Cancer Biology & Medicine最新文献

{"title":"Identification of immune reconstitution and hematopoiesis restoration by scRNA-seq in bone marrow of multiple myeloma patients treated with high-dose melphalan following auto-HSCT.","authors":"Qian Li, Yaling Wang, Hongfeng Yuan, Qiaomei Cai, Lina Zhao, Li Lin, Shuang Gao, Lin Chen, Zhiying Zhang, Jing Ma, Su Liu, Zeng Cao, Haifeng Zhao, Yufei Wang, Shihui Li, Pan Lv, Huihui Zhang, Guowen Wang, Guang Yang, Xiaodong Zhang, Yafei Wang","doi":"10.20892/j.issn.2095-3941.2025.0585","DOIUrl":"10.20892/j.issn.2095-3941.2025.0585","url":null,"abstract":"","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12980031/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147324700","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":"Psychological health mediates the association between diet and upper gastrointestinal cancer: a cross-sectional analysis from a large-scale population-based screening project.","authors":"Yueying Zhang, Shanrui Ma, Xinqing Li, Ru Chen, Shaoming Wang, Wenqiang Wei","doi":"10.20892/j.issn.2095-3941.2025.0472","DOIUrl":"10.20892/j.issn.2095-3941.2025.0472","url":null,"abstract":"<p><strong>Objective: </strong>Upper gastrointestinal (UGI) cancer, including esophageal and gastric cancers, poses a significant health burden. While unhealthy dietary patterns are a recognized risk factor for UGI cancer, the complex interplay with psychological health that influences UGI cancer risk remains underexplored. The current study aimed to determine the association between dietary quality and UGI cancer, and the link with depression and anxiety symptoms.</p><p><strong>Methods: </strong>Cross-sectional data were drawn from the baseline survey of the National Cohort of Esophageal Cancer study that was conducted between 2017 and 2019 in five high-risk regions of China. Dietary quality was evaluated using the Diet Balance Index (DBI)-16. Psychological symptoms were measured with the Generalized Anxiety Disorder 7-item Scale (GAD-7) and the Patient Health Questionnaire (PHQ)-9. Eligible participants underwent endoscopy screening and suspicious cases were confirmed <i>via</i> pathologic biopsies.</p><p><strong>Results: </strong>A total of 434 UGI cancer cases were confirmed among 29,068 participants. Logistic regression models indicated that poor diet quality, reflected by an inadequate intake [low bound score (LBS)] and unbalanced diet [dietary quality distance (DQD)], was associated with psychological distress (e.g., LBS and anxiety: OR = 1.36, 95% CI: 1.19-1.56). UGI cancer participants had more severe psychological symptoms (e.g., anxiety and UGI cancer: OR = 1.20, 95% CI: 1.14-1.26). Path analysis further revealed that psychological symptoms significantly mediate the relationship between poor dietary quality and UGI cancer risk; specifically, anxiety symptoms mediated 27.78% of the LBS-UGI cancer link.</p><p><strong>Conclusions: </strong>The current study revealed a significant association between dietary quality and UGI cancer risk, suggesting that psychological symptoms may have a mediating role. Incorporating dietary and psychological health management into public health strategies is crucial for comprehensive cancer prevention.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13449715/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147282590","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":"Microbiota-host interaction in colorectal cancer: emerging computational technology, multi-omics integration, and mechanisms.","authors":"Yinghong Lu, Jun Yu","doi":"10.20892/j.issn.2095-3941.2025.0762","DOIUrl":"10.20892/j.issn.2095-3941.2025.0762","url":null,"abstract":"<p><p>Colorectal cancer (CRC) remains a major global health burden with the gut microbiome emerging as a critical contributor to tumor initiation and progression. Advances in high-throughput sequencing have deepened our understanding of host-microbe interactions