Seminars in cancer biology最新文献

{"title":"The impact of obesity and lipids on cancer: Insights into mechanisms and potential interventions","authors":"Montserrat Romero ,&nbsp;Yi-Fan Lian ,&nbsp;Albert Piquer ,&nbsp;Núria Borràs-Ferré ,&nbsp;Antonio Zorzano ,&nbsp;Saška Ivanova","doi":"10.1016/j.semcancer.2025.07.006","DOIUrl":"10.1016/j.semcancer.2025.07.006","url":null,"abstract":"<div><div>Obesity and metabolic diseases, such as insulin resistance and type 2 diabetes, are closely linked to different types of cancers. With obesity rates rising globally, its influence on cancer incidence and progression has become increasingly significant. The obesity-cancer axis is thought to be driven by a complex interplay of metabolic and immune factors, including adipokines, lipids, immune cells and gene regulatory mechanisms. These elements work synergistically to promote cancer initiation and progression in the context of obesity. A more precise understanding and targeting these modulators should pave the way to novel therapeutic strategies to disrupt the link between obesity and cancer, improve cancer outcomes, and reduce treatment resistance. This review provides a comprehensive analysis of these factors, many of them derived from adipose tissue, highlightning their roles in shaping the obesity-cancer axis.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"115 ","pages":"Pages 53-74"},"PeriodicalIF":15.7,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144732983","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}

{"title":"Obesity-driven inflammation and cancer risk: A comprehensive review","authors":"D.A. Lamabadusuriya ,&nbsp;H. Jayasena ,&nbsp;A.K. Bopitiya ,&nbsp;A.D. De Silva ,&nbsp;P. Jayasekera","doi":"10.1016/j.semcancer.2025.07.007","DOIUrl":"10.1016/j.semcancer.2025.07.007","url":null,"abstract":"<div><div>Obesity is a growing global health challenge, significantly increasing the risk of metabolic diseases and cancer. This review explores the link between obesity-driven inflammation and cancer risk, emphasizing the key biological mechanisms. Chronic low-grade inflammation in obesity, mediated by dysfunctional adipose tissue, promotes a pro-tumorigenic microenvironment through increased secretion of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β. These factors contribute to insulin resistance, oxidative stress, and immune cell infiltration, fostering tumorigenesis. Adipokine imbalances, particularly elevated leptin and reduced adiponectin levels, further drive cancer progression by enhancing cell proliferation, angiogenesis, and immune evasion. Additionally, obesity-induced hypoxia, endoplasmic reticulum stress, and gut microbiome dysbiosis amplify systemic inflammation and metabolic dysfunction, further increasing cancer susceptibility. Epidemiological evidence highlights strong associations between obesity and cancers such as breast, colorectal, liver, and pancreatic cancer. Given the rising global prevalence of obesity, addressing inflammation-mediated oncogenesis is crucial. Lifestyle modifications, including weight loss through dietary and physical activity interventions, have demonstrated significant cancer risk reduction. Emerging pharmacological approaches targeting inflammatory pathways and adipokine regulation offer promising therapeutic potential. Understanding the mechanisms linking obesity, inflammation, and cancer provides valuable insights for developing targeted prevention and treatment strategies.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"114 ","pages":"Pages 256-266"},"PeriodicalIF":15.7,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144718374","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}

{"title":"Host-microbiota interactions in genitourinary cancer immunotherapy","authors":"Xiao-Feng Xu ,&nbsp;Jin-Long Cui ,&nbsp;Wen-Hua Li ,&nbsp;Yi-Hang Xu ,&nbsp;Shuai Yuan ,&nbsp;Xian-Tao Zeng ,&nbsp;Bing-Hui Li","doi":"10.1016/j.semcancer.2025.07.005","DOIUrl":"10.1016/j.semcancer.2025.07.005","url":null,"abstract":"<div><div>Immunotherapy for genitourinary cancer, including bladder cancer, renal cell carcinoma, and prostate cancer, has made significant progress in recent years; however, it still faces challenges such as low patient response rates, drug resistance and immune-related adverse events. As the “second genome” of the human body, the gut microbiota plays a key factor in modulating the host immune response. Studies have shown that host-microbiome interactions profoundly affect the efficacy and safety of immune checkpoint inhibitors by shaping the tumor immune microenvironment (TIME). This review systematically analyzes the mechanisms by which urinary system-specific microbiota (such as urothelial bacteria and gut microbiota) regulate TIME through metabolic regulation, immune cell function remodeling, and inflammatory signaling networks. We further explore the clinical translational strategy targeting the microbiome to enhance immunotherapy responses, providing new perspectives for precision immunotherapy of urinary tumors.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"115 ","pages":"Pages 1-15"},"PeriodicalIF":15.7,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144718373","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}

