Trends in cancerPub Date : 2024-11-01Epub Date: 2024-08-31DOI: 10.1016/j.trecan.2024.08.001
Lillian M Perez, Smrruthi V Venugopal, Anna St Martin, Stephen J Freedland, Dolores Di Vizio, Michael R Freeman
{"title":"Mechanisms governing lineage plasticity and metabolic reprogramming in cancer.","authors":"Lillian M Perez, Smrruthi V Venugopal, Anna St Martin, Stephen J Freedland, Dolores Di Vizio, Michael R Freeman","doi":"10.1016/j.trecan.2024.08.001","DOIUrl":"10.1016/j.trecan.2024.08.001","url":null,"abstract":"<p><p>Dynamic alterations in cellular phenotypes during cancer progression are attributed to a phenomenon known as 'lineage plasticity'. This process is associated with therapeutic resistance and involves concurrent shifts in metabolic states that facilitate adaptation to various stressors inherent in malignant growth. Certain metabolites also serve as synthetic reservoirs for chromatin modification, thus linking metabolic states with epigenetic regulation. There remains a critical need to understand the mechanisms that converge on lineage plasticity and metabolic reprogramming to prevent the emergence of lethal disease. This review attempts to offer an overview of our current understanding of the interplay between metabolic reprogramming and lineage plasticity in the context of cancer, highlighting the intersecting drivers of cancer hallmarks, with an emphasis on solid tumors.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"1009-1022"},"PeriodicalIF":14.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142112410","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 : 2024-11-01Epub Date: 2024-09-04DOI: 10.1016/j.trecan.2024.08.006
Xinyuan Zhou, Binyu Shi, Gang Huang, Jianjun Liu, Weijun Wei
{"title":"Trends in cancer imaging.","authors":"Xinyuan Zhou, Binyu Shi, Gang Huang, Jianjun Liu, Weijun Wei","doi":"10.1016/j.trecan.2024.08.006","DOIUrl":"10.1016/j.trecan.2024.08.006","url":null,"abstract":"<p><p>Molecular imaging of cancer is a collaborative endeavor, uniting scientists and physicians from diverse fields. Such collaboration is actively developing and translating cutting-edge molecular imaging approaches to enhance the diagnostic landscape of human malignancies. The advent of positron emission tomography (PET) and PET imaging tracers has realized non-invasive target annotation and tumor characterization at the molecular level. In surgical procedures, novel imaging techniques, such as fluorescence or Cherenkov luminescence, help identify tumors and enhance surgical precision. Simultaneously, progress in imaging equipment, innovative algorithms, and artificial intelligence has opened avenues for next-generation cancer screening and imaging, augmenting the efficiency and accuracy of cancer diagnosis. In this review, we provide a panorama of molecular cancer imaging and ongoing developments in the field.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"1023-1037"},"PeriodicalIF":14.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142133893","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 : 2024-11-01Epub Date: 2024-10-01DOI: 10.1016/j.trecan.2024.09.009
Esmeralda García-Torralba, Lorenzo Galluzzi, Aitziber Buqué
{"title":"Prognostic value of atypical B cells in breast cancer.","authors":"Esmeralda García-Torralba, Lorenzo Galluzzi, Aitziber Buqué","doi":"10.1016/j.trecan.2024.09.009","DOIUrl":"10.1016/j.trecan.2024.09.009","url":null,"abstract":"<p><p>The impact of tumor-infiltrating B cells on breast cancer (BRCA) outcomes remains poorly understood. Recent findings from Yang et al. identify an atypical, clonally expanded population of activated Fc receptor-like 4 (FCRL4)<sup>+</sup> B cells that is associated with improved overall survival in patients affected by various tumor types, including BRCA.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"990-991"},"PeriodicalIF":14.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142366683","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 : 2024-11-01Epub Date: 2024-10-02DOI: 10.1016/j.trecan.2024.08.003
Adrian L Harris, David J Kerr, Francesco Pezzella, Domenico Ribatti
{"title":"Accessing the vasculature in cancer: revising an old hallmark.","authors":"Adrian L Harris, David J Kerr, Francesco Pezzella, Domenico Ribatti","doi":"10.1016/j.trecan.2024.08.003","DOIUrl":"10.1016/j.trecan.2024.08.003","url":null,"abstract":"<p><p>The classic cancer hallmark, inducing angiogenesis, was born out of the long-held notion that tumours could grow only if new vessels were formed. The attempts, based on this premise, to therapeutically restrain angiogenesis in hopes of controlling tumour growth have been less effective than expected. This is partly because primary and metastatic tumours can grow without angiogenesis. The discovery of nonangiogenic cancers and the mechanisms they use to exploit normal vessels, called 'vessel co-option,' has opened a new field in cancer biology. Consequently, the cancer hallmark, 'inducing angiogenesis,' has been modified to 'inducing or accessing vasculature.'</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"1038-1051"},"PeriodicalIF":14.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142366682","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 : 2024-11-01Epub Date: 2024-10-02DOI: 10.1016/j.trecan.2024.09.008
Dhanashree Mundhe, Neta Erez
{"title":"Time to heal: inhibiting fibrosis prevents glioblastoma recurrence.","authors":"Dhanashree Mundhe, Neta Erez","doi":"10.1016/j.trecan.2024.09.008","DOIUrl":"10.1016/j.trecan.2024.09.008","url":null,"abstract":"<p><p>New findings by Watson et al. demonstrate that therapy-induced inflammation and fibrosis potentiate glioblastoma recurrence. Post-treatment fibrotic niches shielded surviving tumor cells from immune surveillance, supported their persistence in a dormant state, and enabled rebound growth. Timely inhibition of inflammation and scarring attenuated recurrence, encouraging the use of new combinatorial approaches in glioblastoma therapy.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"987-989"},"PeriodicalIF":14.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142366684","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 : 2024-10-30DOI: 10.1016/j.trecan.2024.10.003
