Carcinogenesis最新文献_第9页

Correction to: MUC1-C dictates neuroendocrine lineage specification in pancreatic ductal adenocarcinomas. 更正：MUC1-C指示胰腺导管腺癌的神经内分泌谱系。

IF 2.9 3区医学

Carcinogenesis Pub Date : 2025-11-21 DOI: 10.1093/carcin/bgaf091

引用次数: 0

Polo-like kinase 4 (PLK4) as a therapeutic target in breast cancer. polo样激酶4 （PLK4）作为乳腺癌的治疗靶点。

IF 3.8 3区医学

Carcinogenesis Pub Date : 2025-11-21 DOI: 10.1093/carcin/bgaf067

Armen Parsyan, Harjot Athwal, Vasudeva Bhat, Alison L Allan

{"title":"Polo-like kinase 4 (PLK4) as a therapeutic target in breast cancer.","authors":"Armen Parsyan, Harjot Athwal, Vasudeva Bhat, Alison L Allan","doi":"10.1093/carcin/bgaf067","DOIUrl":"10.1093/carcin/bgaf067","url":null,"abstract":"Polo-like kinase 4 (PLK4) is a key kinase regulating centriole duplication, centrosome maturation, cytokinesis and other cellular processes. Growing evidence suggests a critical role of PLK4 in the development and progression of various cancers. In many cancer types, its upregulation leads to pro-oncogenic phenotypes, while its pharmacologic inhibition leads to anticancer effects. Functionally, PLK4 affects cancer cell proliferation, growth, motility, invasion, migration, epithelial-mesenchymal transition, apoptosis and other critical oncogenic processes. In breast cancer, PLK4 is associated with centrosome amplification, aneuploidy and chromosomal instability, promoting invasive phenotypes and resistance to cancer cell death. PLK4 shows great promise as a prognostic and predictive biomarker in breast cancer. It is commonly found to be overexpressed in primary human breast cancers and is associated with poor oncologic outcomes, clinicopathologic parameters, and high-risk subtypes. Various compounds, such as CFI-400945, centrinone B, and others have been developed to inhibit PLK4 activity. Preclinical studies have shown that PLK4 inhibitors lead to decreased proliferation, growth and migration and increased breast cancer cell death. Moreover, PLK4 inhibition can serve to enhance the effects of other treatments, including radiotherapy. Clinical studies have been initiated with some of these compounds in cancer patients, including those with breast cancer. This manuscript discusses the role of PLK4 as a promising therapeutic target in breast cancer, one of the most common causes of morbidity and mortality in women.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12637032/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145298576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

HS-10296 (almonertinib) enhances radiosensitivity in EGFR-mutant nonsmall cell lung cancer (including T790M) through inhibition of EGFR downstream signaling and DNA damage repair. HS-10296 （Almonertinib）通过抑制EGFR下游信号传导和DNA损伤修复，增强EGFR突变型NSCLC（包括T790M）的放射敏感性。

IF 3.8 3区医学

Carcinogenesis Pub Date : 2025-11-21 DOI: 10.1093/carcin/bgaf070

Weiqi Liu, Yulian Liu, Yun Xie, Hui Huang, Mengzhi Wan, Ling Zhou, Fei Xu, Min Zhong

