Zihe Xu, Lan Mu, Hao Su, Xiaoting Zhang, Haiyun Shang, Zhuotian Li, Matthew Tak Vai Chan, William Ka Kei Wu, Huarong Chen
{"title":"Probiotics in colorectal cancer: mechanisms, biomarkers, and adjunct strategies.","authors":"Zihe Xu, Lan Mu, Hao Su, Xiaoting Zhang, Haiyun Shang, Zhuotian Li, Matthew Tak Vai Chan, William Ka Kei Wu, Huarong Chen","doi":"10.20892/j.issn.2095-3941.2026.0133","DOIUrl":"10.20892/j.issn.2095-3941.2026.0133","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is among the most common malignant tumors and remains a leading cause of cancer-related mortality worldwide. The gut microbiota and metabolites, which are modulated by host genetics and environmental exposures, have emerged as key contributors to the pathogenesis of CRC. A key feature of gut dysbiosis in CRC is the enrichment of pathogenic bacteria alongside the depletion of beneficial commensals. Probiotic supplementation has been shown to counteract this imbalance and suppress tumor progression. Mechanistically, probiotics suppress CRC development through multifaceted actions, including directly inhibiting tumor cell growth, reducing inflammation, reinforcing the intestinal barrier, and reprogramming host immunity. This review summarizes evidence on the inhibitory role of probiotics in CRC, evaluates the potential of probiotics as predictive biomarkers, and discusses microbiome-modulation strategies designed to enhance immunotherapy and chemotherapy, thereby offering a complementary paradigm for CRC prevention and treatment.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13244304/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147866710","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":"<i>Bifidobacterium animalis</i> suppresses melanoma progression and activates anti-tumor immunity by inhibiting YAP1 expression in CD8+ T cells.","authors":"Chengyi Li, Xuehua Zhang, Yichen Yang, Haotian Zeng, Yanqiang Shi, Jinjin Zhang, Lingjun Liu, Chenwei Zhu, Zhiwen Zhang, Chao Li, Xudong Wang, Xiaowu Bai, Haijun Deng, Qing Li","doi":"10.20892/j.issn.2095-3941.2025.0652","DOIUrl":"10.20892/j.issn.2095-3941.2025.0652","url":null,"abstract":"<p><strong>Objective: </strong>The probiotic, <i>Bifidobacterium animalis</i>, (<i>B. animalis</i>) is known to provide health benefits in humans. This study investigated the role of <i>B. animalis</i> in suppressing malignant melanoma progression and modulating tumor immunity.</p><p><strong>Methods: </strong><i>Bifidobacterium</i> spp. were isolated from human faeces and verified by whole-genome sequencing. The anti-tumor effects were assessed in B16-F10 melanoma cells. <i>B. animalis</i> efficacy was further evaluated in a syngeneic murine model. Immune profiling was performed with flow cytometry and CD8<sup>+</sup> T cell dependency was tested with antibody depletion. Functional metabolites were analyzed by liquid chromatography-mass spectrometry (LC-MS). Transcriptome sequencing elucidated the YAP1 mechanism in CD8<sup>+</sup> T cells. Gut microbiota composition was assessed <i>via</i> shotgun metagenomic sequencing.</p><p><strong>Results: </strong>Among the selected <i>Bifidobacterium</i> spp., <i>B. animalis</i> and its conditioned medium effectively inhibited melanoma cell proliferation. Oral administration of <i>B. animalis</i> significantly reduced the growth of B16-F10 allografts, accompanied by an increase in tumor-infiltrating effector T cells. The bioactive component of <i>B. animalis</i> was identified as a < 3-kDa non-protein fraction containing mannose, which phenocopied the anti-tumor and immunostimulatory effects of <i>B. animalis</i>. Microbiota profiling revealed probiotic enrichment in mannose-treated mice. CD8<sup>+</sup> T cell depletion abrogated mannose efficacy. Combination therapy with <i>B. animalis</i> and anti-PD-1 synergistically enhanced tumor control and T cell activation. Mechanistically, the bioactive fraction and mannose downregulated YAP1 expression in CD8<sup>+</sup> T cells.</p><p><strong>Conclusions: </strong><i>B. animalis</i> suppresses melanoma tumorigenesis in mice by restoring gut microbiota and secreting functional mannose. Mannose enhances anti-PD-1 efficacy by inhibiting YAP1 expression in CD8<sup>+</sup> T cells, thereby improving effector function. <i>B. animalis</i> may serve as a preventive measure for melanoma management.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13244316/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834061","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}
Chuxiong Cheng, Jingsong Wang, Jin Xie, Hanlin Yin, Zhihang Xu, Yuqi Xie, Taochen He, Zhenlai Jiang, Yu Wang, Wenchuan Wu, Wenhui Lou, Jie Wang, Liang Liu, Ning Pu