across genomic, transcriptomic, epigenomic, and metabolomic levels. This review synthesizes current knowledge on how microbial communities shape colorectal carcinogenesis, including induction of genomic instability, remodeling of host transcriptional and epigenetic landscapes, and reprogramming of metabolic pathways within the tumor microenvironment. Integrative multi-omics strategies and advanced computational tools are powerful means for dissecting these complex biological systems. However, analytical challenges, such as data compositionality, sparsity, and high dimensionality, still hinder meaningful interpretation. Emerging technologies, like long-read sequencing and bacterial single-cell spatial transcriptomics, are enhancing the resolution and accuracy of microbiota profiling. Finally, the convergence of advanced experimental models, artificial intelligence-driven computational integration, and precision microbiome medicine are highlighted as key avenues for translating microbiome insights into preventive, diagnostic, and therapeutic innovations in CRC.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13244307/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147282478","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":"Exosomal EPHA2 transfers metastatic potential by stabilizing TGF-βRI and activating the TGF-β/SMAD3 signaling pathway in breast cancer.","authors":"Liming Liu, Yichu Zhang, Xiaoxue Li, Yueni Mo, Lanlan Song, Yidi Jia, Luoming Zhang, Wei Zhou, He Zhang, Hui Guo, Zhiyong Wang, Yanfen Cui, Fei Zhang, Ruifang Niu","doi":"10.20892/j.issn.2095-3941.2025.0440","DOIUrl":"10.20892/j.issn.2095-3941.2025.0440","url":null,"abstract":"<p><strong>Objective: </strong>Intratumoral heterogeneity refers to the presence of distinct subpopulations of cancer cells within a single tumor, which exhibits variations in phenotypic traits, such as proliferation rate, drug sensitivity, and metastatic potential. Dynamic interactions among heterogeneous cell populations have a critical role in tumor progression. Increasing evidence underscores the importance of intercellular communication among heterogeneous cancer cell subpopulations in driving malignancy. However, the molecular mechanisms governing such cancer cell-to-cancer cell interactions are poorly understood.</p><p><strong>Methods: </strong>Exosomes were isolated from highly metastatic breast cancer cells (HM-BCCs) and low metastatic breast cancer cells (LM-BCCs). The role of exosome-mediated intercellular communication on metastatic behavior was assessed using wound healing and Transwell assays. Gene knockdown and overexpression strategies, small-molecule inhibitors, and xenograft mouse models were used to elucidate the role of exosomal EPHA2.</p><p><strong>Results: </strong>Exosomes derived from HM-BCCs considerably enhanced the migratory and invasive capabilities of LM-BCCs <i>in vitro</i> and increased the metastatic potential <i>in vivo</i>. Mechanistically, EPHA2 was identified as a key protein enriched in exosomes from HM-BCCs and was shown to be transferred to LM-BCCs by these vesicles. Exosomal EPHA2 promoted epithelial-to-mesenchymal transition in LM-BCCs when internalized by stabilizing TGF-βRI and activating the transforming growth factor-β/mothers against decapentaplegic homolog 3 (TGF-β/SMAD3) signaling pathway, thereby facilitating the acquisition of a metastatic phenotype.</p><p><strong>Conclusions: </strong>The results underscore the pivotal function of exosomal EPHA2 in mediating the transfer of metastatic potential among heterogeneous breast cancer cell populations. Targeting the EPHA2-TGF-βRI signaling axis may provide a novel therapeutic approach for preventing or limiting breast cancer metastasis.