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LGR5: from stem cell marker to therapeutic target. LGR5：从干细胞标志物到治疗靶点。
IF 21.6 1区 医学
Trends in cancer Pub Date : 2026-06-01 Epub Date: 2026-04-06 DOI: 10.1016/j.trecan.2026.02.006
Peyton C High, Maya G Cappellino, Tiffani A Blackburn, Kendra S Carmon
{"title":"LGR5: from stem cell marker to therapeutic target.","authors":"Peyton C High, Maya G Cappellino, Tiffani A Blackburn, Kendra S Carmon","doi":"10.1016/j.trecan.2026.02.006","DOIUrl":"10.1016/j.trecan.2026.02.006","url":null,"abstract":"<p><p>Leucine-rich repeat-containing G protein-coupled receptor 5 (LGR5) is an established marker of normal and cancer stemlike cells. LGR5 has been implicated in promoting cancer cell plasticity that drives tumorigenesis, metastasis, and therapeutic resistance. LGR5 rapidly and constitutively internalizes and potentiates Wnt (Wingless/Int-1)/β-catenin and adhesion signaling pathways, though its precise mechanisms and interacting partners remain unresolved. An improved understanding of LGR5 signaling may provide invaluable insight into its intricate and important functions in cancer progression. Moreover, several LGR5-targeting therapies, including peptibody- and antibody-drug conjugates and bispecific antibodies, are showing promising efficacy and tolerability in colorectal cancer and other tumor types. This review discusses the cancer-related functions of LGR5 and explores the preclinical and clinical approaches to therapeutically target this enigmatic protein.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"495-509"},"PeriodicalIF":21.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13060024/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147628702","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
Targeting cyclin-dependent kinases in cancer: emerging therapeutics and clinical strategies. 靶向周期蛋白依赖性激酶在癌症：新兴的治疗方法和临床策略。
IF 17.5 1区 医学
Trends in cancer Pub Date : 2026-06-01 Epub Date: 2026-04-22 DOI: 10.1016/j.trecan.2026.03.004
Harold N Tan, Giuseppe Curigliano, Timothy A Yap
{"title":"Targeting cyclin-dependent kinases in cancer: emerging therapeutics and clinical strategies.","authors":"Harold N Tan, Giuseppe Curigliano, Timothy A Yap","doi":"10.1016/j.trecan.2026.03.004","DOIUrl":"10.1016/j.trecan.2026.03.004","url":null,"abstract":"<p><p>Cyclin-dependent kinases (CDKs) regulate cell cycle progression, and their dysregulation is a hallmark of cancer. CDK4/6 inhibitors have shown clinical success against hormone receptor (HR)-positive, Human epidermal growth factor receptor (HER2)-negative breast cancer but encounter adaptive resistance, dose-limiting toxicities, and limited activity in other tumor contexts. Emerging strategies include CDK4-selective, CDK2-selective, and pan-CDK2/4/6 inhibitors designed to overcome resistance and enhance tolerability. In parallel, novel modalities such as proteolysis-targeting degraders, molecular glue degraders, and cyclin-directed agents offer new opportunities to exploit cell cycle vulnerabilities. Several of these candidates have entered early-phase clinical evaluation, marking a new era in CDK-targeted therapy. This review synthesizes recent preclinical and clinical advances, defines key challenges in optimizing efficacy and safety, and outlines future directions for integrating CDK-directed strategies within precision oncology frameworks.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"553-568"},"PeriodicalIF":17.5,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147782321","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
Cancer in 4D: toward Spatiotemporal Hallmark Ecosystems. 四维癌症：时空特征生态系统。
IF 21.6 1区 医学
Trends in cancer Pub Date : 2026-05-01 Epub Date: 2026-03-16 DOI: 10.1016/j.trecan.2026.01.004
Mustafa Sibai, Martin Zacharias, Nicholas McGranahan, Mariam Jamal-Hanjani, Eduard Porta-Pardo
