Molecular Cancer Research最新文献

{"title":"Correction: FBW7 Inhibits Myeloid Differentiation in Acute Myeloid Leukemia via GSK3-Dependent Ubiquitination of PU.1.","authors":"Mukul Mishra, Gatha Thacker, Akshay Sharma, Anil Kumar Singh, Vishal Upadhyay, Sabyasachi Sanyal, Shailendra Prasad Verma, Anil Kumar Tripathi, Madan Lal Brahma Bhatt, Arun Kumar Trivedi","doi":"10.1158/1541-7786.MCR-26-0616","DOIUrl":"https://doi.org/10.1158/1541-7786.MCR-26-0616","url":null,"abstract":"","PeriodicalId":19095,"journal":{"name":"Molecular Cancer Research","volume":"24 9","pages":"801"},"PeriodicalIF":5.8,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148875535","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":"Mapping the Subtype-Specific PARP1 ADP-Ribosylated Proteome in Breast Cancer Cells.","authors":"Sneh Koul, Minjung Kwon, Poulami Tapadar, Yangyang Dai, Weidan Song, Morgan Dasovich, Tulip Nandu, Dan Huang, Cristel V Camacho, W Lee Kraus","doi":"10.1158/1541-7786.MCR-25-1068","DOIUrl":"10.1158/1541-7786.MCR-25-1068","url":null,"abstract":"<p><p>Breast cancers are molecularly heterogeneous, with subtype-specific differences in transcriptional programs, chromatin architecture, and therapeutic responses. Although poly(ADP-ribose) polymerase (PARP) 1 has been extensively studied in the context of DNA repair, emerging evidence implicates its catalytic activity in a broader set of cellular processes, including the regulation of gene expression. In this study, we employed a nicotinamide adenine dinucleotide (NAD+) analogue-sensitive PARP1 chemical genetics approach combined with mass spectrometry to map the ADP-ribosylated proteome across 6 human breast cancer cell lines representing luminal and basal/triple-negative subtypes. We identified thousands of PARP1 substrates and hundreds of Glu/Asp ADP-ribosylation (ADPRylation) sites, revealing both shared and subtype-specific modifications in cell lines maintained under basal growth conditions. Luminal-specific substrates were enriched in chromatin and transcriptional regulators, whereas basal-specific substrates were preferentially linked to translation and RNA processing, highlighting lineage-dependent PARP1 activity. Transcription factors emerged as major substrates, with TFAP2A serving as a proof of concept; it is selectively ADPRylated in luminal cells, and inhibition of PARP1-mediated ADPRylation modulates its promoter occupancy in a subtype-specific manner. Our data provide a new resource for studying subtype-specific PARP1-mediated ADPRylation in breast cancer cells. Collectively, our findings expand the conceptual framework for PARP1 function beyond DNA repair, offering mechanistic insights into subtype-specific gene regulation and potential determinants of PARP inhibitor sensitivity in breast cancer.</p><p><strong>Implications: </strong>PARP1-driven ADPRylation encodes subtype-specific transcriptional programs in breast cancer, revealing a broader role for PARP1 in gene regulation that may influence therapeutic response.</p>","PeriodicalId":19095,"journal":{"name":"Molecular Cancer Research","volume":" ","pages":"770-783"},"PeriodicalIF":5.8,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13327525/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148043167","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":"MIR17HG Expression Is Transcriptionally Regulated by PAX3::FOXO1 and MYCN and is Necessary for Oncogenic Activity in Fusion-Positive Rhabdomyosarcoma.","authors":"Shabir Zargar, Pawan Kumar Raut, Hana Kim, Salah Boudjadi, Rachel A Hoffman, Benjamin Z Stanton, Frederic G Barr","doi":"10.1158/1541-7786.MCR-26-0074","DOIUrl":"10.1158/1541-7786.MCR-26-0074","url":null,"abstract":"<p><p>Alveolar rhabdomyosarcoma (RMS), an aggressive pediatric soft tissue cancer, is driven by the oncogenic fusion transcription factor PAX3::FOXO1 (P3F) or PAX7::FOXO1. In a subset of fusion-positive (FP)-RMS cases, amplification of the MIR17HG locus leads to overexpression of the miR-17-92 cluster of microRNAs (miRNAs). However, miR-17-92 is also highly