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13498882/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147282432","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":"Postbiotics: emerging bioactive agents in cancer therapy.","authors":"Sihan Li, Fashun Li, Jiasheng Tu, Lei Jiang, Xiqun Jiang","doi":"10.20892/j.issn.2095-3941.2025.0511","DOIUrl":"10.20892/j.issn.2095-3941.2025.0511","url":null,"abstract":"<p><p>Postbiotics, considered the functional successors of live probiotics, retain most of probiotics' structural and/or bioactive properties, and are key mediators of probiotic-environment interactions. Beyond influencing tumor proliferation, metastasis, and immune regulation, postbiotics can enhance the effectiveness of current anti-cancer treatments. Postbiotic-based cancer therapy represents an advanced evolution of bacterial treatment with improved safety and treatment potential. However, the field is limited by postbiotics' imprecise definition and lack of standardized manufacturing methods, which together hinder their clinical application. Here, we establish a systematic classification of postbiotics based on their formation processes, focusing on the complex mechanisms underlying their activity in anti-tumor therapy, their therapeutic promise, and their current clinical use and challenges. Our aim is to guide future research, translation, and industrial development.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13115405/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146225647","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":"Single-cell and spatial transcriptome analyses reveal tumor immunometabolism in lymph node metastasis of lung cancer.","authors":"Yang Zhang, Wangyang Zhu, Chaoqiang Deng, Fangqiu Fu, Yushen Li, Ting Ye, Jiaqing Xiang, Yawei Zhang, Yihua Sun, Hong Hu, Yuan Li, Xiaoming Zhang, Haiquan Chen","doi":"10.20892/j.issn.2095-3941.2025.0587","DOIUrl":"https://doi.org/10.20892/j.issn.2095-3941.2025.0587","url":null,"abstract":"<p><strong>Objective: </strong>Progressive metabolic adaptation of tumor cells enables a thriving tumor microenvironment in which immune cells have diminished killing ability. However, whether and how this adaptation plays an active role in lymph node (LN) metastasis of lung cancer remains unclear.</p><p><strong>Methods: </strong>We collected 37 matched samples of primary tumors, metastatic LNs (MetLNs), uninvolved LNs (uiLNs), and peripheral blood from 10 patients with lung cancer. These samples were profiled with single-cell RNA sequencing, T cell receptor/B cell receptor (TCR/BCR) sequencing, and spatial transcriptomics, capturing 671,467 cells in total. Modulator of Cytochrome C Oxidase during Inflammation (MOCCI)-dependent enhancement of oxidative phosphorylation (OXPHOS) and LN metastasis was demonstrated <i>in vivo</i> and <i>in vitro</i>, and its association with adverse prognosis was validated in an independent cohort from Fudan University Shanghai Cancer Center (<i>n</i> = 875). Spatial neighborhood and ligand-receptor analyses were used to examine primary LN metastatic cancer cell (PLMC)-immune interactions.</p><p><strong>Results: </strong>A PLMC subpopulation, characterized by MOCCI-driven OXPHOS reprogramming, was identified. MOCCI increased OXPHOS and promoted LN metastasis <i>in vivo</i> and <i>in vitro</i>, and higher MOCCI levels correlated with poorer prognosis in the cohort. In MetLNs, follicular helper T cells (Tfh) were significantly elevated but exhibited dysfunctional antigen-presentation programs, whereas naïve and memory B cells were enriched yet showed greater clonal diversity with blunted clonal expansion. Spatial analyses linked these features to MOCCI⁺ PLMCs, which, <i>via</i> GDF15-TGFBR2 axis signaling, drive Tfh exhaustion and suppress adjacent B-cell activation.</p><p><strong>Conclusions: </strong>This study delineated transcriptional differences between primary tumors and MetLNs in lung cancer, thereby providing a foundation for further exploration of LN metastasis.