Seminars in cancer biology最新文献

The interplay between cell death and senescence in cancer. 癌症中细胞死亡与衰老之间的相互作用。

IF 12.1 1区医学

Seminars in cancer biology Pub Date : 2024-11-16 DOI: 10.1016/j.semcancer.2024.11.001

Kouhei Shimizu, Hiroyuki Inuzuka, Fuminori Tokunaga

{"title":"The interplay between cell death and senescence in cancer.","authors":"Kouhei Shimizu, Hiroyuki Inuzuka, Fuminori Tokunaga","doi":"10.1016/j.semcancer.2024.11.001","DOIUrl":"10.1016/j.semcancer.2024.11.001","url":null,"abstract":"<p><p>Cellular senescence is a state of permanent proliferative arrest that occurs in response to DNA damage-inducing endogenous and exogenous stresses, and is often accompanied by dynamic molecular changes such as a senescence-associated secretory phenotype (SASP). Accumulating evidence indicates that age-associated increases in the upstream and downstream signals of regulated cell death, including apoptosis, necroptosis, pyroptosis, and ferroptosis, are closely related to the induction of cellular senescence and its phenotype. Furthermore, elevated levels of pro-inflammatory SASP factors with aging can be both a cause and consequence of several cell death modes, suggesting the reciprocal effects of cellular senescence and cells undergoing regulated cell death. Here, we review the critical molecular pathways of the regulated cell death forms and describe the crosstalk between aging-related signals and cancer. In addition, we discuss how targeting regulated cell death could be harnessed in therapeutic interventions for cancer. ABBREVIATIONS: Abbreviations that are not standard in this field are defined at their first occurrence in the article and are used consistently throughout the article.</p>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":" ","pages":""},"PeriodicalIF":12.1,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142668988","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}

引用次数: 0

A systematic review of cardiovascular toxicities induced by cancer immune therapies: Underlying mechanisms, clinical manifestations and therapeutic approaches 癌症免疫疗法诱发心血管毒性的系统综述：潜在机制、临床表现和治疗方法。

IF 12.1 1区医学

Seminars in cancer biology Pub Date : 2024-11-01 DOI: 10.1016/j.semcancer.2024.10.004

Li Liu , Wentao Yao , Mi Wang , Baohui Wang , Fanming Kong , Zhongguo Fan , Guanwei Fan

{"title":"A systematic review of cardiovascular toxicities induced by cancer immune therapies: Underlying mechanisms, clinical manifestations and therapeutic approaches","authors":"Li Liu , Wentao Yao , Mi Wang , Baohui Wang , Fanming Kong , Zhongguo Fan , Guanwei Fan","doi":"10.1016/j.semcancer.2024.10.004","DOIUrl":"10.1016/j.semcancer.2024.10.004","url":null,"abstract":"<div><div>Immunotherapy has revolutionized the management of various types of cancers, even those previously deemed untreatable. Nonetheless, these medications have been associated with inflammation and damage across various organs. These challenges are exemplified by the adverse cardiovascular impacts of cancer immunotherapy, which need comprehensive understanding, clarification, and management integrated into the overall care of cancer patients. Numerous anticancer immunotherapies have been linked to the prevalence and severity of cardiovascular toxicity. These challenges emphasize the importance of conducting fundamental and applied research to elucidate disease causes, discover prognostic indicators, enhance diagnostic methods, and create successful therapies. Despite the acknowledged importance of T cells, there remains a knowledge gap regarding the inciting antigens, the reasons for their recognition, and the mechanisms of how they contribute to cardiac cell injury. In this review, we summarize the molecular mechanism, epidemiology, diagnosis, pathophysiology and corresponding treatment of cardiovascular toxicity induced by immunotherapy, including immune checkpoint inhibitors (ICIs), adoptive cell therapies (ACT), and bi-specific T-cell engagers (BiTEs) among others. By elucidating these aspects, we aim to provide a better understanding of immunotherapies in cancer treatment and offer guidance for their clinical application.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"106 ","pages":"Pages 179-191"},"PeriodicalIF":12.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142507078","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}

引用次数: 0

Unravelling the complexities of resistance mechanism in pancreatic cancer: Insights from in vitro and ex-vivo model systems 揭示胰腺癌抗药性机制的复杂性：体外和体内模型系统的启示。

IF 12.1 1区医学

Seminars in cancer biology Pub Date : 2024-11-01 DOI: 10.1016/j.semcancer.2024.09.002