{"title":"Landscape of non-coding RNAs in cancer treatment-induced cardiovascular toxicity: From mechanistic insights to clinical implications","authors":"Yayu Chen ,&nbsp;Zhishuang Ye ,&nbsp;Rong-Quan He ,&nbsp;Gang Chen ,&nbsp;Daniel Xin Zhang","doi":"10.1016/j.semcancer.2025.07.009","DOIUrl":"10.1016/j.semcancer.2025.07.009","url":null,"abstract":"<div><div>Non-coding RNAs (ncRNAs) are increasingly recognized as crucial regulators in the pathophysiology of cancer treatment–induced cardiovascular toxicity, which largely stems from their capacity to orchestrate a wide range of gene expression networks. Emerging evidence has uncovered complex and critical functions of ncRNAs, including microRNAs, long non-coding RNAs, and circular RNAs, in mediating cardiotoxicity during cancer treatment. Here, we revisit the mechanisms of major anti-cancer treatment modalities and detail how they may lead to cardiovascular toxicity, which involves a myriad of key, interconnected processes, such as apoptosis, DNA damage, oxidative stress, mitochondrial damage, and autophagy. We further underscore the pivotal roles of ncRNAs within the cardio-oncology landscape mechanistically and analyze their clinical potentials to predict, detect, and treat cardiovascular damage in oncology settings. With this review, we aim to provide a comprehensive and up-to-date landscape of ncRNAs in the rapidly revolving field of cancer treatment–related cardiovascular toxicity, highlighting how such fundamental discoveries may guide future clinical applications.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"115 ","pages":"Pages 16-39"},"PeriodicalIF":15.7,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144699379","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}

{"title":"Cancer prevention and interception with antidiabetic and anti-obesity drugs: Current and future perspectives","authors":"Adriana Albini ,&nbsp;Anna Rita Cantelmo ,&nbsp;Lorenzo Mortara ,&nbsp;Douglas M. Noonan ,&nbsp;Giovanni Corso","doi":"10.1016/j.semcancer.2025.07.008","DOIUrl":"10.1016/j.semcancer.2025.07.008","url":null,"abstract":"<div><div>Obesity and type 2 diabetes are major risk factors for cardiovascular diseases and multiple malignancies, and epidemiology reveals an increasing burden of obesity-related cancers, in particular liver, pancreatic and endometrial. Obesity is also clearly associated with an increased risk of breast cancer, particularly in postmenopausal women. Chronic hyperinsulinemia, systemic inflammation, and metabolic dysregulation create a tumor-promoting environment, emphasizing the need for interventions that target metabolic health and can provide cancer prevention or interception. This review examines the potential cancer-preventive effects of antidiabetic and anti-obesity drugs, summarizing current preclinical and clinical evidence on their mechanisms and efficacy. Among these agents, metformin has been extensively studied, demonstrating anticancer properties through AMP-activated protein kinase activation, mammalian target of rapamycin inhibition, and reduced insulin-like growth factor 1 signaling. Glucagon-like peptide-1 receptor agonists, including semaglutide and tirzepatide, promote weight loss, insulin sensitivity, and anti-inflammatory effects, with emerging evidence suggesting direct tumor-suppressive actions. Sodium-glucose cotransporter 2 inhibitors modulate tumor metabolism by reducing glucose availability and mitigating systemic inflammation. Other agents, including dipeptidyl peptidase-4 inhibitors, thiazolidinediones, sulfonylureas, and alpha-glucosidase inhibitors, have shown mixed evidence regarding their potential anticancer effects, necessitating further investigation. While observational studies and meta-analyses suggest a potential reduction in cancer risk with certain antidiabetic and anti-obesity agents, randomized controlled trials specifically assessing cancer prevention are limited. Additionally, long-term safety concerns, including potential tumor-promoting effects in specific contexts, warrant further investigation. Future research should focus on large-scale clinical trials and mechanistic studies to validate the oncologic benefits and risks of these agents.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"115 ","pages":"Pages 40-52"},"PeriodicalIF":15.7,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144699378","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}