{"title":"HS-10296 (almonertinib) enhances radiosensitivity in EGFR-mutant nonsmall cell lung cancer (including T790M) through inhibition of EGFR downstream signaling and DNA damage repair.","authors":"Weiqi Liu, Yulian Liu, Yun Xie, Hui Huang, Mengzhi Wan, Ling Zhou, Fei Xu, Min Zhong","doi":"10.1093/carcin/bgaf070","DOIUrl":"10.1093/carcin/bgaf070","url":null,"abstract":"Nonsmall cell lung cancer (NSCLC) harboring EGFR mutations, including the resistant T790M variant, continues to require improved therapeutic strategies despite the development of EGFR tyrosine kinase inhibitors (TKIs). This study evaluates the radiosensitizing potential of HS-10296 (almonertinib), a third-generation EGFR-TKI, in EGFR-mutant NSCLC models. In vitro studies demonstrated selective growth inhibition in mutant cells (PC-9: half-maximal inhibitory concentration (IC50) = 2.62 μM; H1975: IC50 = 5.22μM at 48 h) compared to wild-type A549 cells (IC50 = 11.42 μM). Clonogenic assays revealed significant radiosensitization in mutant cells (SER: PC-9 = 1.22; H1975 = 1.55) through multiple mechanisms including enhanced DNA damage (1.5-2.0-fold increase in comet tail moments with 4-10× persistent γH2A.X foci), marked suppression of RAD51-mediated DNA repair, and increased apoptosis (combination therapy: 19.53%-20.71% versus monotherapies: 12.08%-14.05%). Mechanistic investigation showed HS-10296 attenuated phosphorylation of EGFR and downstream effectors AKT and ERK, potentially disrupting DNA damage response pathways. In vivo validation using H1975 xenografts demonstrated superior tumor growth inhibition with the combination of HS-10296 and radiotherapy, which correlated with reduced expression of p-EGFR, p-AKT, and RAD51, along with increased γH2A.X levels. These findings establish HS-10296 as a promising radiosensitizer for EGFR-mutant NSCLC through simultaneous targeting of oncogenic signaling via PI3K/AKT and MAPK/ERK pathways and critical DNA repair mechanisms. The study provides compelling preclinical evidence supporting clinical evaluation of HS-10296 combined with radiotherapy for EGFR-driven NSCLC, including tumors with T790M-mediated resistance.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145298594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

BRINP3 promotes lung adenocarcinoma by enhancing CLOCK-mediated transcriptional regulation of CRYZL1 and activating the AKT pathway. BRINP3通过增强时钟介导的CRYZL1转录调控和激活AKT通路来促进肺腺癌。

IF 3.8 3区医学

Carcinogenesis Pub Date : 2025-11-21 DOI: 10.1093/carcin/bgaf039

Ye Zhang, Cheng Huang, Yeye Chen, Lei Liu, Shanqing Li

{"title":"BRINP3 promotes lung adenocarcinoma by enhancing CLOCK-mediated transcriptional regulation of CRYZL1 and activating the AKT pathway.","authors":"Ye Zhang, Cheng Huang, Yeye Chen, Lei Liu, Shanqing Li","doi":"10.1093/carcin/bgaf039","DOIUrl":"10.1093/carcin/bgaf039","url":null,"abstract":"Lung cancer, particularly lung adenocarcinoma (LUAD), is the leading cause of cancer-related death globally. This study investigated the role of BRINP3 in LUAD. Immunohistochemical analysis revealed significantly upregulated BRINP3 expression in LUAD tissues compared to normal tissues, mainly located in the cytoplasm and positively correlated with tumor progression. RNA sequencing data from the TCGA-LUAD database corroborated these findings. Elevated BRINP3 expression was associated with advanced tumor stages, higher malignancy grades, and increased risk of lymphatic metastasis. Functional studies showed that BRINP3 knockdown inhibited cell proliferation, colony formation, and migration, while promoting apoptosis. Conversely, BRINP3 overexpression enhanced these malignant behaviors. Gene expression profiling identified CLOCK and CRYZL1 as potential BRINP3 targets, with BRINP3 interacting with CLOCK to regulate CRYZL1 transcription. Additionally, BRINP3 activated the AKT signaling pathway to promote LUAD progression. In vivo experiments validated the tumor-suppressing effects of BRINP3 knockdown, reducing tumor growth and metastatic potential. In conclusion, BRINP3 played a crucial role in LUAD development and progression by regulating CLOCK-mediated transcriptional regulation of CRYZL1 and activating the AKT signaling pathway. BRINP3 knockdown inhibited LUAD cell malignancy and might represent a potential therapeutic target.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144834052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Analysis of MRPL23 protein expression and its role in prostate cancer pathogenesis. MRPL23蛋白表达及其在前列腺癌发病中的作用分析。

IF 3.8 3区医学

Carcinogenesis Pub Date : 2025-11-21 DOI: 10.1093/carcin/bgaf078

Edyta Podemska, Damian Łukasik, Jędrzej Borowczak, Dariusz Grzanka, Justyna Durślewicz

