Trends in cancerPub Date : 2026-09-01Epub Date: 2026-06-11DOI: 10.1016/j.trecan.2026.05.005
Taniya Murikkinthara Samuel, Samson Mathews Samuel, Elizabeth Varghese, Bini Sreenesh, Dietrich Büsselberg
{"title":"Defying inflammation-driven early-onset colorectal cancer: predict, prevent, and personalize.","authors":"Taniya Murikkinthara Samuel, Samson Mathews Samuel, Elizabeth Varghese, Bini Sreenesh, Dietrich Büsselberg","doi":"10.1016/j.trecan.2026.05.005","DOIUrl":"10.1016/j.trecan.2026.05.005","url":null,"abstract":"<p><p>Early-life exposure to both modifiable and nonmodifiable risk factors may induce chronic low-grade inflammation (CLGI), a silent threat potentially driving the rising incidence of early-onset colorectal cancer (EOCRC). Notably, CLGI could promote EOCRC by altering the proinflammatory and immune microenvironment that supports tumor growth and cancer development. In this review, we examine how risk factors disrupt immune homeostasis and contribute to CLGI in young individuals, thereby promoting the development of EOCRC. Additionally, identifying CLGI-specific biomarkers could aid in early detection and diagnosis, while targeting specific molecular pathways may enable personalized therapeutic interventions for EOCRC by reducing the chronic inflammatory threat. We also highlight the importance of lifestyle changes and interventions to reduce CLGI and address the growing health concern of EOCRC.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"861-876"},"PeriodicalIF":21.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148219665","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 : 2026-09-01Epub Date: 2026-08-06DOI: 10.1016/j.trecan.2026.07.005
Ivan R Siordia, Jonathan R Brody, Dan A Dixon
{"title":"HuR degradation reveals dependencies in BRAF-driven cancers.","authors":"Ivan R Siordia, Jonathan R Brody, Dan A Dixon","doi":"10.1016/j.trecan.2026.07.005","DOIUrl":"10.1016/j.trecan.2026.07.005","url":null,"abstract":"<p><p>Targeting RNA-binding proteins has been shown to be challenging due to the absence of druggable pockets. Recently, Lu et al. identified a molecular glue capable of degrading HuR and suppressing BRAF-mutant colorectal cancer. These findings offer a promising therapeutic pathway for the treatment of a subset of HuR-driven malignancies.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"793-795"},"PeriodicalIF":21.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13449187/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148680135","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 : 2026-09-01Epub Date: 2026-05-20DOI: 10.1016/j.trecan.2026.04.010
Theodoros Papadopoulos, Ariel Pinto, Madelyn J Abraham, Carolina L Naranjo, Manuel F Molina, Marie Hudson, Wilson H Miller, Sonia V Del Rincón
{"title":"Mouse models of immune-related adverse events: progress, challenges, and opportunities.","authors":"Theodoros Papadopoulos, Ariel Pinto, Madelyn J Abraham, Carolina L Naranjo, Manuel F Molina, Marie Hudson, Wilson H Miller, Sonia V Del Rincón","doi":"10.1016/j.trecan.2026.04.010","DOIUrl":"10.1016/j.trecan.2026.04.010","url":null,"abstract":"<p><p>With immune checkpoint inhibitors (ICIs) being an established therapeutic pillar for many cancers, the management of their associated toxicities has emerged as a key clinical challenge. Immune-related adverse events (irAEs) frequently require immunosuppressive therapy, raising the concern that these treatments may dampen the antitumor effects elicited by ICIs. Foundational work in mice enabled the discovery of ICIs, and in this review, we discuss the continued importance of preclinical mouse modeling to understand the molecular mechanisms underpinning the most common irAEs. Mouse models can be used as surrogates to evaluate the effects of immunosuppressive therapies on irAEs, tumor growth, and ICI-mediated antitumor immunity. In reviewing genetic and pharmacological approaches to induce irAEs in mice, we identify key considerations for developing next-generation mouse models of irAEs.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"802-824"},"PeriodicalIF":21.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147983457","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 : 2026-09-01Epub Date: 2026-08-07DOI: 10.1016/j.trecan.2026.07.008
Matthew K Summers
