{"title":"Navigating life as an early career researcher.","authors":"Shruti Bhatt, Yash Chhabra, Merav Cohen, Anniina Färkkilä, Shom Goel, Guideng Li, Sandra Romero-Córdoba","doi":"10.1016/j.trecan.2025.03.006","DOIUrl":"10.1016/j.trecan.2025.03.006","url":null,"abstract":"","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"261-266"},"PeriodicalIF":14.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143744080","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 : 2025-04-01Epub Date: 2025-01-09DOI: 10.1016/j.trecan.2024.12.003
Sepideh Parvanian, Xinying Ge, Christopher S Garris
{"title":"Recent developments in myeloid immune modulation in cancer therapy.","authors":"Sepideh Parvanian, Xinying Ge, Christopher S Garris","doi":"10.1016/j.trecan.2024.12.003","DOIUrl":"10.1016/j.trecan.2024.12.003","url":null,"abstract":"<p><p>Myeloid cells play a crucial dual role in cancer progression and response to therapy, promoting tumor growth, enabling immune suppression, and contributing to metastatic spread. The ability of these cells to modulate the immune system has made them attractive targets for therapeutic strategies aimed at shifting their function from tumor promotion to fostering antitumor immunity. Therapeutic approaches targeting myeloid cells focus on modifying their numbers, genetics, metabolism, and interactions within the tumor microenvironment. These strategies aim to reverse their suppressive functions and redirect them to support antitumor immune responses by inhibiting immunosuppressive pathways, targeting specific receptors, and promoting their differentiation into less immunosuppressive phenotypes. Here, we discuss recent approaches to clinically target tumor myeloid cells, focusing on reprogramming myeloid cells to promote antitumor immunity.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"365-375"},"PeriodicalIF":14.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142966797","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 : 2025-04-01Epub Date: 2024-12-27DOI: 10.1016/j.trecan.2024.11.010
Lin Zhou, Boyang Ma, Marcus Ruscetti
{"title":"Cellular senescence offers distinct immunological vulnerabilities in cancer.","authors":"Lin Zhou, Boyang Ma, Marcus Ruscetti","doi":"10.1016/j.trecan.2024.11.010","DOIUrl":"10.1016/j.trecan.2024.11.010","url":null,"abstract":"<p><p>Chronic damage following oncogene induction or cancer therapy can produce cellular senescence. Senescent cells not only exit the cell cycle but communicate damage signals to their environment that can trigger immune responses. Recent work has revealed that senescent tumor cells are highly immunogenic, leading to new ways to activate antitumor immunosurveillance and potentiate T cell-directed immunotherapies. However, other studies have determined that heterogeneous senescent stromal cell populations contribute to immunosuppression and tumor progression, sparking the development of senotherapeutics to target senescent cells that evade immune detection. We review current findings that provide deeper insights into the mechanisms contributing to the dichotomous role of senescence in immune modulation and how that can be leveraged for cancer immunotherapy.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"334-350"},"PeriodicalIF":14.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11981858/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142898403","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}
Trends in cancerPub Date : 2025-04-01Epub Date: 2025-02-28DOI: 10.1016/j.trecan.2025.01.010
Davide Carra, Silvana C E Maas, Jose A Seoane, Direna Alonso-Curbelo
{"title":"Exposomal determinants of non-genetic plasticity in tumor initiation.","authors":"Davide Carra, Silvana C E Maas, Jose A Seoane, Direna Alonso-Curbelo","doi":"10.1016/j.trecan.2025.01.010","DOIUrl":"10.1016/j.trecan.2025.01.010","url":null,"abstract":"<p><p>The classical view of cancer as a genetically driven disease has been challenged by recent findings of oncogenic mutations in phenotypically healthy tissues, refocusing attention on non-genetic mechanisms of tumor initiation. In this context, gene-environment interactions take the stage, with recent studies showing how they unleash and redirect cellular and tissue plasticity towards protumorigenic states in response to the exposome, the ensemble of environmental factors impinging on tissue homeostasis. We conceptualize tumor-initiating plasticity as a phenotype-transforming force acting at three levels: cell-intrinsic, focusing on mutant epithelial cells' responses to environmental variation; reprogramming of non-neoplastic cells of the host, leading to protumor micro- and macroenvironments; and microbiome ecosystem dynamics. This perspective highlights cell, tissue, and organismal plasticity mechanisms underlying tumor initiation that are shaped by the exposome, and how their functional investigation may provide new opportunities to prevent, detect, and intercept cancer-promoting plasticity.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"295-308"},"PeriodicalIF":14.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143537734","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 : 2025-04-01Epub Date: 2024-12-04DOI: 10.1016/j.trecan.2024.11.002
Francisco Martínez-Jiménez, Diego Chowell
{"title":"Genetic immune escape in cancer: timing and implications for treatment.","authors":"Francisco Martínez-Jiménez, Diego Chowell","doi":"10.1016/j.trecan.2024.11.002","DOIUrl":"10.1016/j.trecan.2024.11.002","url":null,"abstract":"<p><p>Genetic immune escape (GIE) alterations pose a significant challenge in cancer by enabling tumors to evade immune detection. These alterations, which can vary significantly across cancer types, may often arise early in clonal evolution and contribute to malignant transformation. As tumors evolve, GIE alterations are positively selected, allowing immune-resistant clones to proliferate. In addition to genetic changes, the tumor microenvironment (TME) and non-genetic factors such as inflammation, smoking, and environmental exposures play crucial roles in promoting immune evasion. Understanding the timing and mechanisms of GIE, alongside microenvironmental influences, is crucial for improving early detection and developing more effective therapeutic interventions. This review highlights the implications of GIE in cancer development and immunotherapy resistance, and emphasizes the need for integrative approaches.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"286-294"},"PeriodicalIF":14.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11981860/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142781186","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}