{"title":"Analysis of MRPL23 protein expression and its role in prostate cancer pathogenesis.","authors":"Edyta Podemska, Damian Łukasik, Jędrzej Borowczak, Dariusz Grzanka, Justyna Durślewicz","doi":"10.1093/carcin/bgaf078","DOIUrl":"10.1093/carcin/bgaf078","url":null,"abstract":"Prostate cancer (PCa) is the fourth most commonly diagnosed malignancy worldwide and remains a major clinical challenge due to its heterogeneous course and lack of reliable prognostic biomarkers. Mitochondrial ribosomal protein L23 (MRPL23) has recently emerged as a potential contributor to cancer progression, but its role in prostate cancer remains poorly understood. Formalin-fixed, paraffin-embedded (FFPE) tissue samples from 67 PCa patients who underwent radical prostatectomy were analyzed. MRPL23 expression was assessed by immunohistochemistry using a semi-quantitative immunoreactive scale (IRS). Clinicopathological data were collected for correlation analysis. Survival outcomes were evaluated using Kaplan-Meier curves and Cox proportional hazards models. MRPL23 expression differed significantly across all tissue types, with higher levels in prostate cancer tissues compared with normal epithelium, and the highest expression observed in lymph node metastases (P < .001). High MRPL23 expression was associated with shorter overall survival (P = .003) and remained an independent prognostic factor in the multivariate analysis (HR 3.99, 95% CI 1.63-9.77, P = .002). Complementary TCGA analysis confirmed elevated MRPL23 mRNA levels in prostate adenocarcinomas compared with normal tissues (P = .01) and demonstrated that high expression predicted shorter disease-free survival (10-year DFS: 75.98% versus 92.92%, log-rank P = .01). MRPL23 is a potential prognostic biomarker in prostate cancer, linked to aggressive tumor behavior and poor outcomes. Its expression in metastatic tissue suggests a role in disease progression, while TCGA data confirm its prognostic value for recurrence risk. MRPL23 may also serve as a therapeutic target in advanced PCa.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":"46 4","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12716982/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145793399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

An update on the World Trade Center cancer tissue biobank: a scientific resource for molecular and mechanistic studies on WTC-related cancer. 世贸中心癌症组织生物库的最新进展：世贸中心相关癌症分子和机制研究的科学资源。

IF 3.8 3区医学

Carcinogenesis Pub Date : 2025-11-21 DOI: 10.1093/carcin/bgaf063

Wiley M Turner, Angelo Zegarelli, Tara Ivic-Pavlicic, Rachel Brody, Stephanie Tuminello, Emanuela Taioli

{"title":"An update on the World Trade Center cancer tissue biobank: a scientific resource for molecular and mechanistic studies on WTC-related cancer.","authors":"Wiley M Turner, Angelo Zegarelli, Tara Ivic-Pavlicic, Rachel Brody, Stephanie Tuminello, Emanuela Taioli","doi":"10.1093/carcin/bgaf063","DOIUrl":"10.1093/carcin/bgaf063","url":null,"abstract":"World Trade Center (WTC) responders were exposed to a complex mixture of toxins and carcinogens through dust, fumes, and smoke at ground zero. Since then, studies have indicated that WTC responders have elevated cancer rates compared with the general population. While studies have detailed the overarching connection between WTC exposure and cancer, a tissue biobank is needed to enable molecular and mechanistic studies on WTC-related cancers. The cohort includes responders involved in rescue, recovery, or cleanup enrolled in the World Trade Center Health Program (WTCHP) who consented to participate in research. Responders with cancer were identified through WTCHP certification. WTCHP provided data with patients' demographic information, contact details, and cancer diagnoses. Potential participants were contacted by mail, email, or phone for consent and procedure location. If consented, samples were requested from pathology departments. A biobank of cancer tissues from WTC responders has been established with 551 distinct primary cancers from 521 patients. Of these, prostate makes up 39.0%, thyroid 9.8%, melanoma 8.9%, kidney 6.5%, bladder 6.0%, colorectal 5.8%, breast 5.6%, lung 4.7%, head and neck 4.7%, and other cancers 9%. An additional 343 patients have consented for biobank projects and their samples are being requested. To date, we have created a valuable tissue biobank available to the scientific community for high-impact oncology studies in the unique population of WTC responders. By studying links between carcinogenic exposure and cancer sites, exposure signatures, and markers of cancer aggressiveness, this biobank offers an unprecedented opportunity to advance cancer research in an exposed population.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225201","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Non-malignant hematologic conditions and subsequent cancer risk: a prospective cohort study and Mendelian randomization analysis. 非恶性血液病和随后的癌症风险：一项前瞻性队列研究和孟德尔随机分析。