expressed in FP-RMS tumors lacking this amplification, suggesting alternative regulatory mechanisms. Here, we show that P3F and MYCN cooperatively drive miR-17-92 expression in FP-RMS. CRISPR/Cas9-mediated knockout of P3F or MYCN in FP-RMS cell lines substantially reduced miR-17-92 expression. Using a human myoblast line or low P3F FP-RMS variant with inducible P3F or MYCN expression, P3F or MYCN alone induces minimal to low miR-17-92 expression whereas introduction of both MYCN and P3F leads to robust activation of the miR-17-92 cluster and acquisition of oncogenic phenotypes. Chromatin immunoprecipitation sequencing (ChIP-seq) revealed a P3F binding motif located 1.84 Mb upstream of the MIR17HG promoter. CRISPR-mediated deletion of this region in the myoblast system resulted in marked reduction of miR-17-92 expression and impaired oncogenic transformation. Functional inhibition of mature miRNAs of this cluster in FP-RMS cells using miRNA-sponge constructs suppressed proliferation and transformation. In the myoblast model system, transduction studies with exogenous miR-17-92 or miRNA-sponge expression constructs indicated that miR-17-92 is necessary but not sufficient for oncogenic transformation. Implications: These findings establish a cooperative transcriptional axis in FP-RMS involving P3F and MYCN that activates MIR17HG through a distal regulatory element, thereby contributing to oncogenic behavior and uncovering a novel mechanistic vulnerability.</p>","PeriodicalId":19095,"journal":{"name":"Molecular Cancer Research","volume":" ","pages":""},"PeriodicalIF":5.8,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13641197/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148761162","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":"Integrative Transcriptional and Chromatin Analyses Reveal Enhancer-Mediated Regulatory Programs Driving Breast Cancer Metastasis.","authors":"Frances L Heredia, Natalia Maldonado-Vazquez, Homer Fogle, Kamila Wisniewska, Austin A Whitman, Michael R Kelly, Philip M Spanheimer, Lisa A Carey, Hector L Franco","doi":"10.1158/1541-7786.MCR-26-0065","DOIUrl":"10.1158/1541-7786.MCR-26-0065","url":null,"abstract":"<p><p>Breast cancer metastasis remains the leading cause of disease-related mortality, yet the regulatory mechanisms enabling tumor cells to adapt to distant tissue environments remain poorly defined. Here, we generated a multi-omic resource integrating transcriptomic (RNA-seq) and chromatin accessibility (ATAC-seq) profiles from estrogen receptor-positive primary breast tumors and matched liver and lung metastases obtained from the same patients, including diagnostic and postmortem specimens. This design enabled direct intra-patient comparisons of primary and metastatic regulatory landscapes. We identified extensive reprogramming of chromatin accessibility and gene expression in metastatic lesions relative to primary tumors, indicating widespread regulatory remodeling. Peak-to-gene correlation analysis uncovered thousands of metastasis-associated enhancer-gene linkages, with metastatic samples exhibiting significantly increased enhancer connectivity. These rewired enhancer networks preferentially targeted clinically relevant genes, including RIPK4 , ISYNA1, and RAB3D, which were associated with three or more enhancers in metastases but not in primary tumors. Furthermore, ATAC-seq footprinting combined with gene expression analysis revealed distinct, tissue-specific transcription factor activity profiles in liver and lung metastases, including ESR1, that were not explained by transcription factor expression levels alone. Together, these data provide a resource of metastasis-specific regulatory elements and their cognate transcription factors, revealing new regulatory vulnerabilities that may be therapeutically exploitable. Implications: These findings support a model in which breast cancer metastasis is driven by enhancer regulatory reprogramming, allowing tumor cells to adapt to a variety of microenvironments.