specific models outperformed the general model. We further refined our models by selecting the most important features from the initial models. The refined sex-specific predictive models achieved higher accuracy and consistently outperformed the refined comprehensive model, highlighting the value of sex-specific analysis. To ensure robustness, all refined sex-specific models were calibrated and then evaluated using an independent dataset. Random Forest models emerged as the most effective predictors, achieving accuracies of 90.33 % for males and 90.40 % for females on the training dataset, and 81.25 % for males and 89.47 % for females on the independent test dataset. These top-performing models were integrated into Gap-App, a web application that leverages individual gene expression profiles and sex information for personalized survival predictions. As the first online tool bridging complex genomic data with clinical application, Gap-App facilitates more precise, individualized cancer care, marking a significant step in personalized prognosis prediction. This study underscores the importance of incorporating sex differences in predictive modeling and sets the stage for the shift from traditional one-size-fits-all to more personalized and targeted medicine. The Gap-App service is freely available for patients and clinicians at <span><span>www.gap-app.org</span><svg><path></path></svg></span>.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"622 ","pages":"Article 217689"},"PeriodicalIF":9.1,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143794514","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":"TRAIL induces cytokine production via the NFkB2 pathway promoting neutrophil chemotaxis and neutrophil-mediated immune-suppression in triple negative breast cancer cells","authors":"Manjari Kundu ,&nbsp;Yoshimi E. Greer ,&nbsp;Alexei Lobanov ,&nbsp;Lisa Ridnour ,&nbsp;Renee N. Donahue ,&nbsp;Yeap Ng ,&nbsp;Shashi Ratnayake ,&nbsp;Karley White ,&nbsp;Donna Voeller ,&nbsp;Sarah Weltz ,&nbsp;Qingrong Chen ,&nbsp;Stephen J. Lockett ,&nbsp;Maggie Cam ,&nbsp;Daoud Meerzaman ,&nbsp;David A. Wink ,&nbsp;Roberto Weigert ,&nbsp;Stanley Lipkowitz","doi":"10.1016/j.canlet.2025.217692","DOIUrl":"10.1016/j.canlet.2025.217692","url":null,"abstract":"<div><div>Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a potential cancer therapeutic that induces apoptosis in cancer cells while sparing the non-malignant cells in preclinical models. However, its efficacy in clinical trials has been limited, suggesting unknown mechanisms modulating TRAIL activity in patients. We hypothesized that TRAIL treatment elicits transcriptional changes in triple negative breast cancer (TNBC) cells that alter the immune milieu. RNAseq analysis of MDA-MB-231 cells along with validation in additional cell lines demonstrated that TRAIL induced cytokines such as CXCLs 1, 2, 3, 8,11 and IL-6, which are known to modify neutrophil function. Mechanistically, TRAIL dependent induction of the cytokines was predominantly mediated by death receptor 5, caspase-8 and the non-canonical NFKB2 pathway. These cytokines produced by TRAIL-treated TNBC cells enhanced chemotaxis of normal human donor isolated neutrophils. Using TNBC xenograft models<em>,</em> TRAIL induced activation of NFkB2 pathway, cytokine production and increased neutrophil recruitment into the tumors. Moreover, preincubation of neutrophils in supernatants from TRAIL-treated TNBC cells significantly impaired neutrophil function as measured by reduced respiratory burst and cytotoxic effect against TNBC cells. Transcriptomic analysis of neutrophils incubated with either TRAIL alone or supernatant of TRAIL-treated TNBC cells revealed increased expression of inflammatory cytokines, immune modulatory genes, immune checkpoint genes, and genes implicated in delayed neutrophil apoptosis. Functional studies showed that these neutrophils suppress T cell proliferation and augment Treg suppressive phenotype. Collectively, our study demonstrates a novel role of TRAIL-induced NFKB2-dependent cytokine production that promotes neutrophil chemotaxis and neutrophil- mediated immune suppression.