Seminars in cancer biology最新文献

英文中文

Epithelial-mesenchymal transition promotes metabolic reprogramming to suppress ferroptosis

IF 12.1 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-03-07 DOI: 10.1016/j.semcancer.2025.02.013

Wenzheng Guo, Zhibing Duan, Jingjing Wu, Binhua P. Zhou

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.

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引用次数: 0

Targeting mineral metabolism in cancer: Insights into signaling pathways and therapeutic strategies

IF 12.1 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-02-28 DOI: 10.1016/j.semcancer.2025.02.011

Kartik Bhatnagar , Sharon Raju , Ninad Patki , Rajender K. Motiani , Sarika Chaudhary

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.

{"title":"Targeting mineral metabolism in cancer: Insights into signaling pathways and therapeutic strategies","authors":"Kartik Bhatnagar , Sharon Raju , Ninad Patki , Rajender K. Motiani , 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}

引用次数: 0

Clonal hematopoiesis, cardiovascular disease and cancer treatment-induced cardiotoxicity

IF 12.1 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-02-27 DOI: 10.1016/j.semcancer.2025.02.007

Nan Zhang , Xu Tian , Dongkun Sun , Gary Tse , Bingxin Xie , Zhiqiang Zhao , Tong Liu

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.

{"title":"Clonal hematopoiesis, cardiovascular disease and cancer treatment-induced cardiotoxicity","authors":"Nan Zhang , Xu Tian , Dongkun Sun , Gary Tse , Bingxin Xie , Zhiqiang Zhao , 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}

引用次数: 0

Immunosenescence in skeletal muscle: The role-play in cancer cachexia chessboard

IF 12.1 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-02-26 DOI: 10.1016/j.semcancer.2025.02.012

Matteo Giovarelli , Emanuele Mocciaro , Carla Carnovale , Davide Cervia , Cristiana Perrotta , Emilio Clementi

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.

{"title":"Immunosenescence in skeletal muscle: The role-play in cancer cachexia chessboard","authors":"Matteo Giovarelli , Emanuele Mocciaro , Carla Carnovale , Davide Cervia , Cristiana Perrotta , 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}

引用次数: 0

Immunosenescence and immunotherapy in elderly patients with hepatocellular carcinoma

IF 12.1 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-02-26 DOI: 10.1016/j.semcancer.2025.02.010

Dengyong Zhang , Yan Zhu , Zhengchao Shen , Shuoshuo Ma , Sihua Liu , Zheng Lu

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.

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引用次数: 0

Atrial fibrillation in cancer patients: Epidemiology, identification and management

IF 12.1 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-02-22 DOI: 10.1016/j.semcancer.2025.02.006

Chengqi Yu , Leilei Jiang , Liuhua Long , Huiming Yu

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.

癌症和心血管疾病（CVD）是导致全球死亡的主要原因之一，近年来，随着老龄化社会中易感人群基数的增加和治疗方法的改进，这两种疾病的并发率也在不断上升。心房颤动（AF）作为肿瘤患者常见的一种癌症相关心血管毒性反应（CTR-CVT），严重威胁着患者的健康，并可能引发其他心血管并发症。因此，早期发现、及时识别和有效干预房颤对维持肿瘤幸存者的长期生存至关重要。然而，关于心房颤动的相关因果机制尚无定论，临床上也未就最佳治疗方法达成共识。在这篇综述中，我们将整合现有指南和研究，从流行病学、病理生理机制、预测诊断和治疗措施等方面总结肿瘤患者心房颤动的研究现状，并提出一些有待改进的研究方向。希望能提供更全面的综述，为临床应对提供帮助。

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引用次数: 0

Biomarkers, omics and artificial intelligence for early detection of pancreatic cancer 生物标记物、Omics 和人工智能用于胰腺癌的早期检测。

IF 12.1 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-02-20 DOI: 10.1016/j.semcancer.2025.02.009

Kate Murray , Lucy Oldfield , Irena Stefanova , Manuel Gentiluomo , Paolo Aretini , Rachel O’Sullivan , William Greenhalf , Salvatore Paiella , Mateus N. Aoki , Aldo Pastore , James Birch-Ford , Bhavana Hemantha Rao , Pinar Uysal-Onganer , Caoimhe M. Walsh , George B. Hanna , Jagriti Narang , Pradakshina Sharma , Daniele Campa , Cosmeri Rizzato , Andrei Turtoi , Eithne Costello

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.