</p>","PeriodicalId":19095,"journal":{"name":"Molecular Cancer Research","volume":" ","pages":""},"PeriodicalIF":5.8,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13557034/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148679492","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":"Correction: G9a Promotes Invasion and Metastasis of Non-Small Cell Lung Cancer through Enhancing Focal Adhesion Kinase Activation via NF-κB Signaling Pathway.","authors":"Ting Sun, Keqiang Zhang, Rajendra P Pangeni, Jun Wu, Wendong Li, Yong Du, Yuming Guo, Shyambabu Chaurasiya, Leonidas Arvanitis, Dan J Raz","doi":"10.1158/1541-7786.MCR-26-0510","DOIUrl":"https://doi.org/10.1158/1541-7786.MCR-26-0510","url":null,"abstract":"","PeriodicalId":19095,"journal":{"name":"Molecular Cancer Research","volume":"24 8","pages":"715"},"PeriodicalIF":5.8,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148670238","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":"Comparative ASCL1 Interactome Analysis Reveals CDK2-Cyclin A2 as Suppressors of Differentiation in MYCN-Amplified Neuroblastoma.","authors":"Lidiya Mykhaylechko, Roshna L Gomez, Laura M Woods, Evangelia K Papachristou, Revathy Ramachandran, Jethro Lundie-Brown, Rosalind Drummond, Daniel Marcos, Fiona M Y Abou Grealy, Shakhzada Ibragimova, Fahad R Ali, Jason Carroll, Anna Philpott","doi":"10.1158/1541-7786.MCR-24-0943","DOIUrl":"10.1158/1541-7786.MCR-24-0943","url":null,"abstract":"<p><p>Neuroblastoma is a heterogeneous pediatric cancer arising from developmentally arrested neuronal precursors, in which restoring differentiation offers therapeutic promise. Achaete-scute homolog 1 (ASCL1), a proneural transcription factor, is widely expressed in neuroblastoma and can drive either proliferation or differentiation depending on the cellular context. In this study, we show that distinct MYCN-amplified neuroblastoma cell lines exhibit differing differentiation responses to ASCL1 overexpression. By comparing genome-wide ASCL1 chromatin binding, transcriptional changes, and protein-protein interactions, we found that ASCL1 binds more extensively to neuronal proteins in a cell line that is more susceptible to ASCL1-driven differentiation but associates with cell-cycle regulators in less responsive cells. We show that cyclin-dependent kinase 2 (CDK2)-cyclin A2 bind ASCL1 in less responsive cells, with CDK-mediated phosphorylation of ASCL1 limiting the ability of ASCL1 to drive differentiation.</p><p><strong>Implications: </strong>Our study reveals that context-dependent interactions of ASCL1 with protein partners on the chromatin control its ability to reengage a differentiation program in neuroblastoma.</p>","PeriodicalId":19095,"journal":{"name":"Molecular Cancer Research","volume":" ","pages":"675-693"},"PeriodicalIF":5.8,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7619497/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147675425","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":"HLA Class I Expression Is Associated with Increased Immune Cell Density and PTEN Loss in Prostate Cancer.","authors":"Adrianna Amaral, Thiago Vidotto, Juhyung Woo, Michael Rubenstein, Jiayun Lu, Carolina Gomes-Alexandre, Angelo M De Marzo, Karen Sfanos, Janielle Maynard, Ezra Baraban, Laura A Sena, Mark C Markowski, Emmanuel S Antonarakis, Corinne Joshu, Kaushal Asrani, Tamara L Lotan","doi":"10.1158/1541-7786.MCR-25-1264","DOIUrl":"10.1158/1541-7786.MCR-25-1264","url":null,"abstract":"<p><p>Human leukocyte antigen class I (HLA-I) downregulation in prostate cancer may contribute to tumor immune evasion. We digitally quantified HLA-I protein expression in a cohort of racially diverse and molecularly characterized prostatectomy specimens, as well as additional cohorts of metastatic hormone-sensitive prostate cancer (mHSPC) and castration-resistant prostate cancer (mCRPC). We confirm that HLA-I protein expression is negatively associated with intragenic methylation of major HLA-I genes, downregulated in tumor compared with benign glands, but not associated with race, genetic ancestry, or clinicopathologic