{"title":"Gut microbiota and pancreatic cancer: tumorigenesis, progression, and clinical applications.","authors":"Chuxiong Cheng, Jingsong Wang, Jin Xie, Hanlin Yin, Zhihang Xu, Yuqi Xie, Taochen He, Zhenlai Jiang, Yu Wang, Wenchuan Wu, Wenhui Lou, Jie Wang, Liang Liu, Ning Pu","doi":"10.20892/j.issn.2095-3941.2025.0650","DOIUrl":"10.20892/j.issn.2095-3941.2025.0650","url":null,"abstract":"<p><p>Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive malignancies of the digestive system, with a 5-year survival rate of only 13%, which is largely due to late-stage diagnosis and limited therapeutic options. Emerging evidence indicates that the gut microbiota has a critical role in PDAC tumorigenesis, progression, and therapeutic response. This review comprehensively summarizes current insights into gut microbiota-PDAC interactions, highlighting microbial alterations across taxonomic, functional, and clinical dimensions. Gut dysbiosis, which is marked by depletion of beneficial species and enrichment of pathogenic taxa, contributes to carcinogenesis through chronic inflammation, immune dysregulation, and metabolic reprogramming. In particular, the loss of butyrate-producing bacteria reduces anti-inflammatory activity and weakens CD8<sup>+</sup> T cell function, thereby promoting tumor development. In addition to initiation, the gut microbiota also shapes PDAC progression through direct translocation to pancreatic tissue and systemic regulation of the tumor microenvironment (TME), influencing immune cell dynamics and fostering therapeutic resistance. Clinically, distinct microbial signatures are emerging as potential diagnostic and prognostic biomarkers. Moreover, microbiota-targeted interventions, including probiotics, synbiotics, fecal microbiota transplantation (FMT), metabolite supplementation, and dietary modulation, show promise as adjunctive therapeutic strategies. However, significant challenges remain in defining causal mechanisms and translating these findings into practice. Future research should integrate multi-omics profiling with well-designed clinical trials to delineate the gut microbiota-PDAC interaction network, guide precision microbiota-based interventions, and ultimately enable earlier detection and personalized treatment of this lethal disease.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13244306/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147762720","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":"Tumor microenvironment-driven natural killer cell diversity: mechanisms and therapeutic opportunities.","authors":"Yue Duan, Mingzhen Zhou, Xingxian Guo, Tianyu Cao, Yuanyuan Lu, Xiaodi Zhao","doi":"10.20892/j.issn.2095-3941.2025.0829","DOIUrl":"10.20892/j.issn.2095-3941.2025.0829","url":null,"abstract":"<p><p>Natural killer (NK) cells are key effector cells involved in tumor immune surveillance, yet their function within the tumor microenvironment (TME) exhibits considerable complexity and plasticity that cannot be adequately explained by the classical CD56/CD16 dichotomy. This functional diversity arises from the phenotypic adaptability and dynamic differentiation of distinct NK cell subsets shaped by the TME. In this review, we systematically examine the defining characteristics and functional roles of recently identified NK cell subsets in the TME; elucidate the molecular mechanisms governing their regulation; and highlight the functional transitions and cooperative interactions among these subsets. Moreover, building on current evidence, we summarize emerging immunotherapeutic approaches targeting specific NK cell subsets. Together, these perspectives offer new insights and strategic directions for deciphering the multifaceted roles of NK cells in antitumor immunity and advancing the development of subset-targeted therapies.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13498884/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147762992","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}
Yating Bai, Zhihao Lan, Nana Feng, Zhanzhan Zhang, Yang Liu
{"title":"Design principles of nanomaterials for cancer immunotherapy: a mechanistic framework across the cancer immunity cycle.","authors":"Yating Bai, Zhihao Lan, Nana Feng, Zhanzhan Zhang, Yang Liu","doi":"10.20892/j.issn.2095-3941.2025.0737","DOIUrl":"10.20892/j.issn.2095-3941.2025.0737","url":null,"abstract":"<p><p>Cancer immunotherapy has revolutionized oncology by harnessing the immune system to eliminate malignant cells, yet its efficacy remains constrained by insufficient antigen presentation, limited T cell infiltration, and the immunosuppressive tumor microenvironment (TME). Nanotechnology provides strategies to address these barriers by enabling the precise delivery of antigens, adjuvants, cytokines, checkpoint inhibitors, and nucleic acids, while protecting labile cargos and allowing for controlled release. Beyond serving as carriers, nanoparticles can regulate antitumor immunity by enhancing antigen presentation, promoting T cell priming and infiltration, and remodeling the TME. This review outlines key physiological barriers to <i>in vivo</i> nanoparticle delivery and the corresponding engineering optimization strategies, and systematically summarizes representative advances in using nanomaterials to enhance antigen presentation, promote T cell priming and intratumoral infiltration, and remodel the tumor microenvironment. We further discuss major translational limitations, including heterogeneous tumor accumulation, intracellular trafficking bottlenecks, safety considerations, and manufacturing consistency, and finally highlight the realizable potential of nano-immunotherapy to improve both the efficacy and specificity of cancer immunotherapy.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":"23 4","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13115413/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147762994","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}