{"title":"Biomarkers, omics and artificial intelligence for early detection of pancreatic cancer","authors":"Kate Murray , Lucy Oldfield , Irena Stefanova , Manuel Gentiluomo , Paolo Aretini , Rachel O’Sullivan , William Greenhalf , Salvatore Paiella , Mateus N. Aoki , Aldo Pastore , James Birch-Ford , Bhavana Hemantha Rao , Pinar Uysal-Onganer , Caoimhe M. Walsh , George B. Hanna , Jagriti Narang , Pradakshina Sharma , Daniele Campa , Cosmeri Rizzato , Andrei Turtoi , 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}

引用次数: 0

Editorial – Hypoxia as a molecular driver of cancer progression

IF 12.1 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-02-18 DOI: 10.1016/j.semcancer.2025.02.008

Luana Schito , Sergio Rey-Keim

引用次数: 0

Metabolic crosstalk between platelets and cancer: Mechanisms, functions, and therapeutic potential

IF 12.1 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-02-13 DOI: 10.1016/j.semcancer.2025.02.001

Zhixue Chen , Lin Xu , Yejv Yuan , Si Zhang , Ruyi Xue

Platelets, traditionally regarded as passive mediators of hemostasis, are now recognized as pivotal regulators in the tumor microenvironment, establishing metabolic feedback loops with tumor and immune cells. Tumor-derived signals trigger platelet activation, which induces rapid metabolic reprogramming, particularly glycolysis, to support activation-dependent functions such as granule secretion, morphological changes, and aggregation. Beyond self-regulation, platelets influence the metabolic processes of adjacent cells. Through direct mitochondrial transfer, platelets reprogram tumor and immune cells, promoting oxidative phosphorylation. Additionally, platelet-derived cytokines, granules, and extracellular vesicles drive metabolic alterations in immune cells, fostering suppressive phenotypes that facilitate tumor progression. This review examines three critical aspects: (1) the distinctive metabolic features of platelets, particularly under tumor-induced activation; (2) the metabolic crosstalk between activated platelets and other cellular components; and (3) the therapeutic potential of targeting platelet metabolism to disrupt tumor-promoting networks. By elucidating platelet metabolism, this review highlights its essential role in tumor biology and its therapeutic implications.

{"title":"Metabolic crosstalk between platelets and cancer: Mechanisms, functions, and therapeutic potential","authors":"Zhixue Chen , Lin Xu , Yejv Yuan , Si Zhang , Ruyi Xue","doi":"10.1016/j.semcancer.2025.02.001","DOIUrl":"10.1016/j.semcancer.2025.02.001","url":null,"abstract":"<div><div>Platelets, traditionally regarded as passive mediators of hemostasis, are now recognized as pivotal regulators in the tumor microenvironment, establishing metabolic feedback loops with tumor and immune cells. Tumor-derived signals trigger platelet activation, which induces rapid metabolic reprogramming, particularly glycolysis, to support activation-dependent functions such as granule secretion, morphological changes, and aggregation. Beyond self-regulation, platelets influence the metabolic processes of adjacent cells. Through direct mitochondrial transfer, platelets reprogram tumor and immune cells, promoting oxidative phosphorylation. Additionally, platelet-derived cytokines, granules, and extracellular vesicles drive metabolic alterations in immune cells, fostering suppressive phenotypes that facilitate tumor progression. This review examines three critical aspects: (1) the distinctive metabolic features of platelets, particularly under tumor-induced activation; (2) the metabolic crosstalk between activated platelets and other cellular components; and (3) the therapeutic potential of targeting platelet metabolism to disrupt tumor-promoting networks. By elucidating platelet metabolism, this review highlights its essential role in tumor biology and its therapeutic implications.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"110 ","pages":"Pages 65-82"},"PeriodicalIF":12.1,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143425755","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

Unexpected links between cancer and telomere state

IF 12.1 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-02-12 DOI: 10.1016/j.semcancer.2025.01.006

Alessio Lanna

Eukaryotes possess chromosome ends known as telomeres. As telomeres shorten, organisms age, a process defined as senescence. Although uncontrolled telomere lengthening has been naturally connected with cancer developments and immortalized state, many cancers are instead characterized by extremely short, genomically unstable telomeres that may hide cancer cells from immune attack. By contrast, other malignancies feature extremely long telomeres due to absence of ‘shelterin’ end cap protecting factors. The reason for rampant telomere extension in these cancers had remained elusive. Hence, while telomerase supports tumor progression and escape in cancers with very short telomeres, it is possible that different - transfer based or alternative - lengthening pathways be involved in the early stage of tumorigenesis, when telomere length is intact. In this Review, I hereby discuss recent discoveries in the field of telomeres and highlight unexpected links connecting cancer and telomere state. We hope these parallelisms may inform new therapies to eradicate cancers.

引用次数: 0

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