{"title":"The role of deiodinases on metabolic alteration in cancer","authors":"Caterina Miro ,&nbsp;Annunziata Gaetana Cicatiello ,&nbsp;Monica Dentice ,&nbsp;Annarita Nappi","doi":"10.1016/j.semcancer.2025.07.003","DOIUrl":"10.1016/j.semcancer.2025.07.003","url":null,"abstract":"<div><div>Deiodinases are key regulators of Thyroid Hormone (TH) bioavailability, exerting a precise spatial and temporal control over T3 levels in peripheral tissues. By dynamically modulating TH activation and inactivation, deiodinases allow target organs to adapt TH signaling to physiological and pathological demands, highlighting their importance in both health and disease. In cancer, their dysregulated expression reprograms cellular metabolism and shapes the tumor microenvironment (TME). Type 3 deiodinase (D3), frequently upregulated in proliferative and hypoxic tumor regions, fosters cell proliferation and resistance to differentiation. Conversely, type 2 deiodinase (D2) sustains glycolytic metabolism, angiogenesis, and redox disbalance, particularly in aggressive and p53-deficient tumors. Beyond cancer cells, deiodinases activity influences stromal and immune compartments, impacting glutamine metabolism and immune cell plasticity. This complex endocrine-metabolic axis supports tumor adaptation to stress and contributes to the emergence of resistance to therapy. Recent advances reveal the potential of targeting deiodinases to counteract cancer metabolic reprogramming and re-sensitize tumors to treatment. Given the essential and multifaceted roles of deiodinases in cancer biology, a comprehensive understanding of their mechanisms of action, regulation, and clinical implications is critical. This review aims to summarize current knowledge on the roles of deiodinases in cancer metabolism and immunity, focusing on their biochemical properties, regulatory networks, tissue-specific functions, and contributions to disease. In doing so, we seek to highlight emerging concepts in local TH signaling and explore potential avenues for therapeutic intervention targeting deiodinase pathways in precision oncology.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"114 ","pages":"Pages 215-226"},"PeriodicalIF":12.1,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144619968","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}

{"title":"CRISPR/Cas9 genome engineering in PDAC: From preclinical studies to translation and clinical research","authors":"Yanxi Lu ,&nbsp;Jojanneke Stoof ,&nbsp;Yaba Rosette Tanoé ,&nbsp;Naomi Walsh ,&nbsp;Maarten F. Bijlsma ,&nbsp;Huijun Lei ,&nbsp;Tianhui Chen ,&nbsp;Jelena Grahovac ,&nbsp;Robert Grützmann ,&nbsp;Christian Pilarsky","doi":"10.1016/j.semcancer.2025.07.004","DOIUrl":"10.1016/j.semcancer.2025.07.004","url":null,"abstract":"<div><div>CRISPR/Cas9 technology has emerged as a powerful tool in pancreatic ductal adenocarcinoma cancer (PDAC) research, facilitating the study of genes involved in cell signaling pathways, proliferation, migration, invasion, and chemotherapy resistance. In this review, we discuss the evolution of CRISPR technologies from sophisticated editing techniques to broad screening methods, examine the utility of isogenic models and genetically engineered mouse models (GEMMs). We also explore how CRISPR/Cas9 screens can reveal immune-tumor cell interactions, highlighting the multifaceted role of this technology in PDAC research. Moreover, we emphasize the use of CRISPR technology in diagnostics for CAR-T cell therapies, where CRISPR/Cas9 enhances the precision of targeting malignant cells while minimizing off-tumor effects.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"114 ","pages":"Pages 242-255"},"PeriodicalIF":12.1,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144619967","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}