Lanping Jiang, Tianhui Li, Jiayu Wu, Harry Cheuk Hay Lau, Chi Chun Wong, Xingyu Zhou, Alvin Ho Kwan Cheung, Qinyao Wei, Jing Ren, Xiang Zhang, Qing Li, Yongzhan Nie, Jun Yu
{"title":"Dietary nitrate drives gastritis by modulating gastric microbiota and metabolites.","authors":"Lanping Jiang, Tianhui Li, Jiayu Wu, Harry Cheuk Hay Lau, Chi Chun Wong, Xingyu Zhou, Alvin Ho Kwan Cheung, Qinyao Wei, Jing Ren, Xiang Zhang, Qing Li, Yongzhan Nie, Jun Yu","doi":"10.20892/j.issn.2095-3941.2025.0679","DOIUrl":"10.20892/j.issn.2095-3941.2025.0679","url":null,"abstract":"<p><strong>Objective: </strong>Dietary nitrate has been increasingly recognized as a potential carcinogen associated with gastritis. In this study the mechanistic role of a high-nitrate diet (NaD) in driving gastritis was elucidated with a focus on modulation of the gastric microbiota composition and metabolomic profiles.</p><p><strong>Methods: </strong>Animals were randomly assigned to two dietary intervention groups using a C57BL/6 mouse model: a NaD containing 7.5% nitrate; or a standard normal diet (ND). Gastric microbiota composition was characterized based on full-length 16S rRNA sequencing and gastric metabolite profiles were analyzed using high-performance liquid chromatography-mass spectrometry (HPLC/MS). Finally, the roles of the microbiome and metabolites in gastritis development were validated using the human gastric epithelial cell line (GES-1), as well as conventional and germ-free mouse models.</p><p><strong>Results: </strong>NaD induced gastritis in conventional mice compared to ND-fed mice. In addition, NaD incited the infiltration of macrophages and neutrophils with elevated levels of inflammatory cytokine genes (<i>IL-17a, Ccl20, Cxcl5, IL-6,</i> and <i>Ccl2</i>). A significant shift in the composition of the gastric microbiota occurred with an increase in pathogenic bacteria (<i>Enterococcus gallinarum</i>, <i>Prevotella timonensis</i>, and <i>Mycobacterium gordona</i>) and a decrease in probiotics (<i>Roseburia hominis</i>, <i>Clostriduim scindens</i>, and <i>Faecalibacterium prausnitzii</i>). Furthermore, NaD induced alterations in the metabolic profile, marked by an elevated level of 5-hydroxyindoleacetate (5-HIAA), a key downstream metabolite of the tryptophan metabolic pathway. Notably, 5-HIAA also upregulated the levels of inflammatory cytokines in the human gastric epithelial GES-1 cell line. In addition, both <i>E. gallinarum</i> colonization and 5-HIAA exposure significantly increased inflammatory responses in conventional and germ-free mouse models.</p><p><strong>Conclusions: </strong>NaD drives gastritis in mice by inducing gastric microbial dysbiosis and metabolomic dysregulation with elevated 5-HIAA.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13244314/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763519","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":"Evolution in single-cell proteomics drives new frontiers in cancer biology and precision medicine.","authors":"Yi Liu, Yingdong Du, Ran Su, Ruibing Chen","doi":"10.20892/j.issn.2095-3941.2025.0464","DOIUrl":"https://doi.org/10.20892/j.issn.2095-3941.2025.0464","url":null,"abstract":"<p><p>The inherent heterogeneity of cancer leads to varied responses to treatment and underscores the need for the development of precision medicine. Single-cell proteomics is crucial for deciphering intra- and inter-tumor heterogeneity. Mass cytometry and other antibody-based technologies, which enable simultaneous quantification of >100 proteins per cell, have been widely applied in cancer studies. Concurrently, liquid chromatography-tandem mass spectrometry-based single-cell proteomics has dramatically improved protein coverage from approximately 1,000 to >6,500 proteins per cell, driven by enhanced sample preparation, instrumentation, and throughput. These high-throughput capabilities now empower large-scale, protein-level analyses, which have uncovered detailed maps of tumor heterogeneity. The resulting insights deepen our understanding of tumor biology and provide new opportunities for guiding precision cancer medicine.