Molecular Carcinogenesis最新文献

{"title":"LUCAT1 Mediates MYC-Targeted Suppression of Squamous Cell Carcinoma.","authors":"Yifan Wen, Shuo Liu, Zhen Qin, Jingshu Cai, Lingfei Jia, Xin Peng","doi":"10.1002/mc.70117","DOIUrl":"https://doi.org/10.1002/mc.70117","url":null,"abstract":"<p><p>Small-molecule MYC inhibitors that directly target MYC are considered attractive cancer therapeutics. Here, we demonstrate that LUCAT1, a long noncoding RNA, serves as a critical mediator of MYC-driven signaling in head and neck squamous cell carcinoma (HNSCC). The LUCAT1 expression is significantly downregulated in HNSCC cells following treatment with the MYC inhibitor MYCi975. Mechanically, MYC transcriptionally activates LUCAT1 through direct promoter binding, facilitating oncogenic functions. Clinically, elevated LUCAT1 is linked to cervical lymph node involvement in HNSCC and is associated with unfavorable patient outcomes. Functional studies in vitro demonstrated that LUCAT1 knockdown inhibits proliferation, migratory capacity, and invasive activity of HNSCC cells. This suppression also extends to the in vivo growth of tumors. Importantly, LUCAT1 overexpression attenuates the MYCi975 anti-tumor effects on HNSCC, confirming its role in therapeutic resistance. These results establish LUCAT1 as both a biomarker of aggressive disease and a mediator of MYC-driven oncogenesis, proposing LUCAT1 as a candidate synergistic therapeutic target in the treatment of HNSCC with MYC inhibition.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147639405","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":"BTG1 Acts as a Critical Tumor Suppressor Link Between HDAC Inhibition and β-Catenin Signaling Suppression in Diffuse Large B-Cell Lymphoma.","authors":"Kuai Yu, Deyang Guo, Qinhong Li, Qiuyu Su, Zhao Yang, Shuai Wu, Surong Deng","doi":"10.1002/mc.70113","DOIUrl":"https://doi.org/10.1002/mc.70113","url":null,"abstract":"<p><p>Diffuse large B-cell lymphoma (DLBCL) is an aggressive hematologic malignancy with complex pathogenesis and unsatisfactory clinical outcomes. Although histone deacetylase inhibitors (HDACis) have demonstrated therapeutic potential, the molecular mechanisms linking epigenetic regulation to key oncogenic signaling pathways remain incompletely understood. In this study, B-cell translocation gene 1 (BTG1) was identified as a critical tumor suppressor that is epigenetically upregulated by HDAC inhibition in DLBCL cells. Increased BTG1 expression was found to be both necessary and sufficient for HDAC inhibitor-induced cell cycle arrest and autophagy, whereas BTG1 silencing attenuated these effects. Mechanistically, BTG1 suppressed β-catenin signaling by inhibiting the formation of the β-catenin/TCF4 transcriptional complex, leading to reduced expression of downstream targets, including c-Myc and Cyclin D1. Activation of β-catenin signaling reversed the tumor-suppressive effects of BTG1, supporting the functional importance of this pathway. In vivo, the antitumor efficacy of HDAC inhibition in DLBCL xenografts was dependent on the BTG1/β-catenin axis. Collectively, these findings identify a regulatory link between HDAC inhibition and β-catenin signaling mediated by BTG1, providing mechanistic insight into HDAC inhibitor-based therapy in DLBCL.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147639410","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":"RETRACTION: Arsenic Exposure Through Drinking Water Leads to Senescence and Alteration of Telomere Length in Humans: A Case-Control Study in West Bengal, India.","authors":"","doi":"10.1002/mc.70091","DOIUrl":"10.1002/mc.70091","url":null,"abstract":"<p><strong>Retraction: </strong>D. Chatterjee, P. Bhattacharjee, T. J. Sau, J. K. Das, N. Sarma, A. K. Bandyopadhyay, S. S. Roy, and A. K. Giri, \"Arsenic Exposure Through Drinking Water Leads to Senescence and Alteration of Telomere Length in Humans: A Case-Control Study in West Bengal, India,\" Molecular Carcinogenesis 54, no. 9 (2015): 800-809, https://doi.org/10.1002/mc.22150. The above article, published online on 24 March 2014 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by Wiley Periodicals LLC. The retraction has been agreed upon following concerns raised by a third-party regarding duplication between Figures 1a and 1b. Further investigation revealed multiple instances of similar background patterns in the western blots shown in Figures 1d and 4b. The authors provided an alternative image to correct Figure 1b; however evidence of duplication was also identified in this replacement. Given the nature of the concerns, the Publisher considers the results and conclusions to be unreliable. The authors disagree with the retraction.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"537"},"PeriodicalIF":3.