Seminars in cancer biology最新文献

{"title":"The Warburg effect: The hacked mitochondrial-nuclear communication in cancer","authors":"Haowen Jiang ,&nbsp;Jiangbin Ye","doi":"10.1016/j.semcancer.2025.03.006","DOIUrl":"10.1016/j.semcancer.2025.03.006","url":null,"abstract":"<div><div>Mitochondrial-nuclear communication is vital for maintaining cellular homeostasis. This communication begins with mitochondria sensing environmental cues and transmitting signals to the nucleus through the retrograde cascade, involving metabolic signals such as substrates for epigenetic modifications, ATP and AMP levels, calcium flux, etc. These signals inform the nucleus about the cell's metabolic state, remodel epigenome and regulate gene expression, and modulate mitochondrial function and dynamics through the anterograde feedback cascade to control cell fate and physiology. Disruption of this communication can lead to cellular dysfunction and disease progression, particularly in cancer. The Warburg effect is the metabolic hallmark of cancer, characterized by disruption of mitochondrial respiration and increased lactate generation from glycolysis. This metabolic reprogramming rewires retrograde signaling, leading to epigenetic changes and dedifferentiation, further reprogramming mitochondrial function and promoting carcinogenesis. Understanding these processes and their link to tumorigenesis is crucial for uncovering tumorigenesis mechanisms. Therapeutic strategies targeting these disrupted pathways, including metabolic and epigenetic components, provide promising avenues for cancer treatment.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"112 ","pages":"Pages 93-111"},"PeriodicalIF":12.1,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143731590","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 the tumor microenvironment in the dual burden of obesity-cancer link","authors":"Serena Sagliocchi ,&nbsp;Lucia Acampora ,&nbsp;Biagio Barone ,&nbsp;Felice Crocetto ,&nbsp;Monica Dentice","doi":"10.1016/j.semcancer.2025.03.001","DOIUrl":"10.1016/j.semcancer.2025.03.001","url":null,"abstract":"<div><div>Obesity induces systemic perturbations of tissue homeostasis, leading to dyslipidemia, insulin resistance and chronic state of inflammation. Evidence from clinical and preclinical studies links excess of adiposity with increased cancer incidence and suggests that chronic inflammation may contribute to increased cancer risk in obese patients. Over the last decades of obesity research, multifaced and complicated effects of abnormal or excessive expansion of Adipose Tissue have been uncovered. In particular, it is widely described how obesity can exacerbate the tumorigenesis for instance by fueling soluble signals and adipokines and by enhancing tissue inflammation and altering the hormonal balance. Less is known about the paracrine effects of the cancer-associated adipocytes on the tumor cells and still poorly explored is the reciprocal communication between cancer cells and the adipose component of the tumor microenvironment (TME). In this review, we will address the mechanisms by which the peritumoral Adipose Tissue can influence the dynamics of tumoral cells. We will discuss how obesity-induced changes in the tumor microenvironment may enhance tumor growth and aggressive characteristics leading to increased invasiveness and metastatic progression of cancer that leads to a worsen cancer survival in obese subjects. We conclude that targeting the peritumoral adipose component of the TME would be a therapeutic option to prevent cancer development.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"112 ","pages":"Pages 36-42"},"PeriodicalIF":12.1,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143701202","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":"Epithelial-mesenchymal transition promotes metabolic reprogramming to suppress ferroptosis","authors":"Wenzheng Guo,&nbsp;Zhibing Duan,&nbsp;Jingjing Wu,&nbsp;Binhua P. Zhou","doi":"10.1016/j.semcancer.2025.02.013","DOIUrl":"10.1016/j.semcancer.2025.02.013","url":null,"abstract":"<div><div>Epithelial-mesenchymal transition (EMT) is a cellular de-differentiation process that provides cells with the increased plasticity and stem cell-like traits required during embryonic development, tissue remodeling, wound healing and metastasis. Morphologically, EMT confers tumor cells with fibroblast-like properties that lead to the rearrangement