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":8.4,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147762282","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":"Opportunities and challenges of immunotherapy for patients with resectable and potentially resectable stage III non-small cell lung cancer.","authors":"Yuzhen Cui, Jingdong Xu, Junxu Wen, Jianfeng Peng, Jiangao Ren, Ailing Liu, Xiangjiao Meng, Zhaoqin Huang, Anwen Liu","doi":"10.20892/j.issn.2095-3941.2025.0589","DOIUrl":"10.20892/j.issn.2095-3941.2025.0589","url":null,"abstract":"<p><p>The integration of immune checkpoint inhibitors has transformed the therapeutic landscape for patients with resectable and potentially resectable stage III non-small cell lung cancer, providing unprecedented opportunities for curative treatment. Several trials have investigated immune checkpoint inhibitors, either alone or in combination with chemotherapy or radiotherapy, as neoadjuvant and/or adjuvant approaches for resectable and potentially resectable stage III non-small cell lung cancer. This comprehensive review elaborates and deeply analyzes the evolving evidence from landmark clinical trials and emerging treatment strategies. Despite these promising outcomes, significant challenges remain, including optimal treatment modality selection, controversy about adjuvant immunotherapy for patients who have already achieved a pathologic complete response, appropriate endpoint evaluation, and biomarker identification. This review also discusses future directions for optimizing immunotherapy integration in patients with resectable stage III non-small cell lung cancer, emphasizing the need for personalized treatment approaches to maximize patient benefit while addressing unanswered clinical questions.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13326603/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147762673","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}
Ying Zhang, Bingyu Tan, Qianying Zhou, Lixia Xu, Lei Zhou
{"title":"Tumor-resident bacteria in gastrointestinal cancers: from regulatory mechanisms to clinical implications.","authors":"Ying Zhang, Bingyu Tan, Qianying Zhou, Lixia Xu, Lei Zhou","doi":"10.20892/j.issn.2095-3941.2025.0686","DOIUrl":"10.20892/j.issn.2095-3941.2025.0686","url":null,"abstract":"<p><p>The human microbiome is increasingly recognized as a key contributor to the tumor microenvironment (TME). Advances in sequencing technologies have revealed the pivotal role of intratumoral microbiota in the development of gastrointestinal cancers. This review summarizes current knowledge on the characteristics and functional mechanisms of tumor-resident bacteria in colorectal, gastric, and hepatocellular carcinoma. We describe how these microbes affect carcinogenesis and disease progression through multiple pathways, including interactions between the microbiota and the host gut barrier, tumor cells, anti-tumor immunity, and other non-cellular components of the TME. In addition, the translational potential of intratumoral microbiota as diagnostic and prognostic biomarkers, as well as the influence on therapeutic responses, is discussed. A growing understanding of tumor-microbe interactions not only deepens insight into cancer biology but also opens new directions for innovative diagnostic and therapeutic strategies, highlighting the potential of targeting the intratumoral microbiome to improve patient outcomes in gastrointestinal oncology.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13244313/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147728431","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":"From diagnostic marker-to-therapeutic modality: emerging paradigms in tumor biomineralization.","authors":"Fan Liu, Qiqi Cao, Qinglan Chen, Zimo Dong, Anru Wang, Negar Hosseini, Han Han, Yuxuan Shen, Yutong Wu, Liyan Miao, Huabing Chen","doi":"10.20892/j.issn.2095-3941.2026.0008","DOIUrl":"10.20892/j.issn.2095-3941.2026.0008","url":null,"abstract":"<p><p>Biomineralization is a highly regulated, multi-scale biological process that is well-characterized in physiologic contexts but remains poorly understood in pathologic settings. Tumor-associated calcification frequently occurs in clinical practice but is often regarded as an imaging feature rather than an active biological phenomenon. Existing evidence has indicated that tumor calcification is closely linked to cancer progression, prognosis, and underlying biological behavior. This review synthesizes current knowledge on tumor-associated biomineralization from a multidisciplinary perspective, integrating insights from oncology, cell biology, pathology, materials science, and systems biology. The major types and microstructural features of calcium deposition that occur in tumors are summarized and the clinical correlations are discussed. The proposed molecular and cellular mechanisms, including organelle-mediated mineral nucleation, metabolic regulation, differentiation-driven processes, and cell fate-dependent pathways, were further examined. Advances in multi-omics technologies, biomimetic models, and analytical characterization methods are highlighted as critical enablers for mechanistic investigation across biological scales. Finally, emerging strategies that exploit induced tumor calcification using engineered materials as a potential drug free therapeutic and diagnostic approach are discussed. By framing tumor calcification as an active, regulated phenotype, this review aims to provide a unified conceptual framework, identify current knowledge gaps, and encourage future research toward translational applications in cancer diagnosis and treatment.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13115419/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147728370","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}