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146125769","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":"A Comprehensive Gene Expression Analysis of Extensive Cohorts From Colon Adenocarcinoma Uncovered a Set of Genes Regulated by DNA Hypomethylation and Predominantly Influenced by Lipid Raft-Mediated EGFR-RAS-MAPK Signaling.","authors":"Ankan Roy, Niharika, Veerbhan Kesarwani, Ravi Shankar, Samir Kumar Patra","doi":"10.1002/mc.70085","DOIUrl":"10.1002/mc.70085","url":null,"abstract":"<p><p>The regulation of gene expression and its connection to the dynamics of plasma membrane signaling hubs (lipid rafts) have largely remained unexplored to date. Ras signaling plays crucial roles in the initiation and progression of colon adenocarcinoma (COAD) by regulation of gene expression, including DNA methyltransferase 1 (DNMT1). Gene-specific hypermethylation and genome-wide hypomethylation are well characterized in various cancers, including COAD. In view of this, we have examined how the signaling pathway orchestrated by plasma membrane-associated lipid rafts coordinates with the epigenetic modifications that precisely modulate a specific group of (hub) genes involved. First, we have identified COAD-specific hub genes (COL1A1, COL1A2, COL4A1, SPP1, SPARC, and THBS2) through extensive bioinformatics analyses, which revealed that increased expression of these hub genes facilitates the onset and progression of COAD. Comprehensive computational analyses of methylation patterns confirmed that atypical hypomethylation at these gene loci elevates their expression in COAD. Thereafter, we have explored how the dynamics of plasma membrane signaling hubs', such as lipid rafts, influence gene-specific promoter methylation dynamics within the nucleus of COAD cells. Our experimental analyses indicated that the transient destabilization (TD) of lipid rafts through ectopic cholesterol efflux activates the epidermal growth factor (EGF)-independent lipid raft-associated epidermal growth factor receptor (EGFR)-rat sarcoma (RAS)-mitogen-activated protein kinase (MAPK) signaling pathway, leading to increased expression of DNMTs and decreased expression of hub genes in COAD cells. These results strongly suggest that the plasma membrane lipid raft-associated EGFR-RAS-MAPK axis, functioning from membrane signaling hubs, can regulate genes located in various chromosomal locations. Ectopic expressions of DNMT1 impose an epigenetic checkpoint at those target loci by methylation of promoter DNA of the respective genes. We conclude that, gene specific hypomethylation of some genes, including COL1A1, COL1A2, COL4A1, SPP1, SPARC, and THBS2 drives COAD and would serve as potential markers for COAD screening.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"465-492"},"PeriodicalIF":3.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146125721","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":"The 5-Methylcytosine RNA Modification in Hepatitis B Virus-Negative Hepatocellular Carcinoma: Insights From Long-Read Nanopore Sequencing.","authors":"Tianhan Sun, Liying Zhou, XiaoQing Li, Ryan Xiao, Gaoyuan Sun, Lili Zhang, Yifei Li, Wei Huang, Yayu Li, Lu Kuai, Xuanmei Luo, Hongyuan Cui, Meng Chen","doi":"10.1002/mc.70080","DOIUrl":"10.1002/mc.70080","url":null,"abstract":"<p><p>5-Methylcytosine (m5C) RNA modification contributes to tumor initiation and progression. However, its transcriptome-wide distribution patterns and biological implications in hepatitis B virus (HBV)-negative hepatocellular carcinoma (HCC) remain poorly understood. Therefore, this study employs long-read Nanopore direct RNA sequencing to systematically elucidate the mechanisms of m5C-mediated epigenetic reprogramming in HBV-negative HCC. Paired tumor and adjacent normal tissues from three HBV-negative HCC patients were collected for Nanopore sequencing. Transcriptome-wide m5C sites were profiled using the CHEUI tool, followed by a comprehensive comparison between tumor and adjacent normal tissue groups regarding the number of m5C sites, their genomic distribution characteristics, and the expression levels of m5C regulators. Finally, an integrated analysis of transcriptomic and methylation data was conducted to identify m5C-related prognostic indicators in HCC. Tumor tissues exhibited a global increase in m5C sites abundance, with differential modifications enriched on chromosomes 1-3. Genes harboring m5C modifications were significantly enriched in immune and inflammatory pathways, suggesting a potential role for this epitranscriptomic mark in remodeling the tumor immune microenvironment. Consistent upregulation of m5C regulators, including NSUN family members and ALYREF, at both gene and isoform levels, correlated with increased methylation activity. Elevated m5C coupled with decreased CES3 expression were associated with poorer overall survival. Additionally, TMEM234 showed prognostic significance despite unchanged bulk expression in public datasets. m5C modifications are globally altered in HBV-negative HCC and may contribute to post-transcriptional regulation and aberrant expression. These findings highlight the potential of m5C as both a prognostic biomarker and a therapeutic target in HBV-negative HCC.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"397-406"},"PeriodicalIF":3.