Cancer Biology & Medicine最新文献

{"title":"Cancer nanomedicine for therapy: emerging strategies and expanding perspectives.","authors":"Linqi Shi","doi":"10.20892/j.issn.2095-3941.2026.0254","DOIUrl":"10.20892/j.issn.2095-3941.2026.0254","url":null,"abstract":"","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13115402/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147728425","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 m7G RNA modification in gastrointestinal cancers: mechanisms and therapeutic potential.","authors":"Rui Li, Xiaoqing Lu, Zhiyu Guan, Xianli Shi, Rongxin Zhang","doi":"10.20892/j.issn.2095-3941.2025.0698","DOIUrl":"https://doi.org/10.20892/j.issn.2095-3941.2025.0698","url":null,"abstract":"<p><p>The N7-methylguanosine (m7G) modification, an epigenetic transcriptional regulatory mechanism, plays a crucial role in the development of gastrointestinal malignant tumors. This modification, mediated by enzyme complexes such as methyltransferase-like 1 (METTL1)/WD repeat domain 4 (WDR4) and williams-beuren syndrome chromosome region 22 (WBSCR22)/tRNA methyl transferase activator subunit 11-2 (TRMT12), is widely distributed in messenger RNA (mRNA), transfer RNA (tRNA), ribosomal RNA (rRNA), and non-coding RNA. Its abnormal expression is closely associated with the pathogenesis of various gastrointestinal tumors, including hepatocellular carcinoma, colorectal cancer, pancreatic cancer, and esophageal cancer. The METTL1/WDR4 complex enhances the translation efficiency of oncogenes by promoting tRNA m7G modification, thereby facilitating tumor cell proliferation, metastasis, and chemotherapy resistance. More importantly, the m7G modification significantly influences tumor cell resistance to chemotherapy, targeted therapy, and radiation therapy by regulating the epidermal growth factor receptor (EGFR) signaling pathway, autophagy processes, and DNA repair mechanisms. Therefore, m7G modification has dual potential as both a prognostic biomarker and a therapeutic target, and may provide a molecular basis for precision medicine in the treatment of gastrointestinal tumors.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":8.4,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147728422","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":"Unravelling the role of PANoptosis in diseases: from emerging molecular mechanisms-to-therapeutic implications.","authors":"Yi Zhu, Shengming Ou, Xuer Ye, Juncheng Li, Xiaoya Nie, Hongwei Shao, Rongxin Zhang, Jinrong Zhu","doi":"10.20892/j.issn.2095-3941.2026.0012","DOIUrl":"10.20892/j.issn.2095-3941.2026.0012","url":null,"abstract":"<p><p>PANoptosis represents a distinct form of programmed cell death (PCD) that is characterized by the integration of key features from apoptosis, pyroptosis, and necroptosis but cannot be fully explained by any single cell death pathway. A key trigger of PANoptosis is the assembly and activation of the PANoptosome. To date, four types of PANoptosomes have been identified, including PANoptosomes nucleated by Z-DNA binding protein 1 (ZBP1), absent in melanoma 2 (AIM2), receptor-interacting protein kinase 1 (RIPK1), and NOD-like receptor protein 12 (NLRP12). This review summarizes current advances in the molecular regulatory mechanisms underlying PANoptosis and delineates the assembly and activation processes of several PANoptosome complexes. Furthermore, the role of PANoptosis in various pathologic conditions, such as infectious diseases, autoimmune disorders, neurodegenerative diseases, and cancer, are discussed. Recent preclinical and clinical advances in targeting the PANoptosis pathway through small molecule inhibitors, nanomedicines, and combination therapies for the treatment of infectious diseases, inflammatory conditions, and malignancies are also highlighted. However, current research involving the mechanisms underlying PANoptosis are preliminary and the clinical translation faces significant challenges, necessitating further in-depth exploration. This review demonstrates that targeting molecular components and signaling pathways of PANoptosis represents a highly promising therapeutic strategy, aiming to provide a theoretical foundation for the development of novel clinical treatments for related diseases.