Giulia Lencioni , Alessandro Gregori , Belén Toledo , Rita Rebelo , Benoît Immordino , Manoj Amrutkar , Cristina P.R. Xavier , Anja Kocijančič , Deo Prakash Pandey , Macarena Perán , Justo P. Castaño , Naomi Walsh , Elisa Giovannetti

{"title":"Unravelling the complexities of resistance mechanism in pancreatic cancer: Insights from in vitro and ex-vivo model systems","authors":"Giulia Lencioni , Alessandro Gregori , Belén Toledo , Rita Rebelo , Benoît Immordino , Manoj Amrutkar , Cristina P.R. Xavier , Anja Kocijančič , Deo Prakash Pandey , Macarena Perán , Justo P. Castaño , Naomi Walsh , Elisa Giovannetti","doi":"10.1016/j.semcancer.2024.09.002","DOIUrl":"10.1016/j.semcancer.2024.09.002","url":null,"abstract":"<div><div>Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer with poor prognosis and rising global deaths. Late diagnosis, due to absent early symptoms and biomarkers, limits treatment mainly to chemotherapy, which soon encounters resistance. PDAC treatment innovation is hampered by its complex and heterogeneous resistant nature, including mutations in key genes and a stromal-rich, immunosuppressive tumour microenvironment. Recent studies on PDAC resistance stress the need for suitable in vitro and ex vivo models to replicate its complex molecular and microenvironmental landscape. This review summarises advances in these models, which can aid in combating chemoresistance and serve as platforms for discovering new therapeutics. Immortalised cell lines offer homogeneity, unlimited proliferation, and reproducibility, but while many gemcitabine-resistant PDAC cell lines exist, fewer models are available for resistance to other drugs. Organoids from PDAC patients show promise in mimicking tumour heterogeneity and chemosensitivity. Bioreactors, co-culture systems and organotypic slices, incorporating stromal and immune cells, are being developed to understand tumour-stroma interactions and the tumour microenvironment's role in drug resistance. Lastly, another innovative approach is three-dimensional bioprinting, which creates tissue-like structures resembling PDAC architecture, allowing for drug screening. These advanced models can guide researchers in selecting optimal in vitro tests, potentially improving therapeutic strategies and patient outcomes.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"106 ","pages":"Pages 217-233"},"PeriodicalIF":12.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142294447","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}

引用次数: 0

Immunosenescence in digestive system cancers: Mechanisms, research advances, and therapeutic strategies 消化系统癌症中的免疫衰老：机制、研究进展和治疗策略。

IF 12.1 1区医学

Seminars in cancer biology Pub Date : 2024-11-01 DOI: 10.1016/j.semcancer.2024.10.006

Junyan Zhang , Xiaojiao Guan , Xinwen Zhong

{"title":"Immunosenescence in digestive system cancers: Mechanisms, research advances, and therapeutic strategies","authors":"Junyan Zhang , Xiaojiao Guan , Xinwen Zhong","doi":"10.1016/j.semcancer.2024.10.006","DOIUrl":"10.1016/j.semcancer.2024.10.006","url":null,"abstract":"<div><div>Increasing lifespans and external environmental factors have contributed to the increase of age-related diseases, particularly cancer. A decrease in immune surveillance and clearance of cancer cells is the result of immunosenescence, which involves the remodeling of immune organs, the changes and functional decline of immune cell subsets, in association with systemic low-grade chronic inflammation. Stem cells aging in bone marrow and thymic involution are the most important causes of immunosenescence. Senescent cancer cells promote the differentiation, recruitment, and functional upregulation of immune-suppressive cell subsets e.g. regulatory T cells (Tregs), myeloid-derived suppressor cell (MDSC), tumor-associated macrophages (TAMS) through senescence-associated secretory phenotype (SASP) further exacerbating the immunosuppressive microenvironment. For digestive system cancers, age-related damage to the intestinal mucosal barrier, the aging of gut-associated lymphoid tissue (GALT), exposure to xenobiotic stimuli throughout life, and dysbiosis make the local immune microenvironment more vulnerable. This article systematically reviews the research progress of immunosenescence and immune microenvironment in digestive system cancers, as well as the exploration of related therapy strategies, hoping to point out new directions for research in the digestive system cancers.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"106 ","pages":"Pages 234-250"},"PeriodicalIF":12.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142606235","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}

引用次数: 0

Convergent evolution of senescent fibroblasts in fibrosis and cancer with aging 纤维化和癌症中的衰老成纤维细胞随衰老而趋同进化。

