Trends in cancerPub Date : 2025-06-25DOI: 10.1016/j.trecan.2025.06.009
Gaofeng Fan, Yuetong Wang, Ruoning Wang
{"title":"Recharging aged-CAR with NAD<sup>+</sup> to boost immunotherapy.","authors":"Gaofeng Fan, Yuetong Wang, Ruoning Wang","doi":"10.1016/j.trecan.2025.06.009","DOIUrl":"https://doi.org/10.1016/j.trecan.2025.06.009","url":null,"abstract":"<p><p>Impaired cellular metabolism contributes to the age-related decline in T cell function, undermining the response to immunotherapy in older patients with cancer. In a recent study, Hope et al. report that a reduction in intracellular NAD<sup>+</sup> levels compromises metabolic fitness and drives immunosenescence. Notably, restoring NAD<sup>+</sup> levels can reverse age-related chimeric antigen receptor (CAR)-T deterioration, suggesting a promising 'metabolic immunotherapy' that widely benefits older patients with cancer.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":14.3,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144508437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Trends in cancerPub Date : 2025-06-25DOI: 10.1016/j.trecan.2025.06.006
Daolin Tang, Rui Kang
{"title":"Transcriptional regulation of cuproptosis resistance in cancer therapy.","authors":"Daolin Tang, Rui Kang","doi":"10.1016/j.trecan.2025.06.006","DOIUrl":"https://doi.org/10.1016/j.trecan.2025.06.006","url":null,"abstract":"<p><p>Cuproptosis is a newly identified form of copper-dependent cell death. Recent studies show that solid tumors evade this process through transcriptional reprogramming, including hypoxia inducible factor 1 subunit alpha (HIF1A) and NFE2 like BZIP transcription factor 2 (NFE2L2) activation and BTB domain and CNC homolog 1 (BACH1) suppression. Targeting these pathways may restore cuproptosis sensitivity, offering a promising strategy to overcome therapy resistance in cancer.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":14.3,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144508438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Trends in cancerPub Date : 2025-06-19DOI: 10.1016/j.trecan.2025.06.001
Anurag V Prabhu, Carla Azar-Koussa, Zahava Siegfried, Rotem Karni
{"title":"Spliced to kill: RNA mis-splicing derived cancer neoantigens.","authors":"Anurag V Prabhu, Carla Azar-Koussa, Zahava Siegfried, Rotem Karni","doi":"10.1016/j.trecan.2025.06.001","DOIUrl":"10.1016/j.trecan.2025.06.001","url":null,"abstract":"<p><p>One of the major challenges in using neoantigen-based approaches in cancer treatment is the identification of cancer-specific neoantigens, particularly those that are shared by patients. In a recent report, Kim et al. uncover a novel source of cancer neoantigens in splicing factor mutant myeloid malignancies. These mis-spliced neoantigens offer new opportunities for engineered TCR-T cell therapies and neoantigen-based vaccines.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":14.3,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144337073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Trends in cancerPub Date : 2025-06-16DOI: 10.1016/j.trecan.2025.05.007
Rohit Singh, Jon Amund Kyte
{"title":"STEAP1: a promising target in prostate cancer therapy.","authors":"Rohit Singh, Jon Amund Kyte","doi":"10.1016/j.trecan.2025.05.007","DOIUrl":"https://doi.org/10.1016/j.trecan.2025.05.007","url":null,"abstract":"<p><p>The unmet therapeutic need in prostate cancer (PCa), a disease that remains largely incurable after metastasis, underscores the urgency for new treatments. STEAP1 (six transmembrane epithelial antigen of prostate 1) is a cell surface protein highly expressed in >85% prostate tumors but shows little to no presence in normal tissues, making it a promising candidate for targeted therapy. Here, we summarize and discuss recent findings that underscore the promising role of STEAP1 in PCa therapy.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":14.3,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144318036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Trends in cancerPub Date : 2025-06-12DOI: 10.1016/j.trecan.2025.05.005
S Grisaru-Tal, E A Jacobsen, A Munitz
{"title":"Evolving role for eosinophils in cancer: from bench to bedside.","authors":"S Grisaru-Tal, E A Jacobsen, A Munitz","doi":"10.1016/j.trecan.2025.05.005","DOIUrl":"https://doi.org/10.1016/j.trecan.2025.05.005","url":null,"abstract":"<p><p>Eosinophils are increasingly recognized as important immune cells in the tumor microenvironment (TME). Recent technological advancements reveal their heterogeneity and complex context-dependent activities including the ability to elicit pro- or anti-tumorigenic effects. For instance, they can mediate cytotoxicity via highly eosinophil-specific granule proteins and reactive oxygen species, and contribute to antitumor immunity by interacting with various cells including T cells. Clinically, eosinophilia is often observed following various treatments including immunotherapy, where they may be beneficial for therapy. This Review explores eosinophil recruitment, immune interactions, therapeutic potential and methods for studying their activity. Understanding the role of eosinophils in the TME may lead to new therapeutic strategies and position them as targets or biomarkers in precision oncology.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":14.3,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144295026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Trends in cancerPub Date : 2025-06-06DOI: 10.1016/j.trecan.2025.05.006
Antoine Galmiche, Zuzana Saidak, Cliona C Kirwan
{"title":"Advancing cancer precision surgery with the tumor coagulome.","authors":"Antoine Galmiche, Zuzana Saidak, Cliona C Kirwan","doi":"10.1016/j.trecan.2025.05.006","DOIUrl":"https://doi.org/10.1016/j.trecan.2025.05.006","url":null,"abstract":"<p><p>Solid tumors generate a local and systemic procoagulant state, placing cancer patients at risk of hemostatic complications. The interplay between the tumor coagulome, a tumor-intrinsic determinant, and surgery-induced coagulopathy may influence the risk of recurrence following complete surgical resection. Perioperative targeting of the coagulome could advance cancer precision treatment.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":14.3,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144249797","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Trends in cancerPub Date : 2025-06-04DOI: 10.1016/j.trecan.2025.04.012