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":8.4,"publicationDate":"2026-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146225707","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":"VDAC1 protein derived from extracellular vesicles promotes paclitaxel resistance in gastric cancer through autophagy and mitophagy.","authors":"Yanna Bi, Sisi Wei, Zhe Zhang, Yuqing Wang, Yang Wen, Hongquan Wang, Kexin Li, Cong Zhang, Yumin Wang, Lianmei Zhao, Guogui Sun","doi":"10.20892/j.issn.2095-3941.2025.0360","DOIUrl":"10.20892/j.issn.2095-3941.2025.0360","url":null,"abstract":"<p><strong>Objective: </strong>Paclitaxel (PTX), a conventional second-line therapeutic agent for advanced gastric cancer (GC), exhibits compromised clinical efficacy due to acquired chemoresistance in patients, the molecular mechanisms of which remain poorly elucidated. This study aimed to investigate the therapeutic potential of targeting extracellular vesicle (EV) protein in reversing PTX resistance in GC cells and to delineate the underlying molecular pathways involved.</p><p><strong>Methods: </strong>Proteomic profiling was used to identify differentially expressed EV proteins in PTX-resistant GC cells. EVs were isolated <i>via</i> size exclusion chromatography (SEC) and characterized using transmission electron microscopy (TEM), nano-flow cytometry (nano-FCM), and western blot analysis. <i>In vivo</i> functional validation was performed in xenograft tumor models by injecting EV proteins into nude mice <i>via</i> the tail vein (6 groups, <i>n</i> = 4). EVs derived from 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS)-treated cells were administered to tumor-bearing nude mouse model (4 groups, <i>n</i> = 5) to determine the impact of EV-derived voltage-dependent anion channel protein 1 (VDAC1) on PTX resistance. In addition, VDAC1 protein expression was evaluated using immunohistochemical (IHC) assays in 34 clinical specimens from PTX-resistant patients.</p><p><strong>Results: </strong>Proteomic analyses demonstrated a marked upregulation of VDAC1 in EVs secreted by PTX-resistant GC cells. Functional studies revealed that intercellular transfer of EV-derived VDAC1 directly conferred PTX resistance to drug-sensitive cancer cells. Gene set enrichment analysis (GSEA) and adenosine triphosphate (ATP) functional assay further elucidated that VDAC1-mediated chemoresistance was mechanistically linked to the activation of adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) signaling and concomitant suppression of the mammalian target of rapamycin - p70 ribosomal protein S6 kinase (mTOR-p70S6K) pathway. <i>In vivo</i> validation confirmed that systemic delivery of EV-derived VDAC1 significantly reduced PTX sensitivity in GC tumors. Furthermore, DIDS inhibited the expression of the VDAC1 protein in EVs, thereby reducing PTX resistance <i>in vivo</i> and <i>in vitro</i>. IHC analysis revealed that VDAC1 expression was significantly higher in GC patients with PTX resistance compared to PTX-sensitive patients.</p><p><strong>Conclusions: </strong>The findings herein underscore the pivotal role of EV-derived VDAC1 in driving PTX resistance in GC through dual modulation of autophagy and mitophagy, mediated by the AMPK/mTOR signaling axis. Targeting EV-derived VDAC1 has emerged as a promising therapeutic strategy to counteract chemoresistance, providing a novel avenue for improving GC treatment outcomes.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12980039/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146212301","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":"Applying microfluidic technology to interpret the tumor immune microenvironment and cancer immunotherapy.","authors":"Xuhong Chen, Dongxian Tan, Shuaiting Liu, Ruolin Luo, Yang Liu, Miaomiao Zhang, Siqi Li, Jing Xu","doi":"10.20892/j.issn.2095-3941.2025.0541","DOIUrl":"10.20892/j.issn.2095-3941.2025.0541","url":null,"abstract":"<p><p>In the past decade, cancer immunotherapy has emerged as a transformative treatment