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13617947/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147728376","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 foundation model-enhanced CT radiomics signature for the noninvasive assessment of tertiary lymphoid structures and prediction of therapy benefit in gastric cancer.","authors":"Xianchun Gao, Zhe Li, Jun Yu, Jiangpeng Wei, Didi Wen, Ning Han, Linbin Lu, Yongxi Song, Qiong Xiao, Guangtao Wu, Kun Feng, Shibo Wang, Zhongyang Zhang, Dai Zhang, Ling Chen, Zengshan Li, Minwen Zheng, Yong Xia, Yongzhan Nie","doi":"10.20892/j.issn.2095-3941.2026.0076","DOIUrl":"10.20892/j.issn.2095-3941.2026.0076","url":null,"abstract":"","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13617948/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147728410","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":"Poor prognosis outcome tumors, bacteria-infected tumors and nanodrugs: current evidence and hypotheses towards a paradigm change for treatment.","authors":"Henk J Busscher, David W Grainger, JinPu Yu, Da-Yuan Wang","doi":"10.20892/j.issn.2095-3941.2025.0748","DOIUrl":"10.20892/j.issn.2095-3941.2025.0748","url":null,"abstract":"<p><p>New therapies and supportive care have converted several cancer types into chronic conditions. Yet, some tumors exhibit features reproducibly correlated with poor prognosis outcome (PPO-tumors). Bacteria in a tumor environment can inactivate chemotherapeutics and are a feature of PPO-tumors, although standard diagnostic tests for tumor infections do not exist. Optimism is high for nanotechnologic innovations but nanoparticulate chemotherapeutics based on enhanced permeability and retention in a human tumor environment have only shown limited treatment benefits. Moreover, treatment of infected tumors in animals with stimuli-responsive nanocarriers loaded with an antibiotic/chemotherapeutic combination has demonstrated limited benefits compared to treatment with combinations of carrier-free antibiotics and chemotherapeutics. Development of nanoparticulate chemotherapeutics with significant benefits in human clinical use is estimated to take several decades, which is too long for patients with PPO-tumors. Herein we hypothesize the following: 1-all diagnosed PPO-tumors are infected with bacteria; 2-all PPO-tumors in mice and humans exhibit enhanced permeability to chemotherapeutics; and 3-all diagnosed PPO-tumors must be treated from the onset with a combination of carrier-free antibiotics and chemotherapeutics. Each hypothesis was critically evaluated and judged plausible and clinically acceptable. Potential clinical treatment of PPO-tumors, presuming bacterial infection without diagnosis, with an approved antibiotic and chemotherapeutic free drug combination requires a paradigm change in treatment concept towards more lenient antibiotic use. However, many cancer patients already require antibiotics during chemotherapeutic treatment and combined carrier-free antibiotic/chemotherapeutic treatment may provide an immediate pathway to re-sensitize PPO-tumors to clinically used chemotherapeutics and alter the prognosis to a more favourable outcome.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13115410/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147697247","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":"Pyroptosis in cancer: a dual regulator of tumor cell fate and immune activation.","authors":"Yuewen Zhang, Mengshi Luo, Zhiqi Liao, Qiuyang Xu, Ding Ma, Qinglei Gao, Tao Zhu, Yong Fang","doi":"10.20892/j.issn.2095-3941.2025.0826","DOIUrl":"https://doi.org/10.20892/j.issn.2095-3941.2025.0826","url":null,"abstract":"<p><p>Pyroptosis is a form of programmed cell death (PCD) that triggers inflammation. Pyroptosis is activated by specific inflammasomes and caspases, leading to the cleavage of gasdermin protein families, especially gasdermin D (GSDMD) and gasdermin E (GSDME). While pyroptosis has been extensively linked to innate immunity and diseases, such as atherosclerosis, the role in cancer remains an area of active investigation. Studies have suggested that pyroptosis influences tumor behavior, including proliferation and invasion, across different tissue types and genetic backgrounds. This process occurs through both canonical and non-canonical pathways involving GSDMD and GSDME. Tumors tend to thrive in the chronic inflammatory environment created by pyroptosis but tumors are more likely to be eradicated if pyroptosis occurs suddenly and extensively. Indeed, targeting pyroptosis pathways holds promise as an anticancer strategy. To date, several drugs are found to have the ability of inducing pyroptosis to enhance tumor clearance. Moreover, pyroptosis-related genes (PRGs) have emerged as valuable biomarkers for prognosis and monitoring the tumor microenvironment (TME). This review explores the mechanisms underlying endogenous and exogenous pyroptosis in cancer, examines the dual role within tumors, discusses the potential for targeting pyroptosis in cancer treatment and prognosis, and highlights the interactions between pyroptosis and other forms of PCD in cancer.