Molecular Carcinogenesis最新文献

{"title":"HGF/c-Met Promotes Breast Cancer Tamoxifen Resistance Through the EZH2/HOTAIR-miR-141/200a Feedback Signaling Pathway.","authors":"Xiaofeng Lai, Yuan Zhang, Mengyang Li, Shentong Yu, Shuiliang Wang, Shenghang Zhang, Huimin Niu, Li Chen, Xiaopeng Lan, Jian Zhang, Suning Chen","doi":"10.1002/mc.23878","DOIUrl":"10.1002/mc.23878","url":null,"abstract":"<p><p>Tamoxifen is one of the most frequently used endocrine medications for the treatment of estrogen receptor-positive (ER + ) breast cancer (BC). Unfortunately, tamoxifen resistance (TR) brings more challenges to the clinical treatment, and the mechanisms of TR have not yet been fully clarified. HGF/c-Met is closely associated with cancer metastasis, but whether it is involved in TR remains unclear. In our study, we found that the activation of HGF/c-Met was crucial for TR maintenance. Synergistic interaction with HOTAIR and EZH2 accelerated HGF expression by repressing miR-141/200a. Additionally, HGF/c-Met activated NF-κB, forming a positive feedback loop of EZH2/HOTAIR-miR-141/200a-HGF/c-Met-NF-κB. Our findings indicated that HGF/c-Met functioned as an important biomarker for TR, and HGF/c-Met inhibition provided a novel approach to TR treatment.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"769-783"},"PeriodicalIF":3.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143033684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LINC01305 and LAD1 Co-Regulate CTTN and N-WASP Phosphorylation, Mediating Cytoskeletal Reorganization to Promote ESCC Metastasis.","authors":"Hang Yang, Rong Xiong, Ruolan Zhang, Shan Sun, Yingjie Pan, Quanneng Zhao, Jun Bie, Yi Luo, Guiqin Song, Kang Liu","doi":"10.1002/mc.23885","DOIUrl":"10.1002/mc.23885","url":null,"abstract":"<p><p>Esophageal squamous cell carcinoma (ESCC) is prone to metastasis and is a leading cause of mortality. The cytoskeleton is closely related to cell morphology and movement; however, little research has been conducted on ESCC metastasis. In this study, we found that the anchoring filament protein ladinin 1 (LAD1) specifically binds to LINC01305 for co-regulating the level of modulating cortactin proteins (CTTN) and neuronal Wiskott-Aldrich syndrome protein (N-WASP) phosphorylation, which mediates cytoskeletal reorganization and affects the metastasis of ESCC cells. Additionally, LINC01305 and LAD1 jointly promoted the epithelial-mesenchymal transition (EMT) process by activating the phosphoinositide-3-kinase-protein kinase B (PI3K/AKT) signaling pathway. Moreover, LINC01305 and LAD1 were related to the late clinical stage and lymph node metastasis of ESCC. Our study demonstrated that LINC01305 and LAD1 are major determinants of ESCC dissemination and revealed a novel molecular mechanism of cytoskeletal reorganization that controls ESCC metastasis. Trial Registration: N/A.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"756-768"},"PeriodicalIF":3.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11890417/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143008767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Transcription Factor ATF2 Accelerates Clear Cell Renal Cell Carcinoma Progression Through Activating the PLEKHO1/NUS1 Pathway.","authors":"Zheng Lu, Jinge Xu, Junyu Li","doi":"10.1002/mc.23868","DOIUrl":"10.1002/mc.23868","url":null,"abstract":"<p><p>Clear cell renal cell carcinoma (ccRCC) is a common malignant cancer with high mortality rate. Activating transcription factor 2 (ATF2) and pleckstrin homology domain containing O1 (PLEKHO1) were reported to participate in numerous cancers. However, their roles and the detailed mechanisms in ccRCC development remain largely unknown. RT-qPCR and western blot were used to measure the levels of PLEKHO1, ATF2, and nuclear undecaprenyl pyrophosphate synthase 1 (NUS1). Cell proliferation, apoptosis, invasion, migration and stemness were evaluated using CCK-8 assay, flow cytometry, transwell invasion assay, wound-healing assay and sphere formation assay, respectively. Dual-luciferase reporter assay was conducted to verify the relationship between ATF2 and PLEKHO1. The interaction between PLEKHO1 and NUS1 was proved by Co-IP assay. Xenograft models were utilized to evaluate the tumorigenic capability of ccRCC cells upon PLEKHO1 knockdown. PLEKHO1, ATF2 and NUS1 expression were significantly elevated in ccRCC, and PLEKHO1 might be a prognosis biomarker for ccRCC. PLEKHO1 depletion significantly inhibited cell proliferation, invasion, migration, stemness, and induced cell apoptosis in ccRCC cells. ATF2 activated PLEKHO1 expression via transcription regulation, and PLEKHO1 overexpression could reverse the suppressive effects of ATF2 knockdown on the malignant behaviors of ccRCC cells. Moreover, PLEKHO1 directly bound to NUS1, and PLEKHO1 depletion markedly restrained ccRCC progression through targeting NUS1 in vitro and in vivo. Our findings suggested that ATF2 transcriptionally activated PLEKHO1 to promote the development of ccRCC via regulating NUS1 expression.