modality for diverse malignancies. Although impressive clinical efficacy has been demonstrated in some cancer patients, most patients respond poorly to immunotherapies. The complicated architecture and cellular composition of the tumor immune microenvironment (TIME) have substantial roles in the clinical outcomes of immunotherapies. Therefore, employing optimal <i>in vitro</i> models recapitulating the <i>in vivo</i> TIME characteristics is particularly important for interpreting the dynamic complexity of the TIME, evaluating drug efficacy, and developing novel immunotherapeutics. In recent years, microfluidic technology has been shown to be a valuable tool for mimicking dynamic crosstalk among the TIME <i>in vitro</i> through the manipulation of microscale fluids in an integrated device. Cellular behaviors, function and signal transduction, and tumor-immune interactions can be monitored in real time and analyzed in microfluidic chips by combining visualization technologies. Numerous recent studies have shown how to design and fabricate microfluidic chips for reproducing the complex three-dimensional architecture and dynamic changes in the TIME. This review comprehensively examines the application of innovative microfluidic technology in the field of cancer immunology research, focusing on interpreting dynamic crosstalk inside the TIME from bulk-cell to single-cell analyses, evaluating the efficacy of novel immunotherapies and preparing immunotherapeutic agents, and analyzes current limitations. This work aimed to propose a translational roadmap for leveraging microfluidics in elucidating mechanisms, biomarker discovery, high-throughput drug screening, and personalized immunotherapy development.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12980036/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146212121","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":"Expert consensus on the detection and clinical application of tumor mutational burden.","authors":"Zhenying Guo, Chunwei Xu, Shirong Zhang, Yue Hao, Xiaotong Hu, Ming Zhao, Chan Xiang, Yingshi Piao, Pingli Sun, Xueping Xiang, Jing Zhao, Huanwen Wu, Weixing Li, Jinpu Yu, Jingping Yuan, Shuangshuang Wang, Cong Wang, Yun Gu, Bingjian Lv, Liping Zhang, Yueping Liu, Xiaobin Cui, Weizhong Gu, Yining Li, Wei Wang, Wenjun Yang, Weiguo Long, Jingjing Xiang, Hong Mou, Biao Liu, Huajuan Ruan, Yubin Wang, Yongjie Zhu, Feng Wang, Zhonghua Wang, Xiaomin Feng, Xing Liu, Peng Li, Min Deng, Bin Lian, Lili Mao, Qian Wang, Wenxian Wang, Zhengbo Song, Ziming Li, Wenzhao Zhong, Zhijie Wang, Shengxiang Ren, Wenfeng Fang, Yongchang Zhang, Jingjing Liu, Xiuyu Cai, Anwen Liu, Wen Li, Ping Zhan, Hongbing Liu, Tangfeng Lv, Liyun Miao, Lingfeng Min, Yu Chen, Yu Zhang, Feng Wang, Zhansheng Jiang, Gen Lin, Long Huang, Xingxiang Pu, Rongbo Lin, Weifeng Liu, Chuangzhou Rao, Dongqing Lv, Zongyang Yu, Peng Shen, Xiaoyan Li, Chuanhao Tang, Chengzhi Zhou, Junping Zhang, Junli Xue, Hui Guo, Qian Chu, Rui Meng, Jingxun Wu, Rui Zhang, Jin Zhou, Zhengfei Zhu, Yongheng Li, Hong Qiu, Fan Xia, Yuanyuan Lu, Xiaofeng Chen, Rui Ge, Enyong Dai, Yu Han, Jian Zhang, Yinghua Ji, Xianbin Liang, Hongmei Zhang, Xuelei Ma, Xuewen Liu, Yu Yao, Peng Luo, Weiwei Pan, Fei Pang, Fan Wu, Dejian Gu, Li Wang, Liping Wang, Youcai Zhu, Li Lin, Weiwen Li, Xinqing Lin, Jing Cai, Ling Xu, Jisheng Li, Xiaodong Jiao, Kainan Li, Jia Wei, Huijing Feng, Lin Wang, Yingying Du, Wang Yao, Xuefei Shi, Xiaomin Niu, Dongmei Yuan, Yanwen Yao, Yinbin Zhang, Binbin Song, Wenfeng Li, Jianfei Fu, Hong Wang, Mingxiang Ye, Dong Wang, Zhaofeng Wang, Qing Ji, Yuan Fang, Qing Wei, Zhen Wang, Bin Wan, Donglai Lv, Xiaofeng Li, Shengjie Yang, Jing Kang, Jiatao Zhang, Chao Zhang, Lin Shi, Yina Wang, Bihui Li, Zhang Zhang, Ke Wang, Zhefeng Liu, Nong Yang, Lin Wu, Xiaobing Chen, Gu Jin, Zhongwu Li, Miao Li, Guansong Wang, Jiandong Wang, Meiyu Fang, Yong Fang, Xiaojia Wang, Jing Chen, Yiping Zhang, Xixu