of cytoskeleton (loss of stiffness) and decrease of membrane rigidity by incorporating high level of poly-unsaturated fatty acids (PUFA) in their phospholipid membrane. Although large amounts of PUFA in membrane reduces rigidity and offers capabilities for tumor cells with the unbridled ability to stretch, bend and twist in metastasis, these PUFA are highly susceptible to lipid peroxidation, which leads to the breakdown of membrane integrity and, ultimately results in ferroptosis. To escape the ferroptotic risk, EMT also triggers the rewiring of metabolic program, particularly in lipid metabolism, to enforce the epigenetic regulation of EMT and mitigate the potential damages from ferroptosis. Thus, the interplay among EMT, lipid metabolism, and ferroptosis highlights a new layer of intricated regulation in cancer biology and metastasis. Here we summarize the latest findings and discuss these mutual interactions. Finally, we provide perspectives of how these interplays contribute to cellular plasticity and ferroptosis resistance in metastatic tumor cells that can be explored for innovative therapeutic interventions.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"112 ","pages":"Pages 20-35"},"PeriodicalIF":12.1,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586697","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":"Targeting mineral metabolism in cancer: Insights into signaling pathways and therapeutic strategies","authors":"Kartik Bhatnagar ,&nbsp;Sharon Raju ,&nbsp;Ninad Patki ,&nbsp;Rajender K. Motiani ,&nbsp;Sarika Chaudhary","doi":"10.1016/j.semcancer.2025.02.011","DOIUrl":"10.1016/j.semcancer.2025.02.011","url":null,"abstract":"<div><div>Cancer remains the second leading cause of death worldwide, emphasizing the critical need for effective treatment and control strategies. Essential minerals such as copper, iron, zinc, selenium, phosphorous, calcium, and magnesium are integral to various biological processes and significantly influence cancer progression through altered metabolic pathways. For example, dysregulated copper levels promote tumor growth, while cancer cells exhibit an increased dependency on iron for signaling and redox reactions. Zinc influences tumor development through pathways such as Akt-p21. Selenium, primarily through its role in selenoproteins, exhibits anticancer potential but may also contribute to tumor progression. Similarly, dietary phosphate exacerbates tumorigenesis, metastasis, and angiogenesis through signaling pathway activation. Calcium, the most abundant mineral in the body, is tightly regulated within cells, and its dysregulation is a hallmark of various cancers. Magnesium deficiency, on the other hand, promotes cancer progression by fostering inflammation and free radical-induced DNA mutations. Interestingly, magnesium also plays a dual role, with low levels enhancing epithelial-mesenchymal transition (EMT), a critical process in cancer metastasis. This complex interplay of essential minerals underscores their potential as therapeutic targets. Dysregulation of these minerals and their pathways could be exploited to selectively target cancer cells, offering novel therapeutic strategies. This review summarizes current research on the abnormal accumulation or depletion of these microelements in tumor biology, drawing evidence from animal models, cell lines, and clinical samples. We also highlight the potential of these minerals as biomarkers for cancer diagnosis and prognosis, as well as therapeutic approaches involving metal chelators, pharmacological agents, and nanotechnology. By highlighting the intricate roles of these minerals in cancer biology, we aim to inspire further research in this critical yet underexplored area of oncology.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"112 ","pages":"Pages 1-19"},"PeriodicalIF":12.1,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143537635","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":"Clonal hematopoiesis, cardiovascular disease and cancer treatment-induced cardiotoxicity","authors":"Nan Zhang ,&nbsp;Xu Tian ,&nbsp;Dongkun Sun ,&nbsp;Gary Tse ,&nbsp;Bingxin Xie ,&nbsp;Zhiqiang Zhao ,&nbsp;Tong Liu","doi":"10.1016/j.semcancer.2025.02.007","DOIUrl":"10.1016/j.semcancer.2025.02.007","url":null,"abstract":"<div><div>Clonal hematopoiesis (CH) arises when a substantial proportion of mature blood cells is derived from a single hematopoietic stem cell