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"620 ","pages":"Article 217692"},"PeriodicalIF":9.1,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitigating ambient RNA and doublets effects on single cell transcriptomics analysis in cancer research","authors":"Madhu Sudhana Saddala ,&nbsp;Midhuna Sree Chittineni ,&nbsp;Niharitha Hariharan ,&nbsp;Anijah L. Rias ,&nbsp;Ganji Purnachandra Nagaraju","doi":"10.1016/j.canlet.2025.217693","DOIUrl":"10.1016/j.canlet.2025.217693","url":null,"abstract":"<div><div>In cancer biology, where understanding the tumor microenvironment at high resolution is vital, ambient RNA contamination becomes a considerable problem. This hinders accurate delineation of intratumoral heterogeneity, complicates the identification of potential biomarkers, and decelerates advancements in precision oncology. To solve this problem, several computational approaches are created to determine the ambient RNA contribution from scRNA-seq datasets. Techniques like SoupX and DecontX assist in assessing and eliminating ambient RNA contamination from primary gene expression profiles. Practical solutions like CellBender employ deep learning techniques to concurrently address ambient RNA contamination and background noise, offering a contemporary end-to-end strategy for data preparation. This high-quality, reliable data enables clinicians and researchers to make effective decisions that will help ensure interventions are rooted in reproducible evidence, giving hope for developing more effective targeted therapies.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"620 ","pages":"Article 217693"},"PeriodicalIF":9.1,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787972","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":"MK2 promotes p16 negative head and neck cancer migration, invasion, and metastasis","authors":"Deri Morgan ,&nbsp;Dakota DD. Okwuone ,&nbsp;Kiersten L. Berggren ,&nbsp;Levi Arnold ,&nbsp;Alyssa Schmidt ,&nbsp;Colby Spiess ,&nbsp;Hannah Smith ,&nbsp;Ravi Yada ,&nbsp;Nathan Hendrikse ,&nbsp;Rashna Madan ,&nbsp;Devin Shrock ,&nbsp;Chris Lominska ,&nbsp;Mengjia Hu ,&nbsp;Malgorzata Witek ,&nbsp;Steven Soper ,&nbsp;Yuting Lin ,&nbsp;Hao Gao ,&nbsp;Dennis J. McCance ,&nbsp;Sufi M. Thomas ,&nbsp;David Beebe ,&nbsp;Gregory N. Gan","doi":"10.1016/j.canlet.2025.217690","DOIUrl":"10.1016/j.canlet.2025.217690","url":null,"abstract":"<div><div>For patients with locally advanced, p16-negative head and neck squamous cell carcinoma (HNSCC), overall survival remains poor due to primary locoregional failure and distant metastasis following curative therapy. We aimed to understand how MAPKAPK2 (MK2) regulates HNSCC tumor cell migration and invasion, important first steps in cancer metastases. The TCGA database and HNSCC tissue microarrays were used to show that MK2 expression was associated with more advanced cancers and faster cancer recurrence rates. We observed that silencing of tumor MK2 in human cell lines (shRNA) caused a significant reduction in tumor cell migration-invasion in a complex HNSCC microphysiologic system used to recapitulate the tumor microenvironment. Murine cells (Ly2) with MK2 silenced (CRISPR-Cas9) also demonstrated reduced migration and invasion using 2D and 3D monoculture cell migration-invasions assays. Ly2 cells are orthotopic p16-negative murine metastatic cells that spontaneously metastasize, and we observed that MK2 inhibition via genetic (Cas9/CRISPR) or pharmacologic (PF-3644022) methods led to a significant reduction in the number of circulating tumor cells, fewer lymph node and lung metastases, and MK2 inhibited mice showed improved overall survival. Our findings suggest that HNSCC MK2 regulates tumor cell migration-invasion and may be a promising therapeutic target to reduce metastases.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"622 ","pages":"Article 217690"},"PeriodicalIF":9.1,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787973","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":"Apigenin inhibits recurrent bladder cancer progression by targeting VEGF-β","authors":"Zhen-Duo Shi ,&nbsp;Ying Liu ,&nbsp;Zi-Qi Tao ,&nbsp;Liu Chao ,&nbsp;Zheng-Guo Zhang ,&nbsp;Fang Sun ,&nbsp;Fu-Kang Yuan ,&nbsp;Qing-Fang Ma ,&nbsp;Zong-Yun Li ,&nbsp;Zhe-Sheng Chen ,&nbsp;Shao-Yuan Wu ,&nbsp;Cong-Hui Han","doi":"10.1016/j.canlet.2025.217676","DOIUrl":"10.1016/j.canlet.2025.217676","url":null,"abstract":"<div><div>Bladder cancer is a major global health concern with high incidence and mortality rates. Both muscle-invasive