IF 3.8 3区医学

Carcinogenesis Pub Date : 2025-11-21 DOI: 10.1093/carcin/bgaf085

Weiwei Chen, Jiacong Li, Hengyu Cui, Lijuan Dai, Yuefan Shen, Xueni Cheng, Lu He, Qingyuan Zhuang, Mingming He, Mingyang Song, Dong Hang

{"title":"Non-malignant hematologic conditions and subsequent cancer risk: a prospective cohort study and Mendelian randomization analysis.","authors":"Weiwei Chen, Jiacong Li, Hengyu Cui, Lijuan Dai, Yuefan Shen, Xueni Cheng, Lu He, Qingyuan Zhuang, Mingming He, Mingyang Song, Dong Hang","doi":"10.1093/carcin/bgaf085","DOIUrl":"10.1093/carcin/bgaf085","url":null,"abstract":"No studies have examined the association between non-malignant hematologic diseases and the risk of various cancers. To examine the associations between non-malignant hematologic diseases and cancer risk, we performed a cohort study and Mendelian randomization analysis. The association between hematologic diseases and incident cancer risk was assessed using time-varying Cox proportional hazards regression with multivariable hazard ratios (HRs) and 95% confidence intervals (CIs). Over a total of 5 031 372 person-years of follow-up in the UK Biobank, 32 589 (6.8%) patients were diagnosed with hematologic diseases, with 2279 incident cancer cases. Multivariable time-varying Cox regression models revealed that any hematologic disease was positively associated with total cancer (HR = 1.19; 95% CI, 1.14-1.24), hematologic cancer (HR = 1.92; 95% CI, 1.69-2.17), and digestive system cancer risks (HR = 1.36; 95% CI, 1.25-1.48). Nine hematologic diseases were associated with higher hematologic cancer risk, and six of the hematologic diseases were also associated with higher risks of four types of digestive system cancer (liver, stomach, esophageal, and small intestine cancers). Mendelian randomization analysis supported the positive association of agranulocytosis with leukemia, coagulation defects and spleen diseases with lymphoma, and unspecified anemia with small intestine cancer. This study indicates that non-malignant hematologic diseases are associated with an increased risk of cancer, particularly cancers in the hematological and digestive systems.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145573328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Lung cancer chemo-interception by sulfasalazine and disulfiram codelivered using a nano self-emulsifying drug delivery system in mice. 采用纳米自乳化给药系统，磺胺氮嗪和双硫仑共给药对小鼠肺癌的化疗阻断作用。

IF 3.8 3区医学

Carcinogenesis Pub Date : 2025-11-21 DOI: 10.1093/carcin/bgaf075

Fekadu Kassie, Kevin Wang, Katherine Bang, Mohammed Riaz Hasan Chowdhury, Jeffrey Wang, Sunil Prabhu, Xueqing Liang, Davis Seelig, Preshita Desai