lineage. It is considered to be a premalignant state that predisposes individuals to an increased risk of cancers. Recently, emerging evidence has demonstrated a strong association between CH and both the incidence and mortality of cardiovascular diseases (CVD), with the relative risks being comparable to those attributed to traditional cardiovascular risk factors. In addition, CH has been suggested to play a role in CVD and anti-cancer treatment-related cardiotoxicity amongst cancer survivors. Moreover, certain forms of chemotherapy and radiation therapy have been shown to promote the clonal expansion of specific CH-related mutations. Consequently, CH may play a substantial role in the realm of cardio-oncology. In this review, we discuss the association between CH with cancer and CVD, with a special focus on anti-cancer treatment-related cardiotoxicity, discuss possible future research avenues and propose a systematic approach for clinical practice.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"111 ","pages":"Pages 89-114"},"PeriodicalIF":12.1,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143537632","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":"Immunosenescence in skeletal muscle: The role-play in cancer cachexia chessboard","authors":"Matteo Giovarelli ,&nbsp;Emanuele Mocciaro ,&nbsp;Carla Carnovale ,&nbsp;Davide Cervia ,&nbsp;Cristiana Perrotta ,&nbsp;Emilio Clementi","doi":"10.1016/j.semcancer.2025.02.012","DOIUrl":"10.1016/j.semcancer.2025.02.012","url":null,"abstract":"<div><div>With the increase in life expectancy, age-related conditions and diseases have become a widespread and relevant social burden. Among these, immunosenescence and cancer cachexia play a significant often intertwined role. Immunosenescence is the progressive aging decline of both the innate and adaptive immune systems leading to increased infection susceptibility, poor vaccination efficacy, autoimmune disease, and malignancies. Cancer cachexia affects elderly patients with cancer causing severe weight loss, muscle wasting, inflammation, and reduced response to therapies. Whereas the connections between immunosenescence and cancer cachexia have been raising attention, the molecular mechanisms still need to be completely elucidated. This review aims at providing the current knowledge about the interplay between immunosenescence, skeletal muscle, and cancer cachexia, analyzing the molecular pathways known so far to be involved. Finally, we highlight potential therapeutic strategies suited for elderly population aimed to block immunosenescence and to preserve muscle mass in cachexia, also presenting the analysis of the current state-of-the-art of related clinical trials.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"111 ","pages":"Pages 48-59"},"PeriodicalIF":12.1,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143520060","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}

{"title":"Immunosenescence and immunotherapy in elderly patients with hepatocellular carcinoma","authors":"Dengyong Zhang ,&nbsp;Yan Zhu ,&nbsp;Zhengchao Shen ,&nbsp;Shuoshuo Ma ,&nbsp;Sihua Liu ,&nbsp;Zheng Lu","doi":"10.1016/j.semcancer.2025.02.010","DOIUrl":"10.1016/j.semcancer.2025.02.010","url":null,"abstract":"<div><div>Liver cancer, more specifically hepatocellular carcinoma (HCC), is a global health issue and one of the dominant causes of cancer death around the world. In the past few decades, remarkable advances have been achieved in the systemic therapy of HCC. Immune checkpoint inhibitors (ICIs) have become a therapy mainstay for advanced HCC and have shown promise in the neoadjuvant therapy before resection. Despite these significant advancements, the compositions and functions of the immune system occur various alterations with age, called “immunosenescence”, which may affect the antitumor effects and safety of ICIs, thus raising concerns that immunosenescence may impair elderly patients’ response to ICIs. Therefore, it is important to learn more about the immunosenescence characteristics of elderly patients. However, the real-world elderly HCC patients may be not accurately represented by the elderly patients included in the clinical trials, affecting the generalizability of the efficacy and safety profiles from the clinical trials to the real-world elderly patients. This review summarizes the characteristics of immunosenescence and its influence on HCC progression and immunotherapy efficacy as well as provides the latest progress in ICIs available for HCC and discusses their treatment efficacy and safety on elderly patients. In the future, more studies are needed to clarify the mechanisms of immunosenescence in HCC, and to find sensitive screening tools or biomarkers to identify the patients who may benefit from ICIs.