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":8.4,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147697220","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":"Machine learning-based clinical decision support tool for advanced ESCC in the immunotherapy era: a multi-center study.","authors":"Hui Bai, Xiaofeng Wang, Qifeng Wang, Jiacheng Li, Chengcheng Fan, Xiao Liu, Yujin Xu, Qin Xiao, Hao Zhang, Bingyi Wang, Qingsong Pang, Biqi Chen, Mian Xi, Zhiyong Yuan, Jianzhong Cao, Baoqing Chen, Wencheng Zhang","doi":"10.20892/j.issn.2095-3941.2025.0597","DOIUrl":"https://doi.org/10.20892/j.issn.2095-3941.2025.0597","url":null,"abstract":"<p><strong>Objective: </strong>We aimed to develop clinical decision support tools for patients with treatment-naïve advanced esophageal squamous cell carcinoma (ESCC).</p><p><strong>Methods: </strong>Patients who received first-line immunochemotherapy with or without radiotherapy between 2018 and 2023 across 9 centers were included in the current study. Candidate predictors were routine clinical variables such as patient demographics, tumor characteristics, and treatment details. Feature selection was conducted using the least absolute shrinkage and selection operator (LASSO), Boruta, and stepwise feature selection method. The models were fitted using 4 machine learning algorithms and a Cox proportional hazards model was set as a benchmark, comparing model predictive performance by computing the time-dependent area under the receiver operator curve (tAUC). Concordance index (C-index), Brier score, calibration plots, precision-recall (PR) curves, decision curve analysis (DCA), and held-out testing and external validation were utilized for evaluating model robustness, transportability, and clinical utility. SHapley Additive exPlanations (SHAP) analysis was used to rank feature importance and explain the models.</p><p><strong>Results: </strong>A total of 1,048 patients were included, comprising the training/test (<i>n</i> = 828) and validation cohorts (<i>n</i> = 220). The random survival forest model that was constructed following feature selection using Boruta [Boruta-random survival forest (RSF)] showed the highest predictive performance. The tAUCs for 6-, 12-, and 18-month OS were 0.886, 0.775, and 0.772, respectively, in the training set, which significantly outperformed all other models (<i>P</i>-adjust < 0.05). This superiority persisted in the external validation cohort (all tAUCs > 0.750). The Boruta-RSF model exhibited excellent calibration and the highest clinical net benefit on DCA. A publicly accessible web calculator (https://escc.shinyapps.io/ESCC/) was implemented, enabling individualized overall survival prediction under varying treatment scenarios.</p><p><strong>Conclusions: </strong>The Boruta-RSF model, leveraging routinely available clinical variables with the corresponding web calculator, facilitates personalized prognostic assessment and optimization of treatment strategies.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":8.4,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147688346","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":"Metabolic regulation of tumor-associated macrophage function and immunotherapy in cancer.","authors":"Mingyue Zhao, Rui Chen, Ping Gao","doi":"10.20892/j.issn.2095-3941.2025.0626","DOIUrl":"10.20892/j.issn.2095-3941.2025.0626","url":null,"abstract":"<p><p>Tumor-associated macrophages (TAMs), essential components of the tumor immune microenvironment (TIME), undergo metabolic reprogramming as part of functional adaptation. Tumor cells modulate TAMs through multiple mechanisms, including metabolic cross-feeding, cytokine production, extracellular vesicles, tumor-derived proteins (such as GRP78) and pathogen-associated patterns (such as Lipopolysaccharide) signaling mediators. In turn, metabolic alterations in TAMs fine-tune TAM function <i>via</i> intricate signaling networks with outcomes that vary across cancer types. These functional and phenotypic shifts enable TAMs to influence malignant cells and other TIME components, such as T cells, NK cells, and fibroblasts, through the secretion of inflammatory factors and changes in surface marker expression. This process establishes an extensive network of interconnected cellular crosstalk. In this review the metabolic alterations-intracellular signaling-TAM biology axis is linked to cancer progression contributions and the implications for immunotherapy across diverse malignancies. Building on these insights, current preclinical and clinical studies with a focus on TAMs were surveyed and the advantages and challenges of TAM-targeted therapeutic strategies were systematically evaluated. We anticipate that these perspectives will spur further investigation into TAM-specific immune targets and accelerate the development of next-generation cancer immunotherapies.