bladder cancer (MIBC) and recurrent non-muscle-invasive bladder cancer (NMIBC) present significant challenges in treatment. Apigenin, a naturally occurring flavonoid, has shown promise in inhibiting the growth of bladder cancer cells, however, its therapeutic mechanism remains unclear. Single-cell RNA sequencing (scRNA-seq) data analysis and drug target screening were performed. Differentially expressed genes (DEGs) and potential therapeutic targets of apigenin were identified. Molecular docking was utilized to evaluate the binding affinity between apigenin and VEGF-β. <em>In vitro</em> assays were conducted to evaluate the association of VEGF-β and apigenin. Drug target screening identified 51 common targets between apigenin and bladder cancer, with VEGF-β emerging as a dominant gene. Molecular docking confirmed a high binding affinity between apigenin and VEGF-β. VEGF-β was significantly upregulated in fibroblasts from recurrent bladder cancer, correlating with increased tumor malignancy. Enhanced cell communication in VEGF-β-positive fibroblasts contributed to tumor progression. <em>In vitro</em> experiments demonstrated that VEGF-β promotes tumor cell proliferation, migration, and invasion. Apigenin significantly inhibits bladder cancer progression by targeting VEGF-β. The upregulation of VEGF-β in fibroblasts from recurrent bladder cancer highlights its potential as a diagnostic marker and therapeutic target. This study underscores the promise of apigenin as a chemopreventive and therapeutic agent for recurrent bladder cancer.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"620 ","pages":"Article 217676"},"PeriodicalIF":9.1,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ADAM12 promotes temozolomide resistance in glioblastoma by activating the TNF-α - NF-κB pathway","authors":"Chunchao Cheng ,&nbsp;Longtao Cui ,&nbsp;Xiaoteng Cui ,&nbsp;Qi Zhan ,&nbsp;Jiasheng Ju ,&nbsp;Biao Hong ,&nbsp;Yanping Huang ,&nbsp;Yaqing Ding ,&nbsp;Hanyi Xu ,&nbsp;Tian Qiu ,&nbsp;Chunsheng Kang ,&nbsp;Xiaomin Liu ,&nbsp;Qixue Wang ,&nbsp;Liang Zeng","doi":"10.1016/j.canlet.2025.217684","DOIUrl":"10.1016/j.canlet.2025.217684","url":null,"abstract":"<div><div>Development of temozolomide (TMZ) resistance is a critical factor contributing to a poor prognosis in glioma patients. TMZ resistance is also closely associated with the phosphorylation level of NF-κB, yet targeted inhibition of NF-κB activity in glioma can be leveraged to overcome TMZ resistance. ADAM12, a protein significantly overexpressed in glioma cells, is implicated in the pathogenesis and progression of glioma, yet its role in the development of TMZ resistance is completely understood. We found that knockdown of ADAM12 was shown to arrest the glioma cell cycle, enhance apoptosis, inhibit DNA damage repair mechanisms, and sensitize glioma cells to TMZ. Targeting ADAM12 <em>in vivo</em> was found to increase the sensitivity of glioma cells to TMZ. Survival analysis indicated that ADAM12 serves as a prognostic marker for TMZ treatment. Using ELISA and protein interaction predictions via docking simulation, we identified the TNF-α shedding function of ADAM12 as a critical regulator of glioma progression. Furthermore, in glioma cell lines with unmethylated MGMT, the knockdown of ADAM12 enhanced sensitivity to TMZ by inhibiting the TNF-α/NF-κB pathway and reducing MGMT expression. In all, these results demonstrated that ADAM12 aids in shedding of membrane-bound TNF-a to drive TMZ resistance in glioma.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"620 ","pages":"Article 217684"},"PeriodicalIF":9.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143779248","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":"CAR T-Cell therapy in chronic myeloid leukemia patients with lymphoid blast crisis: A multicenter clinical analysis","authors":"Yujie Liu ,&nbsp;Yuqing Tu ,&nbsp;Zhiling Yan ,&nbsp;Jinyan Xiao ,&nbsp;Biqi Zhou ,&nbsp;Tianhui Liu ,&nbsp;Lijuan Qi ,&nbsp;Depei Wu ,&nbsp;Yongxian Hu ,&nbsp;Yang Cao ,&nbsp;Yang Xu","doi":"10.1016/j.canlet.2025.217688","DOIUrl":"10.1016/j.canlet.2025.217688","url":null,"abstract":"","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"621 ","pages":"Article 217688"},"PeriodicalIF":9.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143779249","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}