{"title":"Deubiquitinase inhibition exposes a subtype-specific vulnerability in SCLC-P.","authors":"Matthew K Summers","doi":"10.1016/j.trecan.2026.07.008","DOIUrl":"10.1016/j.trecan.2026.07.008","url":null,"abstract":"<p><p>In a recent study published in Cell Press Blue, Huang et al. show that deubiquitinase-dependent stabilization of POU2F3 (POU class 2 homeobox 3), primarily driven by USP2 (Ubiquitin-Specific Protease 2), sustains the growth of the small cell lung cancer (SCLC)-P subtype of SCLC, revealing a strategy to exploit transcription factor dependence by disrupting protein stability.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"791-792"},"PeriodicalIF":21.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148685894","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 : 2026-09-01DOI: 10.1016/j.trecan.2026.08.002
Jether Amos Espinosa, Madeline Y Mayday, Abigail R Robb, Gina Lee, Diane S Krause
{"title":"RBM15 in leukemogenesis: an emerging regulator at the interface of RNA biology and hematopoiesis.","authors":"Jether Amos Espinosa, Madeline Y Mayday, Abigail R Robb, Gina Lee, Diane S Krause","doi":"10.1016/j.trecan.2026.08.002","DOIUrl":"10.1016/j.trecan.2026.08.002","url":null,"abstract":"<p><p>RNA-binding motif protein 15 (RBM15) is a key regulator of hematopoiesis and leukemogenesis, linking RNA metabolism, epitranscriptomic regulation, and lineage specification. Identified through the RBM15::MKL1 fusion in acute megakaryoblastic leukemia (AMKL), RBM15 functions within the N<sup>6</sup>-methyladenosine (m<sup>6</sup>A) writer complex, where its RNA-recognition motifs and Spen paralog and ortholog C-terminal domain enable site-specific methylation and protein recruitment. In hematopoietic stem and progenitor cells, RBM15 supports stem cell quiescence, self-renewal, and balanced lineage output, with additional roles in B cell, myeloid, and megakaryocytic differentiation. Mechanistically, RBM15 links m<sup>6</sup>A deposition to chromatin regulation, RNA export, and splicing. This review summarizes RBM15 structure, function, and regulation and highlights its emerging roles in leukemia, including AMKL and myelodysplastic syndromes, while outlining key questions for future studies.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":21.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13596041/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148876107","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 : 2026-09-01Epub Date: 2026-05-20DOI: 10.1016/j.trecan.2026.04.008
Tingjie Yuan, Jean Paul Thiery, Klaus Pantel, Daniel J Smit
{"title":"Epithelial-mesenchymal plasticity in breast cancer: from cell states to clinical vulnerability.","authors":"Tingjie Yuan, Jean Paul Thiery, Klaus Pantel, Daniel J Smit","doi":"10.1016/j.trecan.2026.04.008","DOIUrl":"10.1016/j.trecan.2026.04.008","url":null,"abstract":"<p><p>Epithelial-mesenchymal transition (EMT) in breast cancer is better understood as epithelial-mesenchymal plasticity (EMP), a dynamic and reversible spectrum of epithelial, hybrid, and mesenchymal states. In this review, we discuss how EMP is deployed differently across hormone receptor-positive/HER2-negative, HER2-positive, and triple-negative/claudin-low breast cancers, with distinct implications for metastasis, immune evasion, liquid biopsy, and therapeutic resistance. We highlight the regulatory networks and microenvironmental cues that shape state transitions and emphasize that hybrid and plasticity-high states may be more clinically informative than terminal mesenchymal states alone. We propose that progress will depend on subtype-aware, biomarker-guided strategies that resolve carcinoma cell state in space and time and therapeutically exploit EMT-associated vulnerabilities.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"838-848"},"PeriodicalIF":21.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147983456","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 : 2026-09-01Epub Date: 2026-06-02DOI: 10.1016/j.trecan.2026.05.003
Claudia Cifuentes Caballero, Ilaria Delle Fontane, Helen C Hope, Nicola Vannini