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13326602/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147688421","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":"Circadian-driven transcriptional programs govern metastatic progression.","authors":"Jie Wang, Hao Pan, Xuan Wang, Yuru Ren, Yiwen Huang, Yizhou Liu, Hejin Lai, Zhimin Fei, Ning Pu, Yu Wang","doi":"10.20892/j.issn.2095-3941.2025.0491","DOIUrl":"10.20892/j.issn.2095-3941.2025.0491","url":null,"abstract":"<p><p>Circadian rhythms orchestrate 24-h oscillations in gene expression to govern diverse physiologic functions. Mounting evidence suggests that circadian disruption, resulting from aberrant light exposure, shift work, or genetic mutations in core clock genes (e.g., <i>BMAL1</i> and <i>PER2</i>), promotes tumorigenesis and progression by dysregulating proliferation, apoptosis, cell cycle progression, metabolic reprogramming, and senescence. Critically, the circadian clock exerts spatiotemporal control over the tumor microenvironment, a dynamic ecosystem central to metastatic efficiency. This review synthesizes emerging mechanisms underlying circadian regulation of tumor microenvironment (TME) components during the metastatic cascade: 1) extracellular matrix (ECM) dynamics. Circadian oscillation of matrix metalloproteinases remodels collagen alignment at invasive edges. 2) Stromal crosstalk. Rhythmic secretion of cytokine by cancer-associated fibroblasts or macrophages gates intravasation efficiency on circulating tumor cells. 3) Immune-extravasation axis. Diurnal variations in endothelial adhesion molecules (ICAM-1/VCAM-1) regulate CTC extravasation, synchronized with neutrophil infiltration peaks. In this review how circadian perturbations (e.g., jet lag-induced cortisol spikes or CRY1 knockout) alter cytokine networks (TGF-β/IL-6), hypoxia responses, and metabolic symbiosis within the TME were dissected. This work unveiled chronotherapeutic targets to disrupt metastasis timing by integrating recent single-cell RNA-seq and intravital imaging data. However, details regarding the molecular mechanisms underlying TME have not been established. We anticipate that upcoming research will deepen our comprehension of these complex interactions, facilitating the creation of novel strategies for cancer therapy.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13617944/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147670642","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":"How the gut microbiome affects the immunotherapy response in hepatocellular carcinoma.","authors":"Mengrui Wu, Yating Zhang, Jun Yu","doi":"10.20892/j.issn.2095-3941.2025.0761","DOIUrl":"10.20892/j.issn.2095-3941.2025.0761","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) remains a major global health challenge with limited long-term survival despite advances in surgical, locoregional, and systemic treatments. Although immune checkpoint blockade (ICB) has reshaped HCC therapy, only a subset of patients achieves durable responses, reflecting substantial heterogeneity in tumor biology and immune microenvironments. Dysbiosis, involving the loss of beneficial bacteria, like <i>Lactobacillus reuteri</i> and <i>Akkermansia muciniphila</i>, and the expansion of pathogens, such as <i>Klebsiella pneumoniae</i> and <i>Catenibacterium mitsuokai</i>, drives HCC by promoting microbial translocation and chronic inflammation. This process is mediated by microbiota-derived metabolites. Pro-carcinogenic agents, like deoxycholic acid (DCA) and quinolinic acid, induce inflammation and activate oncogenic pathways, while protective short-chain fatty acids (SCFAs), like acetate and butyrate, modulate T-cell and ILC3 responses to influence antitumor immunity. Tryptophan catabolites, acting <i>via</i> the aryl hydrocarbon receptor (AhR), further fine tune immune and barrier functions. In addition, emerging data implicate intratumoral microbiota as active modulators of immune suppression and metastatic behavior. These mechanistic insights have accelerated the development of microbiome-targeted interventions, such as probiotics, prebiotics, engineered bacterial strains, and fecal microbiota transplantation, to enhance ICB responsiveness. This review synthesizes current advances linking the gut microbiome to HCC immunobiology and highlights emerging therapeutic strategies aimed at optimizing immunotherapy through precise microbial modulation.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13244310/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147670563","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}