{"title":"The impact of sarcopenic obesity on cancer clinical outcomes","authors":"Bahadır Köylü ,&nbsp;Cem Sulu ,&nbsp;Volkan Demirhan Yumuk ,&nbsp;Perran Fulden Yumuk","doi":"10.1016/j.semcancer.2025.07.002","DOIUrl":"10.1016/j.semcancer.2025.07.002","url":null,"abstract":"<div><div>Sarcopenic obesity is a distinct clinical condition characterized by the coexistence of excess fat and reduced muscle mass. Although the prevalence of sarcopenic obesity varies depending on the definition used, it is increasingly recognized as a significant health concern, regardless of age and underlying disease. Despite limited understanding of the crosstalk between sarcopenic obesity and cancer, emerging evidence suggests that sarcopenic obesity not only promotes a metabolic and inflammatory environment conducive to cancer progression but also profoundly impacts treatment efficacy, safety, and survival outcomes. This review provides a concise overview of the key aspects of sarcopenic obesity, with a particular focus on its role in the cancer setting. We also assess existing evidence on its influence on oncological outcomes in both early and advanced stages of the various solid tumor types.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"114 ","pages":"Pages 203-214"},"PeriodicalIF":12.1,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144588547","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}

{"title":"From awareness to action: Revolutionizing cardio-oncology in China","authors":"Aman Wang,&nbsp;Jiwei Liu","doi":"10.1016/j.semcancer.2025.06.011","DOIUrl":"10.1016/j.semcancer.2025.06.011","url":null,"abstract":"<div><div>Cardio-oncology is an emerging interdisciplinary field focused on the intersection of cancer and cardiovascular disease. With the rising incidence of both cancer and cardiovascular disease in China, establishing a strong cardio-oncology framework has become essential. This review examines the historical development, clinical practices, and key milestones of cardio-oncology in China, emphasizing the importance of multidisciplinary teams, specialized guidelines, and international collaborations. Additionally, it discusses the current challenges and future opportunities for advancing cardio-oncology within China’s healthcare landscape.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"114 ","pages":"Pages 195-202"},"PeriodicalIF":12.1,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144588546","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}

{"title":"Reopening Pandora’s box: Is there a role for HDL in breast cancer?","authors":"Maria Isabela Bloise Alves Caldas Sawada ,&nbsp;Monique de Fatima de Mello Santana ,&nbsp;Milena Gomes Vancini ,&nbsp;Marisa Passarelli","doi":"10.1016/j.semcancer.2025.07.001","DOIUrl":"10.1016/j.semcancer.2025.07.001","url":null,"abstract":"<div><div>Plasma lipid and lipoprotein profiles are recognized as key modulators in breast cancer (BC) development. Notably, the association between high-density lipoprotein cholesterol (HDLc) and BC remains controversial, with studies reporting positive, negative, or no correlation. This inconsistency may arise from the clinical metrics used to quantify high-density lipoproteins (HDL), such as HDLc and apolipoprotein (apo) A-1, which may not accurately reflect HDL functionality in modulating the tumor microenvironment. Moreover, HDL particles isolated from plasma may undergo modifications influenced by tumor activity, varying with disease stage, severity, and treatment. In this review, we are critically reopening Pandora´s box analyzing evidence on HDLc plasma levels and HDL functionality in BC. Specifically, HDL contributes to tumor regulation by removing excess cellular cholesterol, thereby limiting sterol availability for cell replication and metastasis. Additionally, HDL exerts antioxidant and anti-inflammatory effects and acts as a carrier of bioactive proteins, lipids, and microRNAs, facilitating their delivery to target cells and modulating intracellular signaling and gene expression. Collectively, HDL functionality may serve as a predictor of therapeutic response and clinical outcomes in BC.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"114 ","pages":"Pages 227-241"},"PeriodicalIF":12.1,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144584724","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}