Luana Schito, Sergio Rey-Keim
{"title":"Transcriptional regulation of hypoxic cancer cell metabolism and artificial intelligence.","authors":"Luana Schito, Sergio Rey-Keim","doi":"10.1016/j.trecan.2024.10.003","DOIUrl":"https://doi.org/10.1016/j.trecan.2024.10.003","url":null,"abstract":"<p><p>Gene expression regulation in hypoxic tumor microenvironments is mediated by O<sub>2</sub> responsive transcription factors (O<sub>2</sub>R-TFs), fine-tuning cancer cell metabolic demand for O<sub>2</sub> according to its availability. Here, we discuss key O<sub>2</sub>R-TFs and emerging artificial intelligence (AI)-based applications suitable for the interrogation of O<sub>2</sub>R-TF relationships specifying cancer cell metabolic adaptations to hypoxia.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":14.3,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142558877","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 : 2024-10-25DOI: 10.1016/j.trecan.2024.10.001
Jerry Tyler DeWitt, Megha Raghunathan, Svasti Haricharan
{"title":"Nonrepair functions of DNA mismatch repair proteins: new avenues for precision oncology.","authors":"Jerry Tyler DeWitt, Megha Raghunathan, Svasti Haricharan","doi":"10.1016/j.trecan.2024.10.001","DOIUrl":"https://doi.org/10.1016/j.trecan.2024.10.001","url":null,"abstract":"<p><p>DNA damage repair (DDR) proteins are well recognized as guardians of the genome that are frequently lost during malignant transformation of normal cells across cancer types. To date, their tumor suppressor functions have been generally regarded as a consequence of their roles in maintaining genomic stability: more genomic instability increases the risk of oncogenic transformation events. However, recent discoveries centering around DNA mismatch repair (MMR) proteins suggest a broader impact of the loss of DDR proteins on cellular processes beyond genomic instability. Here, we explore the clinical implications of nonrepair roles for DDR proteins, using the growing evidence supporting roles for DNA MMR proteins in cell cycle and apoptosis regulation, metabolic function, the cellular secretome, and immunomodulation.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":14.3,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142569617","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":"A new enhancer for anti-PD-1/PD-L1 immunotherapy: PCSK9 inhibition.","authors":"Shengbo Sun, Zhengyang Yang, Hongwei Yao, Zhongtao Zhang","doi":"10.1016/j.trecan.2024.10.002","DOIUrl":"https://doi.org/10.1016/j.trecan.2024.10.002","url":null,"abstract":"<p><p>Anti-programmed cell death protein 1 (PD-1)/PD-1 ligand 1 (PD-L1) immunotherapy has shown promising results in cancer treatment, improving clinical outcomes and prolonging patient survival. However, most patients exhibit low response rates to PD-1/PD-L1 blockade, highlighting the urgent need for new enhancers. Increasing data now demonstrate that inhibiting proprotein convertase subtilisin/kexin type 9 (PCSK9), a serine proteinase, can enhance the antitumor efficacy of anti-PD-1/PD-L1 immunotherapy.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":14.3,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142508856","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 : 2024-10-21DOI: 10.1016/j.trecan.2024.09.010
Pavel Vodicka, Sona Vodenkova, Natalie Danesova, Ludmila Vodickova, Renata Zobalova, Kristyna Tomasova, Stepana Boukalova, Michael V Berridge, Jiri Neuzil
{"title":"Mitochondrial DNA damage, repair, and replacement in cancer.","authors":"Pavel Vodicka, Sona Vodenkova, Natalie Danesova, Ludmila Vodickova, Renata Zobalova, Kristyna Tomasova, Stepana Boukalova, Michael V Berridge, Jiri Neuzil","doi":"10.1016/j.trecan.2024.09.010","DOIUrl":"https://doi.org/10.1016/j.trecan.2024.09.010","url":null,"abstract":"<p><p>Mitochondria are vital organelles with their own DNA (mtDNA). mtDNA is circular and composed of heavy and light chains that are structurally more accessible than nuclear DNA (nDNA). While nDNA is typically diploid, the number of mtDNA copies per cell is higher and varies considerably during development and between tissues. Compared with nDNA, mtDNA is more prone to damage that is positively linked to many diseases, including cancer. Similar to nDNA, mtDNA undergoes repair processes, although these mechanisms are less well understood. In this review, we discuss the various forms of mtDNA damage and repair and their association with cancer initiation and progression. We also propose horizontal mitochondrial transfer as a novel mechanism for replacing damaged mtDNA.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":14.3,"publicationDate":"2024-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142508857","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 : 2024-10-05DOI: 10.1016/j.trecan.2024.09.005
Venkata Narasimha Kadali, Ofer Shoshani
{"title":"Aberrant nuclei with amplified DNA in cancer.","authors":"Venkata Narasimha Kadali, Ofer Shoshani","doi":"10.1016/j.trecan.2024.09.005","DOIUrl":"https://doi.org/10.1016/j.trecan.2024.09.005","url":null,"abstract":"<p><p>Gene amplification in the form of extrachromosomal DNA (ecDNA) or intrachromosomal homogenous staining regions (HSRs) is an emerging hallmark in cancer. Recent studies implicate abnormal nuclear structures in the biogenesis and evolution of amplified DNA. Here, we discuss how the interplay between aberrant nuclei and gene amplification drives cancer therapy resistance and metastasis.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":14.3,"publicationDate":"2024-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142381736","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}