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"111 ","pages":"Pages 60-75"},"PeriodicalIF":12.1,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143520061","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":"Atrial fibrillation in cancer patients: Epidemiology, identification and management","authors":"Chengqi Yu ,&nbsp;Leilei Jiang ,&nbsp;Liuhua Long ,&nbsp;Huiming Yu","doi":"10.1016/j.semcancer.2025.02.006","DOIUrl":"10.1016/j.semcancer.2025.02.006","url":null,"abstract":"<div><div>Cancer and cardiovascular disease (CVD) are among the leading causes of death globally, and the rate of coexistence of the two diseases has been increasing in recent years, with the elevation of the susceptible population base in aging societies and the improvement of therapeutic approaches. Atrial fibrillation (AF), as a common type of cancer-related cardiovascular toxicity (CTR-CVT) in oncology patients, is a serious threat to patients' health and may lead to other cardiovascular complications. Therefore, early detection, timely recognition, and effective intervention of AF are essential to maintain long-term survival of tumor survivors. However, the causal mechanisms regarding its association are still inconclusive, and there is no consensus in the clinic on the optimal treatment. In this review, we will integrate existing guidelines and studies to summarize the current state of research on atrial fibrillation in oncology patients in terms of epidemiology, pathophysiological mechanisms, predictive diagnostics, and therapeutic measures, and propose some research directions to be improved. We hope to provide a more comprehensive review and provide assistance in clinical response.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"111 ","pages":"Pages 39-47"},"PeriodicalIF":12.1,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143479813","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":"Biomarkers, omics and artificial intelligence for early detection of pancreatic cancer","authors":"Kate Murray ,&nbsp;Lucy Oldfield ,&nbsp;Irena Stefanova ,&nbsp;Manuel Gentiluomo ,&nbsp;Paolo Aretini ,&nbsp;Rachel O’Sullivan ,&nbsp;William Greenhalf ,&nbsp;Salvatore Paiella ,&nbsp;Mateus N. Aoki ,&nbsp;Aldo Pastore ,&nbsp;James Birch-Ford ,&nbsp;Bhavana Hemantha Rao ,&nbsp;Pinar Uysal-Onganer ,&nbsp;Caoimhe M. Walsh ,&nbsp;George B. Hanna ,&nbsp;Jagriti Narang ,&nbsp;Pradakshina Sharma ,&nbsp;Daniele Campa ,&nbsp;Cosmeri Rizzato ,&nbsp;Andrei Turtoi ,&nbsp;Eithne Costello","doi":"10.1016/j.semcancer.2025.02.009","DOIUrl":"10.1016/j.semcancer.2025.02.009","url":null,"abstract":"<div><div>Pancreatic ductal adenocarcinoma (PDAC) is frequently diagnosed in its late stages when treatment options are limited. Unlike other common cancers, there are no population-wide screening programmes for PDAC. Thus, early disease detection, although urgently needed, remains elusive. Individuals in certain high-risk groups are, however, offered screening or surveillance. Here we explore advances in understanding high-risk groups for PDAC and efforts to implement biomarker-driven detection of PDAC in these groups. We review current approaches to early detection biomarker development and the use of artificial intelligence as applied to electronic health records (EHRs) and social media. Finally, we address the cost-effectiveness of applying biomarker strategies for early detection of PDAC.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"111 ","pages":"Pages 76-88"},"PeriodicalIF":12.1,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143476743","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}

{"title":"Editorial – Hypoxia as a molecular driver of cancer progression","authors":"Luana Schito ,&nbsp;Sergio Rey-Keim","doi":"10.1016/j.semcancer.2025.02.008","DOIUrl":"10.1016/j.semcancer.2025.02.008","url":null,"abstract":"","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"111 ","pages":"Pages 36-38"},"PeriodicalIF":12.1,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143469011","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}