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12973161/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146030384","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":"A Genome-Wide Association Study of Colorectal Cancer Mortality Outcomes Among Individuals of African and Admixture Ancestry.","authors":"Thomas Lawler, Jirong Long, Rene Welch, Irene Ong, Oluwatoyosi Ogunmuyiwa, Rida A Khatri, Martha Shrubsole, Shaneda Warren Andersen","doi":"10.1002/mc.70086","DOIUrl":"10.1002/mc.70086","url":null,"abstract":"<p><p>African Americans have the highest colorectal cancer (CRC) mortality rates in the United States. We performed the first genome-wide association study (GWAS) of overall and CRC-specific mortality among African Americans with incident CRC to identify genetic contributors to CRC outcomes. Participants enrolled in the Southern Community Cohort Study in 2002-2009; incident CRC and mortality were identified via state cancer registries and the National Death Index. SNPs were genotyped across the genome via Illumina platforms and imputed using the Michigan Imputation Server with Minimac4. Associations with mortality were estimated as hazard ratios (HRs) with 95% confidence intervals (CIs) using Cox proportional hazards models, adjusted for age, sex, stage, and five principal components for ancestry. In total, 500 Black-identifying participants were analyzed, including 316 deaths and 184 CRC-specific deaths. Two novel loci in linkage disequilibrium (r² = 1) within LTBP1 were associated with higher CRC-specific mortality risk: rs34071846 and rs12712337 (per allele HR: 2.74, CI: 1.91-3.92, p = 3.78 × 10^-8). An additional variant mapped to a gene for a noncoding RNA was associated with CRC-specific mortality: rs10103953 (per allele HR: 0.52, CI: 0.42-0.66, p = 2.03 × 10^-8). One loci mapping to MCTP2 was associated with lower overall mortality risk: rs7171579 (per allele HR: 0.59, CI: 0.50-0.71, p = 2.13 × 10^-8). In conclusion, evidence from the present study supports LTBP1 and MCTP2 as important to CRC mortality.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"422-433"},"PeriodicalIF":3.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12973162/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146086481","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":"A Combination of Xanthohumol and Ursolic Acid in the Diet Leads to Synergistic Inhibition of Prostate Cancer Progression.","authors":"Rachel Clark, Achinto Saha, G Lavender Hackman, Chelsea A Friedman, Ruggiero Gorgoglione, Stefano Tiziani, John DiGiovanni","doi":"10.1002/mc.70087","DOIUrl":"10.1002/mc.70087","url":null,"abstract":"<p><p>Prostate cancer (PCa) is the second most common cancer and second leading cause of cancer death for American men. Chemoprevention by using phytochemicals offers a promising approach to improve outcomes due to their ability to act on cancer cell metabolism and growth while maintaining low toxicity profiles. The goal of this study was to assess the combination of xanthohumol (XAN) and ursolic acid (UA) given in the diet for synergistic efficacy against PCa progression and identify potential mechanisms of action. PCa cells were treated with the combination to evaluate cell survival and colony formation. Two mouse models of PCa were used to evaluate tolerability and efficacy of dietary administration of the combination and to further understand mechanism(s) of action. The combination of XAN + UA reduced PCa cell survival and colony formation. The combination given in the diet significantly and synergistically inhibited growth of HMVP2 PCa allograft tumors and also inhibited PCa progression in HiMyc mice. Mechanistically, inhibition of polyamine synthesis and epithelial-to-mesenchymal transition contributed to the inhibition of HMVP2 allograft tumor growth, while the inhibition of PCa progression in HiMyc mice was associated with activation of the unfolded protein response pathway and apoptosis. Further studies in cultured PCa cells revealed additional effects of the combination on several oncogenic signaling pathways (e.g, phospho-STAT3) and cell cycle regulatory proteins (e.g, cyclin D1, phospho-Rb).</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"508-522"},"PeriodicalIF":3.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12973155/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146150414","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":"PI3K Activity Mediates the Epithelial to Mesenchymal Transition Process in MCF10A Cells and Tumor Growth and Metastasis in a Murine Model of Breast Cancer.","authors":"Rocio Castillo-Sanchez, Alejandra Ordoñez-Moreno, Pablo Torres-Alamilla, Pedro Cortes-Reynosa, Hector Quezada, Eduardo Perez Salazar","doi":"10.1002/mc.70089","DOIUrl":"10.1002/mc.70089","url":null,"abstract":"<p><p>Breast cancer represents the leading cause of mortality among women worldwide. Triple negative breast cancer (TNBC) subtype does not express estrogen receptor, progesterone receptor and Her2, as well as presents a high expression of Ki67. In addition, TNBC presents the highest incidence of metastasis. Erythropoietin (EPO) is a hematopoietic cytokine that is produced in the kidney; however, EPO is also produced in non-hematopoietic cells. Treatment of breast cancer patients with EPO is associated with poor prognosis and decrease of survival. Epithelial to mesenchymal transition (EMT) is a reversible process in which epithelial cells decrease or lose their epithelial characteristics and acquire properties of mesenchymal cells. EMT is implicated in normal processes and tumor progression. We previously demonstrated that EPO induces an EMT process in MCF10A mammary non-tumorigenic epithelial cells. In this study, we demonstrate that PI3K activity mediates the EMT process induced by EPO in MCF10A cells. Moreover, Balb/cJ mice inoculated with TNBC 4T1 cells and treated with EPO develop mammary tumors with more weight and volume and an increase in the total number of metastatic nodules in lungs and liver through PI3K activity compared with untreated Balb/cJ mice inoculated with 4T1 cells. In conclusion, PI3K activity mediates the EMT process in MCF10A cells and the growth of mammary tumors and metastasis to lungs and liver induced by EPO in Balb/cJ mice inoculated with TNBC 4T1 cells.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"434-447"},"PeriodicalIF":3.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146113819","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":"CCNL1 Activates the NF-κB Pathway Through DVL3 Inhibition and PI3K/AKT Pathway Promotion in Breast Cancer.","authors":"Dan Zhang, Runfen Cheng, Jiaxin Gao, Jiyuan Han, Chunsheng Ni, Song Wang, Xiulan Zhao, Baocun Sun, Tieju Liu","doi":"10.1002/mc.70090","DOIUrl":"10.1002/mc.70090","url":null,"abstract":"<p><p>Cyclin L1 (CCNL1) is highly expressed in multiple cancer types and has been linked to poor prognosis. However, the expression pattern of CCNL1 in breast cancer and its specific role in regulating breast cancer progression remain largely unknown. This study used cell and molecular biology techniques to examine how CCNL1 regulates the proliferation, invasion, migration, and epithelial-mesenchymal transition (EMT) of breast cancer cells. The applied methods encompassed plasmid transfection, Transwell assay, wound-healing assay, Western blot analysis, co-immunoprecipitation (Co-IP), and rescue assay. For the analysis of CCNL1-related factors and pathways, bioinformatics platforms including Metascape and HURI were also employed. CCNL1 is highly expressed in breast cancer cells and is associated with a poor prognosis. CCNL1 overexpression increased breast cancer cell invasion and migration and accelerated proliferation. Overexpression of CCNL1 was found to upregulate the mesenchymal marker Vimentin and downregulate the epithelial marker E-cadherin expression. There is close relationship between CCNL1, the NF-κB and PI3K/AKT signaling pathways. The direct interaction is verified between CCNL1 and DVL3 by Co-IP, indicating a negative correlation between the two proteins. CCNL1 overexpression affects breast cancer cells' paclitaxel sensitivity through the PI3K/AKT pathway. CCNL1 activates the NF-κB signaling pathway through its interaction with DVL3; additionally, it promotes the PI3K/AKT pathway. Together, these two mechanisms enable CCNL1 to exert a regulatory role in the progression of breast cancer.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"448-464"},"PeriodicalIF":3.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146113806","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":"AOC3 Loss Promotes Imatinib Resistance in GIST by Stabilizing HK2 and Enhancing H3K18la-Driven Myc Transcription.","authors":"Zhiyuan Guo, Linsen Zhou, Zhiqiang Wang, Haohai Jiang, Xinguo Zhu","doi":"10.1002/mc.70084","DOIUrl":"10.1002/mc.70084","url":null,"abstract":"<p><p>Gastrointestinal stromal tumor (GIST) frequently develops resistance to imatinib (IM). This study identifies AOC3 downregulation as a critical contributor to IM resistance. Analyzing clinical samples and IM-sensitive/resistant GIST cell lines, we found AOC3 significantly decreased in resistant states. Functionally, AOC3 knockdown promoted IM resistance, enhanced glycolytic activity, and increased lactate production. Mechanistically, AOC3 loss attenuated ubiquitin-mediated degradation of HK2, stabilizing this glycolytic enzyme and boosting lactate generation. Subsequent histone lactylation, notably at H3K18, enriched at the Myc promoter and stimulated its transcription. Crucially, HK2 overexpression reversed AOC3's suppressive effects on glycolysis, lactylation, Myc expression, and IM resistance. In vivo xenograft models confirmed these findings. We conclude that AOC3 acts as a tumor suppressor by promoting HK2 degradation; its loss triggers a HK2/glycolysis/lactylation/Myc axis driving IM resistance, positioning AOC3 as a promising prognostic biomarker and therapeutic target in GIST.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"407-421"},"PeriodicalIF":3.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146030482","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}