{"title":"Lung cancer chemo-interception by sulfasalazine and disulfiram codelivered using a nano self-emulsifying drug delivery system in mice.","authors":"Fekadu Kassie, Kevin Wang, Katherine Bang, Mohammed Riaz Hasan Chowdhury, Jeffrey Wang, Sunil Prabhu, Xueqing Liang, Davis Seelig, Preshita Desai","doi":"10.1093/carcin/bgaf075","DOIUrl":"10.1093/carcin/bgaf075","url":null,"abstract":"Although preclinical studies consistently indicate that sulfasalazine (SAS) and disulfiram (DSF) are promising agents for the prevention and treatment of lung cancer, their clinical efficacy is limited. This discrepancy is attributed to the poor bioavailability of the drugs. Therefore, in the present study, we explored whether delivery of lower doses of SAS and DSF in nano self-emulsifying drug delivery systems (Nano-SEDDS) improves their potency and efficacy in suppressing malignant progression of lung tumors. Mice were treated with the tobacco smoke carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and once lung adenoma developed, high doses of free SAS (250 mg/kg) + DSF (100 mg/kg) or SEDDS formulations containing lower doses of SAS + DSF (40 mg/kg SAS + 8, 16 or 40 mg/kg DSF) were administered by oral gavage, every other day, for 10 weeks. Although the doses of SAS and DSF contained in SAS + DSF-SEDDS were about 6-fold and 3-15-fold lower, respectively, than the doses of the respective free drugs, SAS + DSF-SEDDS was more effective than free SAS + DSF in reducing the multiplicity of bigger lung tumors (≥1 mm). These effects were paralleled by significant reductions in the multiplicity of adenoma with progression and adenocarcinoma histopathological lesions. Also, lung tumors from mice treated with SAS + DSF-SEDDS exhibited an increase in the level of 4-hydroxynonenal (4-HNE) and malondialdehyde (MDA), lipid peroxidation products. Overall, our results show that the Nano-SEDDS formulation of SAS + DSF is a promising approach to enhance the potency and efficacy of the drugs for lung cancer chemo-interception and treatment.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13370244/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145376146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

MAPK3 modulates enhancer-promoter interactions of SKAP2 in acute myeloid leukemia. MAPK3调控SKAP2在急性髓性白血病中的增强子-启动子相互作用

IF 3.8 3区医学

Carcinogenesis Pub Date : 2025-11-21 DOI: 10.1093/carcin/bgaf073

Yanping Hu, Fang Chen, Tingjie Wang, Bo Wang, Zhizhong Wang, Jiawen Zheng, Yifen Shen, Yihang Shen, Jie Ma, Yongjun Guo

{"title":"MAPK3 modulates enhancer-promoter interactions of SKAP2 in acute myeloid leukemia.","authors":"Yanping Hu, Fang Chen, Tingjie Wang, Bo Wang, Zhizhong Wang, Jiawen Zheng, Yifen Shen, Yihang Shen, Jie Ma, Yongjun Guo","doi":"10.1093/carcin/bgaf073","DOIUrl":"10.1093/carcin/bgaf073","url":null,"abstract":"The regulation of gene expression through chromatin architecture plays a critical role in acute myeloid leukemia (AML). In this study, the influence of MAPK3 on CTCF-mediated chromatin interactions in AML was examined, focusing on gene regulation and chromatin architecture. Immunoprecipitation coupled with mass spectrometry (IP-MS) was conducted to identify CTCF-binding proteins in AML cell lines. Chromatin immunoprecipitation sequencing (ChIP-seq) was used to assess the impact of MAPK3 modulation on CTCF DNA binding, following treatment with an MAPK3 activator or inhibitor. Additionally, chromatin interactions were evaluated using 3C-qPCR, and specific enhancer sites at the SKAP2 locus were deleted using CRISPR-Cas9. Results demonstrated that IP-MS identified MAPK3 as a key CTCF-binding protein, indicating its potential role in AML chromatin regulation. MAPK3 significantly influences CTCF binding at distal intergenic regions upstream of SKAP2, as confirmed by ChIP-seq. Chromatin interaction analyses revealed that CTCF-regulated enhancer-promoter interactions at SKAP2 are modulated by MAPK3 activity. Furthermore, deletion of enhancer regions E4 and E6 led to decreased SKAP2 expression. These findings highlight the critical role of MAPK3 in regulating CTCF-mediated chromatin interactions and suggest that targeting MAPK3-regulated chromatin remodeling could be a novel therapeutic strategy for AML.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145370081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction to: Triple-negative breast cancer molecular subtypes and potential detection targets for biological therapy indications. 更正：三阴性乳腺癌分子亚型和生物治疗适应症的潜在检测靶点。

IF 3.8 3区医学

Carcinogenesis Pub Date : 2025-11-21 DOI: 10.1093/carcin/bgaf086

引用次数: 0