Zhu, Yi Shen, Shenglin Ma, Biyun Wang, Lu Si, Yong Song, Yuanzhi Lu, Aijun Liu, Yuchen Han","doi":"10.20892/j.issn.2095-3941.2025.0351","DOIUrl":"10.20892/j.issn.2095-3941.2025.0351","url":null,"abstract":"<p><p>As an emerging biomarker, tumor mutational burden (TMB) has attracted increasing attention from clinicians in predicting the efficacy of tumor immunotherapy. Currently, TMB is detected primarily by whole-exome sequencing or targeted panel sequencing on high-throughput sequencing platforms. However, the lack of uniformity in detection methods, threshold settings, and reporting formats, as well as the significant differences in TMB values among different cancer types, have hindered the standardized application of this biomarker in clinical practice. This consensus focuses on the definition, standardization of detection, clinical significance, and limitations of TMB, and provides consensus recommendations for the clinical application of TMB in real-world practice in China. This consensus is aimed at helping clinicians and laboratory personnel understand the clinical significance and testing standards of TMB, promoting more accurate interpretation of test results, and improving patient care.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12980037/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146212084","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":"Coordinated DNA methyltransferase 3A and methyltransferase-like 7A activity reprograms the tumor microenvironment through discoidin domain receptor 1 signaling.","authors":"Zhengyang Bai, Dan Yang, Jiayi Li, Yaobang Liu, Bin Lian, Jinping Li","doi":"10.20892/j.issn.2095-3941.2025.0261","DOIUrl":"10.20892/j.issn.2095-3941.2025.0261","url":null,"abstract":"<p><strong>Objective: </strong>Breast cancer is the most common malignancy in women and is characterized by a high recurrence rate that severely impacts patient survival. Regulatory T cells (Tregs) in the tumor microenvironment (TME) promote immune evasion and metastasis, increasing recurrence risk. This study determined how the epigenetic regulators, DNMT3A and METTL7A, modulate Treg infiltration <i>via</i> the <i>DDR1/STAT3/CXCL5</i> axis and influence breast cancer recurrence and prognosis.</p><p><strong>Methods: </strong>RNA sequencing (RNA-seq) was used to identify differentially expressed genes (DEGs), followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment. Machine learning algorithms, including least absolute shrinkage and selection operator (LASSO), supported vector machine-recursive feature elimination (SVM-RFE) and ElasticNet identified DDR1 as a key gene. Validation included RT-qPCR, western blot, MSP, MeRIP-qPCR, and Co-IP to assess epigenetic regulation. Functional assays (CCK-8, Transwell, and Treg differentiation/chemotaxis) and xenograft models evaluated the role of <i>DDR1</i> in tumor progression and recurrence.</p><p><strong>Results: </strong>DNMT3A upregulated <i>DDR1 via</i> DNA methylation, while METTL7A enhanced <i>DDR1</i> mRNA stability <i>via</i> m6A modification. Co-regulation activated the <i>DDR1/STAT3/CXCL5</i> axis, which boosted cancer cell proliferation, migration, and invasion. CXCL5 secretion increased Treg infiltration and accelerated tumor growth <i>in vivo</i>. <i>DDR1</i> silencing reversed these effects, confirming that <i>DDR1</i> has a pivotal role in breast cancer recurrence.</p><p><strong>Conclusions: </strong>DNMT3A and METTL7A were shown to cooperatively regulate <i>DDR1</i> <i>via</i> DNA/m6A methylation, which drives Treg-mediated immune suppression and recurrence. This study provided novel insights and therapeutic targets for breast cancer prognosis and treatment.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":"23 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12911440/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146212260","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}