IF 12.1 1区医学

Seminars in cancer biology Pub Date : 2024-11-01 DOI: 10.1016/j.semcancer.2024.10.002

Jin Young Lee , Tien Peng

{"title":"Convergent evolution of senescent fibroblasts in fibrosis and cancer with aging","authors":"Jin Young Lee , Tien Peng","doi":"10.1016/j.semcancer.2024.10.002","DOIUrl":"10.1016/j.semcancer.2024.10.002","url":null,"abstract":"<div><div>Aging is associated with stereotyped changes in the tissue microenvironment that increase susceptibility to diseases of the elderly, including organ fibrosis and cancer. From a tissue perspective, fibrosis and cancer can both be viewed as non-healing wounds with pathogenic activation of tissue repair pathways in the stroma. If fibrosis and cancer represent an example of the convergent evolution of maladaptive stromal responses in distinct pathologies, what are the analogous cell types that might emerge in both diseases that share similarities in identity and function? In this review, we explore how senescent fibroblasts form a nexus that connects the aging organ with both fibrosis and cancer. The advent of single cell sequencing, coupled with improved detection of cell types with senescent traits in vivo, have allowed us to identify senescent fibroblasts with similar identities in both fibrosis and cancer that share pro-fibrotic programs. In addition to their ability to reorganize the extracellular matrix in diseased states, these pro-fibrotic senescent fibroblasts can also promote epithelial reprogramming and immune rewiring, which drive disease progression in fibrosis and cancer. Finally, the identification of common pathogenic cell types in fibrosis and cancer also presents a therapeutic opportunity to target both diseases with a shared approach.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"106 ","pages":"Pages 192-200"},"PeriodicalIF":12.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142473763","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}

引用次数: 0

BubR1 and SIRT2: Insights into aneuploidy, aging, and cancer BubR1 和 SIRT2：对非整倍体、衰老和癌症的见解

IF 12.1 1区医学

Seminars in cancer biology Pub Date : 2024-11-01 DOI: 10.1016/j.semcancer.2024.10.005

Renju Pun , Niti Kumari , Rodaina Hazem Monieb, Sachin Wagh, Brian J. North

{"title":"BubR1 and SIRT2: Insights into aneuploidy, aging, and cancer","authors":"Renju Pun , Niti Kumari , Rodaina Hazem Monieb, Sachin Wagh, Brian J. North","doi":"10.1016/j.semcancer.2024.10.005","DOIUrl":"10.1016/j.semcancer.2024.10.005","url":null,"abstract":"<div><div>Aging is a significant risk factor for cancer which is due, in part, to heightened genomic instability. Mitotic surveillance proteins such as BubR1 play a pivotal role in ensuring accurate chromosomal segregation and preventing aneuploidy. BubR1 levels have been shown to naturally decline with age and its loss is associated with various age-related pathologies. Sirtuins, a class of NAD<sup>+</sup>-dependent deacylases, are implicated in cancer and genomic instability. Among them, SIRT2 acts as an upstream regulator of BubR1, offering a critical pathway that can potentially mitigate age-related diseases, including cancer. In this review, we explore BubR1 as a key regulator of cellular processes crucial for aging-related phenotypes. We delve into the intricate mechanisms through which BubR1 influences genomic stability and cellular senescence. Moreover, we highlight the role of NAD<sup>+</sup> and SIRT2 in modulating BubR1 expression and function, emphasizing its potential as a therapeutic target. The interaction between BubR1 and SIRT2 not only serves as a fundamental regulatory pathway in cellular homeostasis but also represents a promising avenue for developing targeted therapies against age-related diseases, particularly cancer.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"106 ","pages":"Pages 201-216"},"PeriodicalIF":12.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142560557","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}

引用次数: 0

Origins and molecular effects of hypoxia in cancer 癌症中缺氧的起源和分子效应。

IF 12.1 1区医学

Seminars in cancer biology Pub Date : 2024-10-18 DOI: 10.1016/j.semcancer.2024.10.001

Sergio Rey-Keim , Luana Schito

引用次数: 0

Ferroptosis and immunosenescence in colorectal cancer 结直肠癌中的铁蛋白沉积症和免疫衰老

IF 12.1 1区医学

Seminars in cancer biology Pub Date : 2024-10-16 DOI: 10.1016/j.semcancer.2024.10.003