{"title":"The impact of aging on antitumor immunity and cancer immunotherapy.","authors":"Claudia Cifuentes Caballero, Ilaria Delle Fontane, Helen C Hope, Nicola Vannini","doi":"10.1016/j.trecan.2026.05.003","DOIUrl":"10.1016/j.trecan.2026.05.003","url":null,"abstract":"<p><p>Aging is the first risk factor associated with cancer, predominantly due to cumulative somatic mutations and a profound decline in antitumor immunity. The aging process remodels immune function across hematopoietic, adaptive, and innate compartments through interconnected processes, including hematopoietic stem cell dysfunction, loss of metabolic fitness, altered B and T cell phenotypes, myeloid skewing, and a complex interplay between cellular senescence and inflammaging. These changes collectively establish an immunosuppressive landscape that weakens natural tumor surveillance and constrains responses to cancer immunotherapies. Given the shift toward an aging global population and the disproportionate cancer burden in older individuals, we emphasize the clinical relevance of patient-stratification strategies. We further discuss emerging approaches aimed at rejuvenating immune function to improve immunotherapy outcomes in older patients.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"849-860"},"PeriodicalIF":21.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148151703","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 : 2026-09-01Epub Date: 2026-06-10DOI: 10.1016/j.trecan.2026.04.009
Nicole L Michmerhuizen, Richard W Kriwacki, Charles G Mullighan
{"title":"Condensates in fusion oncoprotein-driven leukemia: new biology and therapeutic opportunities.","authors":"Nicole L Michmerhuizen, Richard W Kriwacki, Charles G Mullighan","doi":"10.1016/j.trecan.2026.04.009","DOIUrl":"10.1016/j.trecan.2026.04.009","url":null,"abstract":"<p><p>Chromosomal rearrangements leading to the formation of fusion oncoproteins (FOs) are drivers of leukemia and other cancers. Many such FOs are now known to localize in nuclear or cytoplasmic condensates formed through the process of phase separation (PS). FO-associated condensates facilitate the spatiotemporal organization of key macromolecules required for oncogenic transformation. NUP98 fusions provided the first example of FO-associated condensates in leukemia, and other leukemic drivers subsequently illustrated the shared and distinct mechanisms by which PS contributes to leukemogenesis. Improved understanding of FO-associated condensates has, in turn, revealed new opportunities for therapeutic targeting. Pharmacologic approaches, including the dissolution of condensates, inhibition of key condensate components, or modification of condensate material properties, may translate to more effective treatments for patients with FO-driven cancer.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"825-837"},"PeriodicalIF":21.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13344903/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148212548","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 : 2026-09-01Epub Date: 2026-08-04DOI: 10.1016/j.trecan.2026.07.004
Elizabeth A White
{"title":"Lightning doesn't strike twice in HPV-positive adenosquamous carcinoma.","authors":"Elizabeth A White","doi":"10.1016/j.trecan.2026.07.004","DOIUrl":"10.1016/j.trecan.2026.07.004","url":null,"abstract":"<p><p>Cancers containing histologically distinct cell populations could arise from multiple transforming events, from transdifferentiation late in tumor evolution, or from a single progenitor cell. Poulain and colleagues show that glandular and squamous cells in adenosquamous carcinomas caused by human papillomavirus infection are descendants of a common ancestor.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"796-797"},"PeriodicalIF":21.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148702456","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 : 2026-08-21DOI: 10.1016/j.trecan.2026.07.009
Vincent J Guen, Robert A Weinberg
{"title":"Cancer cell plasticity: new insights from developmental programs.","authors":"Vincent J Guen, Robert A Weinberg","doi":"10.1016/j.trecan.2026.07.009","DOIUrl":"https://doi.org/10.1016/j.trecan.2026.07.009","url":null,"abstract":"<p><p>Tumors represent a heterogeneous set of neoplastic diseases, each composed of an intricate network of cancer cells residing in multiple alternative phenotypic states. Transitions between these phenotypic states, often termed 'phenotypic plasticity', enable them to execute specific steps in tumor progression and to develop therapeutic resistance. The phenotypic plasticity of tumor cells is mediated, in part, by cellular processes that orchestrate normal embryonic development and are hijacked by tumors. In this review, we discuss the contributions of these developmental programs to cancer cell phenotypic plasticity. We focus on epithelial-mesenchymal transition and ciliogenesis programs and discuss new insights into the mechanistic roles of these cellular processes in cancer progression and response to treatment.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":21.6,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148798503","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}