parameters in primary prostate cancer. Compared with matched primary tumor tissue, HLA-I expression is higher in HSPC pelvic lymph node metastases, and increased primary tumor expression is inversely associated with metastasis among self-identified White patients, but not Black patients. HLA-I expression in primary tumors is positively correlated with infiltrating immune cell densities, consistent with its established role in tumor cell immunogenicity. Surprisingly, primary tumors with PTEN loss show significantly higher HLA-I expression than those with intact PTEN, and this finding is validated in preclinical cell line and animal models, with a similar (nonsignificant) trend in mCRPC.</p><p><strong>Implications: </strong>The novel finding that PTEN loss is associated with higher tumoral HLA-I expression is concordant with observed increased immune cell infiltrates in tumors lacking PTEN and may be relevant for precision medicine therapeutic approaches.</p>","PeriodicalId":19095,"journal":{"name":"Molecular Cancer Research","volume":" ","pages":"703-714"},"PeriodicalIF":5.8,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13383058/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147818022","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":"YTHDC1 Promotes Triple-Negative Breast Cancer Cell Proliferation and Stemness by Regulating BACH1 mRNA Stability in an m6A-Dependent Manner.","authors":"Shulin Huang, Haihui Gong, Jing Xie, Ou Yue","doi":"10.1158/1541-7786.MCR-25-0602","DOIUrl":"10.1158/1541-7786.MCR-25-0602","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) is an aggressive malignancy with high mortality and limited treatment options, yet the role of YTH domain-containing protein 1 (YTHDC1) in its progression remains unclear. In this study, we investigated the function and mechanism of YTHDC1 in TNBC using in vitro assays, including quantitative real-time polymerase chain reaction, Western blot, cell counting kit-8, colony formation, and sphere formation assays, to assess cell proliferation and stemness. Fluorescence in situ hybridization and RNA immunoprecipitation (RIP) were performed to examine YTHDC1 binding to BTB domain and CNC homology 1 (BACH1) mRNA, and actinomycin D treatment was used to evaluate BACH1 mRNA stability upon YTHDC1 silencing. Additionally, rescue experiments further assessed whether BACH1 overexpression could reverse the effects of YTHDC1 knockdown. We found that YTHDC1 was significantly upregulated in TNBC tissues and cells. Silencing YTHDC1 suppressed cell proliferation, colony formation, and sphere formation and reduced the expression of stemness markers (Nanog, Oct4, and SOX2). Mechanistically, YTHDC1 silencing inhibited the nuclear export of BACH1 mRNA, leading to an increased nucleoplasmic ratio. RIP assays further revealed the enrichment of both YTHDC1 and N6-methyladenosine (m6A) modifications on BACH1 mRNA, and YTHDC1 knockdown significantly decreased BACH1 mRNA stability. Importantly, BACH1 overexpression rescued the inhibitory effects of YTHDC1 silencing on TNBC cell proliferation and stemness marker expression. Together, these findings demonstrate that YTHDC1 regulates BACH1 expression through an m6A-dependent mechanism, thereby contributing to TNBC progression.</p><p><strong>Implications: </strong>Our findings provide a rationale for further investigation of the YTHDC1-BACH1 axis as a potential therapeutic target in TNBC.</p>","PeriodicalId":19095,"journal":{"name":"Molecular Cancer Research","volume":" ","pages":"694-702"},"PeriodicalIF":5.8,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147777126","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":"E3 Ubiquitin Ligase ITCH Enhances P53 Ubiquitination-Dependent Degradation and Drives Osteosarcoma Tumorigenesis.","authors":"Jin Zeng, Haibo Zhan, Jun Xiao, Fang Huang, Weiguo Bian","doi":"10.1158/1541-7786.MCR-25-0687","DOIUrl":"10.1158/1541-7786.MCR-25-0687","url":null,"abstract":"<p><p>Osteosarcoma remains a highly aggressive malignant tumor with strong metastatic potential and