Yao Wang , Xinran Cao , Chunbaixue Yang , Jianchun Fan , Xingmei Zhang , Xueliang Wu , Wei Guo , Shoutian Sun , Ming Liu , Lifen Zhang , Tian Li

{"title":"Ferroptosis and immunosenescence in colorectal cancer","authors":"Yao Wang , Xinran Cao , Chunbaixue Yang , Jianchun Fan , Xingmei Zhang , Xueliang Wu , Wei Guo , Shoutian Sun , Ming Liu , Lifen Zhang , Tian Li","doi":"10.1016/j.semcancer.2024.10.003","DOIUrl":"10.1016/j.semcancer.2024.10.003","url":null,"abstract":"<div><div>Colorectal cancer (CRC), ranked as the globe’s third leading malignancy. Despite advancements in therapeutic approaches, the mortality rate remains distressingly high for those afflicted with advanced stages of the disease. Ferroptosis is a programmed form of cell death. The ways of ferroptosis mainly include promoting the accumulation of cellular ROS and increasing the level of cellular Labile iron pool (LIP). Immunosenescence is characterized by a gradual deterioration of the immune system’s ability to respond to pathogens and maintain surveillance against cancer cells. In CRC, this decline is exacerbated by the tumor microenvironment, which can suppress the immune response and promote tumor progression. This paper reviews the relationship between iron prolapse and immune senescence in colorectal cancer, focusing on the following aspects: firstly, the different pathways that induce iron prolapse in colorectal cancer; secondly, immune-immune senescence in colorectal cancer; and lastly, the interactions between immune senescence and iron prolapse in colorectal cancer, e.g., immune-immune senescent cells often exhibit increased oxidative stress, leading to the accumulation of ROS, and consequently to lipid peroxidation and induction of iron-induced cell death. At the same time, ferroptosis induces immune cell senescence as well as alterations in the immune microenvironment by promoting the death of damaged or diseased cells and leading to the inflammation usually associated with it. In conclusion, by exploring the potential targets of ferroptosis and immune senescence in colorectal cancer therapy, we hope to provide a reference for future research.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"106 ","pages":"Pages 156-165"},"PeriodicalIF":12.1,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142473765","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}

引用次数: 0

PROTAC as a novel anti-cancer strategy by targeting aging-related signaling 以衰老相关信号为靶点，将 PROTAC 作为一种新型抗癌策略。

IF 12.1 1区医学

Seminars in cancer biology Pub Date : 2024-10-03 DOI: 10.1016/j.semcancer.2024.09.004

Yunhua Peng , Donghua Liu , Daoyuan Huang , Hiroyuki Inuzuka , Jing Liu

引用次数: 0

DAMPs in immunosenescence and cancer 免疫衰老和癌症中的 DAMPs。

IF 12.1 1区医学

Seminars in cancer biology Pub Date : 2024-09-29 DOI: 10.1016/j.semcancer.2024.09.005

Fangquan Chen , Hu Tang , Xiutao Cai , Junhao Lin , Rui Kang , Daolin Tang , Jiao Liu

{"title":"DAMPs in immunosenescence and cancer","authors":"Fangquan Chen , Hu Tang , Xiutao Cai , Junhao Lin , Rui Kang , Daolin Tang , Jiao Liu","doi":"10.1016/j.semcancer.2024.09.005","DOIUrl":"10.1016/j.semcancer.2024.09.005","url":null,"abstract":"<div><div>Damage-associated molecular patterns (DAMPs) are endogenous molecules released by cells in response to injury or stress, recognized by host pattern recognition receptors that assess the immunological significance of cellular damage. The interaction between DAMPs and innate immune receptors triggers sterile inflammation, which serves a dual purpose: promoting tissue repair and contributing to pathological conditions, including age-related diseases. Chronic inflammation mediated by DAMPs accelerates immunosenescence and influences both tumor progression and anti-tumor immunity, underscoring the critical role of DAMPs in the nexus between aging and cancer. This review explores the characteristics of immunosenescence and its impact on age-related cancers, investigates the various types of DAMPs, their release mechanisms during cell death, and the immune activation pathways they initiate. Additionally, we examine the therapeutic potential of targeting DAMPs in age-related diseases. A detailed understanding of DAMP-induced signal transduction could provide critical insights into immune regulation and support the development of innovative therapeutic strategies.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"106 ","pages":"Pages 123-142"},"PeriodicalIF":12.1,"publicationDate":"2024-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142353128","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}

引用次数: 0