Trends in cancerPub Date : 2025-04-01Epub Date: 2024-11-07DOI: 10.1016/j.trecan.2024.10.005
Stanislav Drapela, Bruna M Garcia, Ana P Gomes, Ana Luísa Correia
{"title":"Metabolic landscape of disseminated cancer dormancy.","authors":"Stanislav Drapela, Bruna M Garcia, Ana P Gomes, Ana Luísa Correia","doi":"10.1016/j.trecan.2024.10.005","DOIUrl":"10.1016/j.trecan.2024.10.005","url":null,"abstract":"<p><p>Cancer dormancy is a phenomenon defined by the entry of cancer cells into a reversible quiescent, nonproliferative state, and represents an essential part of the metastatic cascade responsible for cancer recurrence and mortality. Emerging evidence suggests that metabolic reprogramming plays a pivotal role in enabling entry, maintenance, and exit from dormancy in the face of the different environments of the metastatic cascade. Here, we review the current literature to understand the dynamics of metabolism during dormancy, highlighting its fine-tuning by the host micro- and macroenvironment, and put forward the importance of identifying metabolic vulnerabilities of the dormant state as therapeutic targets to eradicate recurrent disease.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"321-333"},"PeriodicalIF":14.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11981868/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142606455","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}
Trends in cancerPub Date : 2025-04-01Epub Date: 2025-01-28DOI: 10.1016/j.trecan.2025.01.002
Lisa Pavinato, Arianna Baggiolini
{"title":"Oncogenic competence: balancing mutations, cellular state, and microenvironment.","authors":"Lisa Pavinato, Arianna Baggiolini","doi":"10.1016/j.trecan.2025.01.002","DOIUrl":"10.1016/j.trecan.2025.01.002","url":null,"abstract":"<p><p>Cancer development is driven by mutations, yet tumor-causing mutations only lead to tumor formation within specific cellular contexts. The reasons why certain mutations trigger malignant transformation in some contexts but not others remain often unclear. Both intrinsic and extrinsic factors play a key role in driving carcinogenesis by leading the cells toward a state of 'oncogenic competence'. This state is shaped by the transcriptional and epigenetic programs that define a specific cell in time and space. These programs arise from the interplay between genetic mutations, cellular lineage, differentiation state, and microenvironment. A deeper understanding of oncogenic competence is essential to uncover the mechanisms behind tumor initiation and, ultimately, advance the development of novel targeted therapies for cancer treatment and prevention.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"276-285"},"PeriodicalIF":14.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143060830","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 : 2025-04-01Epub Date: 2025-02-21DOI: 10.1016/j.trecan.2025.01.012
Long Cheng, Yibo Wang, Ying Zhang
{"title":"Dying to survive: harnessing inflammatory cell death for better immunotherapy.","authors":"Long Cheng, Yibo Wang, Ying Zhang","doi":"10.1016/j.trecan.2025.01.012","DOIUrl":"10.1016/j.trecan.2025.01.012","url":null,"abstract":"<p><p>Immunotherapy has transformed cancer treatment paradigms, but its effectiveness depends largely on the immunogenicity of the tumor. Unfortunately, the high resemblance of cancer to normal tissues makes most tumors immunologically 'cold', with a poor response to immunotherapy. Danger signals are critical for breaking immune tolerance and mobilizing robust, long-lasting antitumor immunity. Recent studies have identified inflammatory cell death modalities and their power in providing danger signals to trigger optimal tumor suppression. However, key mediators of inflammatory cell death are preferentially silenced during early tumor immunoediting. Strategies to rejuvenate inflammatory cell death hold great promise for broadening immunotherapy-responsive tumors. In this review, we examine how inflammatory cell death enhances tumor immunogenicity, how it is suppressed during immunoediting, and the potential of harnessing it for improved immunotherapy.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"376-402"},"PeriodicalIF":14.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143477049","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 : 2025-04-01Epub Date: 2025-01-02DOI: 10.1016/j.trecan.2024.12.002
Jan Hochstadt, Sarai Martínez Pacheco, María Casanova-Acebes
{"title":"Embracing diversity: macrophage complexity in cancer.","authors":"Jan Hochstadt, Sarai Martínez Pacheco, María Casanova-Acebes","doi":"10.1016/j.trecan.2024.12.002","DOIUrl":"10.1016/j.trecan.2024.12.002","url":null,"abstract":"<p><p>Macrophages are myeloid cells that receive, integrate, and respond to tumoral cues. Tumors evolve and are shaped by macrophages, with tumor-associated macrophage (TAM)-tumor sculpting capacities going beyond an increase in their cellular mass. Longitudinal and local heterogeneity of TAM states is now possible with the use of single-cell and spatial transcriptomics. However, understanding TAM biology and its fundamental functional programs is still challenging, probably because of the lack of models that fully integrate TAM complexity. Here, we aim to review TAM diversity not only at the level of single-cell phenotypes but also by integrating complex physiological signals that determine their complexity and plasticity in tumors.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"351-364"},"PeriodicalIF":14.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142927838","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":"Tackling the next decade of cancer research.","authors":"Raza Ali, Brittany Jenkins, Wouter Karthaus, Jana Lipkova, Sandra Misale, Jens Puschhof, Melody Smith, Santosha Vardhana, Xin Zhou","doi":"10.1016/j.trecan.2025.03.004","DOIUrl":"10.1016/j.trecan.2025.03.004","url":null,"abstract":"","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"267-273"},"PeriodicalIF":14.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143710487","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}