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"617-628"},"PeriodicalIF":3.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142952061","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TRIM36 Inhibits the Development of AOM/DSS-Induced Colitis-Associated Colorectal Cancer by Promoting the Ubiquitination and Degradation of GRB7.","authors":"Ju Wu, Zhengbo Yang, Xi Chen, Shuangshuang Hou, Nanbo Li, Yaoyuan Chang, Jiajun Yin, Jian Xu","doi":"10.1002/mc.23871","DOIUrl":"10.1002/mc.23871","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is among the most common cancer types for both sexes. Tripartite motif 36 (TRIM36) has been reported to be aberrantly expressed in several cancer types, suggesting its involvement in cancer progression. However, the role of TRIM36 in the colorectal carcinogenesis remain unknown. In our in vivo experiments, we investigated the role of TRIM36 in AOM/DSS-induced colitis-associated carcinogenesis using TRIM36-knockout (TRIM36 KO) mice. Subsequently, we overexpressed and knocked down TRIM36 expression in two CRC cell lines to further confirm the role of TRIM36 in vitro. The UALCAN database revealed a significant decrease in TRIM36 levels in CRC tissues, including colon adenocarcinoma and rectum adenocarcinoma. A significant correlation was observed between TRIM36 levels and the histological subtype, individual cancer stage, and nodal metastasis status. The downregulation of TRIM36 in CRC tissues was further confirmed using our own collected clinical specimens. Low expression of TRIM36 was found to be associated with unfavorable overall survival and recurrence-free survival in CRC. TRIM36 KO promoted inflammation, inhibited autophagy, and facilitated the development of AOM/DSS-induced CRC. TRIM36 overexpression inhibited proliferation, migration, and invasion, while activated autophagy in CRC cells. TRIM36 directly bound to and regulated the ubiquitination of GRB7 protein. The tumor-suppressive role of TRIM36 in CRC cells was mediated by GRB7. The TRIM36/GRB7 axis may represent a promising therapeutic target for the treatment of CRC.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"668-679"},"PeriodicalIF":3.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142971484","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Computed Tomography-Based Radiomics and Genomics Analyses for Survival Prediction of Stage III Unresectable Non-Small Cell Lung Cancer Treated With Definitive Chemoradiotherapy and Immunotherapy.","authors":"Yuxin Geng, Tianwen Yin, Yikun Li, Kaixing He, Bingwen Zou, Jinming Yu, Xiao Sun, Tao Zhang, Feifei Teng","doi":"10.1002/mc.23883","DOIUrl":"10.1002/mc.23883","url":null,"abstract":"<p><p>The standard therapy for locally unresectable advanced non-small cell lung cancer (NSCLC) is comprised of chemoradiotherapy (CRT) before immunotherapy (IO) consolidation. However, how to predict treatment outcomes and recognize patients that will benefit from IO remain unclear. This study aimed to identify prognostic biomarkers by integrating computed tomography (CT)-based radiomics and genomics. Specifically, our research involved 165 patients suffering from unresectable Stage III NSCLC. Cohort 1 (IO following CRT) was divided into D1 (n = 74), D2 (n = 32), and D3 (n = 26) sets, and the remaining 33 patients treated with CRT alone were grouped in D4. According to the CT images of primary tumor regions, radiomic features were analyzed through the least absolute shrinkage and selection operator (LASSO) regression. The Rad-score was figured out to forecast the progression-free survival (PFS). According to the Rad-score, patients were divided into high and low risk groups. Next-generation sequencing was implemented on peripheral blood and tumor tissue samples in the D3 and D4 cohorts. The maximum somatic allele frequency (MSAF) about circulating tumor DNA levels was assessed. Mismatch repair and switching/sucrose non-fermenting signaling pathways were significantly enriched in the low-risk group compared to the high-risk group (p < 0.05). Moreover, patients with MSAF ≥ 1% and those showing a decrease in MSAF after treatment significantly benefited from IO. This study developed a radiomics model predicting PFS after CRT and IO in Stage III NSCLC and constructed a radio-genomic map to identify underlying biomarkers, supplying valuable insights for cancer biology.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"733-743"},"PeriodicalIF":3.