Zihan Xia, Olivier De Wever
{"title":"The plasticity of cancer-associated fibroblasts.","authors":"Zihan Xia, Olivier De Wever","doi":"10.1016/j.trecan.2025.04.012","DOIUrl":"https://doi.org/10.1016/j.trecan.2025.04.012","url":null,"abstract":"<p><p>The plasticity of cancer-associated fibroblasts (CAFs) refers to their ability to adopt a spectrum of distinct phenotypes or states in response to dynamic changes within the tumor microenvironment (TME). Recent advances in single-cell technologies have enabled detailed characterization of the heterogeneity and spatial complexity of CAF subpopulations across multiple tumor types. Notably, CAF subtypes undergo dynamic transitions during tumor progression and therapy pressure. This review systematically summarizes the current knowledge on CAF plasticity shaped by both intrinsic and extrinsic factors, delineates research gaps, and highlights CAF phenotypic switching as a potential therapeutic opportunity.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":14.3,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144235350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Trends in cancerPub Date : 2025-06-03DOI: 10.1016/j.trecan.2025.05.003
Jessica L Chitty, Thomas R Cox
{"title":"The extracellular matrix in cancer: from understanding to targeting.","authors":"Jessica L Chitty, Thomas R Cox","doi":"10.1016/j.trecan.2025.05.003","DOIUrl":"https://doi.org/10.1016/j.trecan.2025.05.003","url":null,"abstract":"<p><p>Significant advances in matrix biology research have enhanced our understanding of individual matrix components and extracellular matrix (ECM) signalling. The dysregulation of the ECM during the development of solid tumours is a critical area of investigation. Despite recent progress, further investigation into the role of the ECM in cancer progression and therapeutic targeting remains essential for improving outcomes. This study is especially relevant for ECM-rich cancers, such as pancreatic cancer, which is characterised by dense fibrosis that impacts all stages of tumour development, including initiation, progression, and chemoresistance. Currently, no matrix-targeting agents have achieved mainstream clinical implementation. Challenges in this field include insufficient integration of new technologies, and limited understanding of cross disciplinary influences and of the complex, multifunctional nature of the ECM. In this review, we highlight key areas of matrix biology research that are crucial for advancing cancer treatment.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":14.3,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144226864","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Trends in cancerPub Date : 2025-06-01Epub Date: 2025-03-19DOI: 10.1016/j.trecan.2025.02.007
Yiming Luo, Ye Yuan, Dan Liu, Haoxin Peng, Lin Shen, Yang Chen
{"title":"Targeting novel immune checkpoints in the B7-H family: advancing cancer immunotherapy from bench to bedside.","authors":"Yiming Luo, Ye Yuan, Dan Liu, Haoxin Peng, Lin Shen, Yang Chen","doi":"10.1016/j.trecan.2025.02.007","DOIUrl":"10.1016/j.trecan.2025.02.007","url":null,"abstract":"<p><p>The B7-H family of immune checkpoint molecules is a crucial component of the immune regulatory network for tumors, offering new opportunities to modulate the tumor microenvironment (TME). The B7-H family - which includes B7-H2 (inducible T cell costimulatory ligand, ICOSL), B7-H3, B7-H4, B7-H5 (V-domain immunoglobulin suppressor of T cell activation, VISTA), B7-H6, and B7-H7 (HHLA2) - is known for its diverse roles in regulating innate and adaptive immunity. These molecules can exhibit co-stimulatory or co-inhibitory effects on T cells, influencing processes such as T cell activation, differentiation, and effector functions, and they are involved in the recruitment and polarization of various immune cells. This review explores the structural characteristics, receptor-ligand interactions, and signaling pathways associated with each B7-H family member. We also discuss the family's impact on tumor immunity and potential therapeutic strategies.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"540-559"},"PeriodicalIF":14.3,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670797","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Trends in cancerPub Date : 2025-06-01Epub Date: 2025-03-08DOI: 10.1016/j.trecan.2025.02.004
Lizhi Pang, Yuyun Huang, Jean Huang-Gao, Peiwen Chen
{"title":"Protease regulation of tumor-immune cell symbiosis.","authors":"Lizhi Pang, Yuyun Huang, Jean Huang-Gao, Peiwen Chen","doi":"10.1016/j.trecan.2025.02.004","DOIUrl":"10.1016/j.trecan.2025.02.004","url":null,"abstract":"<p><p>Proteases play a crucial role in cancer progression and are traditionally known for their protumorigenic role by degrading the extracellular matrix (ECM). Emerging evidence indicates that proteases, such as caspases, cathepsins, and ubiquitin-specific proteases (USPs), regulate diverse immunomodulatory substrates or signals in the tumor microenvironment (TME), generating symbiotic interactions between cancer cells and immune cells. These interactions are critical for tumor progression and immunotherapy resistance across cancer types. In this review, we highlight recent insights into protease-mediated tumor-immune cell crosstalk, emphasizing how this symbiosis affects tumor progression and immunosuppression. Moreover, we discuss therapeutic strategies that exploit protease-mediated tumor-immune cell interactions to inhibit tumor progression and sensitize immunologically 'cold' tumors to immunotherapies, especially immune checkpoint inhibitor (ICI) therapy.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"560-574"},"PeriodicalIF":14.3,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12158644/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143587199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}