limited therapeutic options. E3 ubiquitin ligases, particularly the HECT-type family, regulate oncogenic pathways via targeted protein degradation. Among them, Itchy E3 ubiquitin protein ligase (ITCH) has been implicated in poor prognosis in multiple cancers. However, its functional effects and clinical relevance in osteosarcoma pathogenesis remain completely unexplored. Herein, ITCH expression in osteosarcoma tissues was detected using qRT-PCR, Western blot, and IHC. In vitro and in vivo, the function of ITCH was evaluated by soft agar colony formation assay, Transwell assay, CCK8 assay, wound healing assay, immunofluorescence, flow cytometric analysis, and xenograft tumor assay. Downstream targets were further investigated using proteomic analysis, Western blot, and immunoprecipitation. ITCH was aberrantly overexpressed in osteosarcoma tissues, exhibiting a strong negative correlation with patient survival. Mechanistically, ITCH directly bound P53 and mediated its ubiquitination and degradation. ITCH-driven P53 loss enhanced malignant phenotypes, whereas ITCH knockdown restored P53 stability. This study demonstrates that ITCH functions as an oncogene in osteosarcoma by targeting P53 for degradation and suggests ITCH as a promising therapeutic target.</p><p><strong>Implications: </strong>These findings define a molecular mechanism underlying the oncogenic role of ITCH through P53 ubiquitination-dependent degradation.</p>","PeriodicalId":19095,"journal":{"name":"Molecular Cancer Research","volume":" ","pages":"637-648"},"PeriodicalIF":5.8,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13434300/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147628158","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 SNHG15/miR-451a/Caveolin-1 Axis Promotes Oxaliplatin Resistance in Gastric Cancer Cells by Regulating Fatty Acid β-Oxidation.","authors":"Yi Wang, Zhongshi Hong, Jintian Song, Jianping Jiang, Zhihui Jiang, Shu Chen, Luchuan Chen, Hui Yu, Chengzhi Qiu, Shenghong Wei","doi":"10.1158/1541-7786.MCR-25-0154","DOIUrl":"10.1158/1541-7786.MCR-25-0154","url":null,"abstract":"<p><p>Gastric cancer is a common malignant tumor of the digestive tract. Chemotherapy resistance severely limits the therapeutic effect of this disease. The competing endogenous RNA regulatory network is widely involved in the occurrence and development of various cancers and is also closely related to the generation of drug resistance. However, the underlying molecular mechanism remains to be further elucidated. This study investigated the molecular mechanism by which the long noncoding RNA SNHG15/miR-451a/Caveolin-1 (CAV1) axis mediates oxaliplatin resistance in gastric cancer through regulating fatty acid β-oxidation. Through analysis using The Cancer Genome Atlas database and qRT-PCR, it was found that SNHG15 was highly expressed in gastric cancer tissues, whereas miR-451a was lowly expressed. Bioinformatics prediction combined with dual luciferase and RNA immunoprecipitation experiments confirmed that SNHG15 could act as a molecular sponge for miR-451a, and CAV1 was the downstream target gene of miR-451a. Functional experiments demonstrated that the knockdown of miR-451a or overexpression of CAV1 could promote cell proliferation, inhibit apoptosis, and alleviate G0-G1-phase arrest while enhancing fatty acid β-oxidation. In vivo experiments further confirmed that the SNHG15/miR-451a/CAV1 axis affected gastric cancer oxaliplatin resistance by regulating fatty acid β-oxidation.</p><p><strong>Implications: </strong>This study revealed that SNHG15 inhibits miR-451a to upregulate CAV1 expression, thereby regulating fatty acid β-oxidation and influencing gastric cancer oxaliplatin resistance, providing new biomarkers and potential therapeutic targets for gastric cancer oxaliplatin resistance.</p>","PeriodicalId":19095,"journal":{"name":"Molecular Cancer Research","volume":" ","pages":"660-674"},"PeriodicalIF":5.8,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147675401","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}