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11890425/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143008764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adipose Secreted Slit2-C Suppresses Breast Cancer Invasion Through cAMP/PKA Transition.","authors":"Haolin Hu, Kexuan Li, Lifei Han, Yangyang Gu, Zhenling Ji","doi":"10.1002/mc.23915","DOIUrl":"https://doi.org/10.1002/mc.23915","url":null,"abstract":"<p><p>Adipose tissue activation plays a positive role in breast cancer outcomes, consistent with the improved outcomes observed through exercise and weight loss mediated by brown and beige fat. However, the underlying mechanism of this process remains unclear. C-terminal fragment of Slit2 (Slit2-C), endogenously produced by brown or beige adipose cells could increase the thermogenic process of adipose cells in autocrine and paracrine manners. Here, we show that Slit2-C dominantly reduces breast cancer cell invasion through cAMP/PKA mediated inhibition of epithelial-mesenchymal transition. In the process, Slit2-C plays a vital role as a positive regulator of cAMP/PKA signaling in breast cancer. As a result, the overexpression of Slit2-C leads to a reduction in cancer cell invasion and an increase in both the epithelial phenotype and thermogenesis. Besides, inhibiting PKA phosphorylation with H89 reversed the reduced invasion process seen in human breast cancer cells overexpressing Slit2-C, which suggests that the effect of Slit2-C on reducing invasion is mediated through the activation of PKA signaling. Taken together, our study suggests that the modulation of the Slit2-C/cAMP/PKA axis might be a potential targeting therapeutic intervention in aggressive breast cancers.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143764490","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypoxia Promotes Malignant Progression of Colorectal Cancer by Inducing POSTN⁺ Cancer-Associated Fibroblast Formation.","authors":"Jian Qin, Shangshang Hu, Yuhan Chen, Mu Xu, Qianni Xiao, Jinwei Lou, Muzi Ding, Huiling Sun, Tao Xu, Yuqin Pan, Shukui Wang","doi":"10.1002/mc.23882","DOIUrl":"10.1002/mc.23882","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is one of the most common malignancies. Hypoxia can promote the occurrence and development of CRC. However, how hypoxia regulates the CRC immune microenvironment needs to be further explored. The bulk RNA sequencing data and clinicopathological information of CRC patients were enrolled from The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) databases. The single-cell RNA sequencing (scRNA-seq) datasets of CRC were collected from and analyzed from the GEO database and the ArrayExpress database. The score of the hypoxia gene set was estimated using the \"ssGSEA\" algorithm in the \"GSVA\" R package. The functional characteristics of CAF subtypes were studied by bioinformatics analysis and in vitro experiments, and a prognostic model was constructed based on machine learning correlation. Hypoxia is associated with poor prognosis in CRC patients. Periostin (POSTN) + Fib is a cancer-associated fibroblast (CAF) closely associated with hypoxia, and high infiltration of POSTN + Fib is associated with adverse outcomes in overall survival (OS) and relapse-free survival (RFS) in CRC patients. Hypoxia can induce POSTN expression and secretion in CAFs. Hypoxia-induced increase of POSTN expression in CAFs can significantly promote the migration and proliferation of CRC cells. Hypoxia-induced increase of POSTN expression in CAFs can significantly promote the proliferation and migration of CRC cells. The POSTN⁺Fib Hypoxia-Related Risk Model (PFHRM) can predict the survival and immunotherapy response of CRC patients. Our study identified a POSTN⁺Fib cell subpopulation closely associated with hypoxia, which promotes the malignant progression of CRC. The development of PFHRM provides a theoretical basis for improving patient survival and prognosis.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"716-732"},"PeriodicalIF":3.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143008766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glutamine, Serine and Glycine at Increasing Concentrations Regulate Cisplatin Sensitivity in Gastric Cancer by Posttranslational Modifications of KDM4A.","authors":"Junhao Fu, Yuqi Ni, Yuqing Hu, Wanfen Tang, Jianfei Fu, Yue Wang, Shian Yu, Wenxia Xu","doi":"10.1002/mc.23881","DOIUrl":"10.1002/mc.23881","url":null,"abstract":"<p><p>Gastric cancer is a common digestive system tumor with a high resistance rate that reduces the sensitivity to chemotherapy. Nutrition therapy is an important adjuvant approach to favor the prognosis of gastric cancer. Dietary amino acids contribute greatly to gastric cancer progression by mediating tumor gene expressions, epigenetics, signal transduction, and metabolic remodeling. In the present study, 20 types of amino acids were screened and glutamine, glycine and serine were identified as the critical regulators of cisplatin (DDP) sensitivity in gastric cancer cells. Moreover, KDM4A acetylation drove the reduced chemotherapy sensitivity in gastric cancer cells by maintaining protein stability and activating DNA repair ability when the concentrations of glutamine (Gln), serine (Ser), and glycine (Gly) decreased. Conversely, Gln/Ser/Gly at increasing concentrations stimulated ubiquitination degradation of KDM4A, which in turn elevated the sensitivity of gastric cancer cells to chemotherapy. Our findings unveiled the role of amino acid nutrition in regulating chemotherapy sensitivity of gastric cancer and the underlying mechanism, thus providing a scientific basis for expanding the clinical significance of nutrition therapy for gastric cancer patients.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"703-715"},"PeriodicalIF":3.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143008765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PTPN2 Expression in Hypopharyngeal Squamous Cell Carcinoma and Its Clinical Significance.","authors":"Xue Li, Hua Feng, Hengheng Jian, Shilan Zhang, Zhaoli Liao Tai, Xiaoyu Wang, Fengzhi Lu, Zuwei Liu, Tingchao Li, Yangsong Ji, Youxuan Liu, Zuxia Ma","doi":"10.1002/mc.23872","DOIUrl":"10.1002/mc.23872","url":null,"abstract":"<p><p>This study aimed to explore PTPN2 expression levels in Hypopharyngeal Squamous Cell Carcinoma (HPSCC) tissues and their relationship with the clinical characteristics and prognosis of HPSCC patients. PTPN2, a protein tyrosine phosphatase, has recently emerged as a promising target for cancer immunotherapy, and in many previous studies, PTPN2 may have a significant role in the growth, differentiation, metabolism and immune response of head and neck malignant tumors. In this study, PTPN2 expression in Head and Neck Squamous Cell Carcinoma (HNSCC) and other cancer tissues was analyzed using datasets derived from the Sangerbox database. Furthermore, we analyzed data on PTPN2 mRNA levels across various clinical stages of HNSCC (I, II, III, and IV), which was extracted from the Gene Expression Profiling Interactive Analysis (GEPIA) database. Clinical data from patients who underwent surgical resection for hypopharyngeal malignancies at the Third Affiliated Hospital of Zunyi Medical University between January 2013 and January 2024 were also obtained and analyzed. The patient specimens were categorized into two groups (the HPSCC tumor and paracarcinoma tissue groups) and compared for PTPN2 expression using Immunohistochemistry (IHC), Immunofluorescence (IF), and Western Blot (WB) analyses. According to the results, HPSCC patients were mostly elderly males with a history of tobacco and alcohol abuse. Furthermore, the most common site of HPSCC onset was piriform sinuses, and the disease was often diagnosed in the middle or advanced stages. Additionally, HPSCC tissues exhibited PTPN2 upregulation. Moreover, PTPN2 expression did not correlate significantly with patients' gender, Smoking Index (SI), alcohol abuse, tumor diameter, Hypertension (HTN), diabetes, and M stage. On the other hand, it correlated with HPSCC patients' T-stage, N-stage, Overall Survival (OS), and clinical stage. Based on these findings, we deduced that high PTPN2 expression could be involved in HPSCC patients' poor prognosis.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"629-637"},"PeriodicalIF":3.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142952057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic Potential of IL-37 in Cervical Cancer: Suppression of Tumour Progression and Enhancement of CD47-Mediated Macrophage Phagocytosis.","authors":"Yuan Feng, Lianlian Feng, Bingyu Wang, Teng Zhang, Baoxia Cui","doi":"10.1002/mc.23855","DOIUrl":"10.1002/mc.23855","url":null,"abstract":"<p><p>As a promising therapeutic approach, immunotherapy is being extensively investigated in cervical cancer. Although immunotherapy has been validated to improve progression-free survival and overall survival in clinical trials, the overall response rate for cervical cancer remains inadequate, necessitating further improvement. Interleukin (IL)-37, an emerging immunomodulator, exhibits antitumour potentials by inhibiting tumour progression and regulating tumour-associated macrophage recognition. We found a significant downregulation of IL-37 expression in cervical cancer, correlated with a poor prognosis. Moreover, the upregulation of IL-37 expression exhibited a suppressive effect on various tumorigenic processes, suppressing the proliferation, invasion, migration, apoptosis and angiogenesis of tumour cells. We also found that the upregulation of IL-37 suppressed cluster of differentiation 47 (CD47) expression in tumour cells via suppression of the signal transducer and activator of transcription 3 (STAT3) expression and phosphorylation, thereby enhancing macrophage recognition and phagocytosis to tumour cells, ultimately reducing immune evasion. Overall, our study highlighted the crucial role of IL-37 in antitumour efficacy and downregulating the expression of CD47 in tumour cells to reduce immune evasion, suggesting the potential of IL-37 as a prognostic biomarker in cervical cancer and offering innovative therapeutic strategies to improve cancer treatment outcomes.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"425-439"},"PeriodicalIF":3.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11814915/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142770380","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}