{"title":"Cancer in 4D: toward Spatiotemporal Hallmark Ecosystems.","authors":"Mustafa Sibai, Martin Zacharias, Nicholas McGranahan, Mariam Jamal-Hanjani, Eduard Porta-Pardo","doi":"10.1016/j.trecan.2026.01.004","DOIUrl":"10.1016/j.trecan.2026.01.004","url":null,"abstract":"<p><p>The Hallmarks of Cancer framework provided a unifying description of tumor capabilities, but in its static form, it cannot capture where in a tumor these traits occur, when they arise, or how they reorganize under selection pressure. Here, we propose Spatiotemporal Hallmark Ecosystems as a new lens that redefines the functional unit of selection in cancer evolution. In this view, hallmarks are not fixed consequences of mutations but context-dependent phenotypes that are enabled or constrained by local tissue and microenvironmental conditions. This perspective resolves critical paradoxes, explaining why identical mutations yield divergent outcomes, why premalignant states persist without transformation, and how therapeutic resistance emerges not just from clonal selection but also from 'ecological buffering' by the tumor architecture. By shifting the analysis from the individual cell to the ecosystem, we outline a path toward predictive biomarkers and spatially aware strategies that target the structural stability of the tumor.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"404-419"},"PeriodicalIF":21.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147469130","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 lysosomal requiem for glioblastoma cells. 胶质母细胞瘤细胞的溶酶体安魂曲。
IF 21.6 1区 医学
Trends in cancer Pub Date : 2026-05-01 Epub Date: 2026-03-11 DOI: 10.1016/j.trecan.2026.01.012
Laura Merlet, Margaux Le Guyon, Julie Gavard
{"title":"A lysosomal requiem for glioblastoma cells.","authors":"Laura Merlet, Margaux Le Guyon, Julie Gavard","doi":"10.1016/j.trecan.2026.01.012","DOIUrl":"10.1016/j.trecan.2026.01.012","url":null,"abstract":"<p><p>Once viewed solely as degradative compartments, lysosomes shape cell fate through signaling, metabolism, and communication. In glioblastoma, their rewiring underlies plasticity, invasion, and resistance to therapies. This forum explores lysosomal dynamics in brain tumors and therapeutic strategies targeting lysosomal vulnerabilities, offering fresh perspectives for precision approaches in this lethal cancer.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"386-389"},"PeriodicalIF":21.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147445296","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
IL33 in pancreatic cancer-pro- or antitumor? il - 33在胰腺癌中的作用是促肿瘤还是抗肿瘤？
IF 17.5 1区 医学
Trends in cancer Pub Date : 2026-05-01 Epub Date: 2026-03-10 DOI: 10.1016/j.trecan.2026.01.009
Supriya Sharma, Ajay Dixit
{"title":"IL33 in pancreatic cancer-pro- or antitumor?","authors":"Supriya Sharma, Ajay Dixit","doi":"10.1016/j.trecan.2026.01.009","DOIUrl":"10.1016/j.trecan.2026.01.009","url":null,"abstract":"<p><p>Interleukin 33 (IL33) in the tumor microenvironment of pancreatic cancer has been linked to both pro- and antitumor immune responses, suggesting a context-dependent role. Herein, we discuss the current understanding and challenges of therapeutically targeting IL33 signaling in pancreatic cancer.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"390-392"},"PeriodicalIF":17.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147435806","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
FGFR rearrangements: oncogenic drivers and therapeutic targets. FGFR重排：致癌驱动因素和治疗靶点。
IF 21.6 1区 医学
Trends in cancer Pub Date : 2026-05-01 Epub Date: 2026-03-04 DOI: 10.1016/j.trecan.2026.01.010
Julia Yemelyanenko, Jos Jonkers, Daniel Zingg
{"title":"FGFR rearrangements: oncogenic drivers and therapeutic targets.","authors":"Julia Yemelyanenko, Jos Jonkers, Daniel Zingg","doi":"10.1016/j.trecan.2026.01.010","DOIUrl":"10.1016/j.trecan.2026.01.010","url":null,"abstract":"<p><p>Genomic amplifications and hotspot mutations affecting fibroblast growth factor receptors (FGFRs) have long been recognized as oncogenic drivers across human cancers. However, recent studies have uncovered FGFR in-frame fusions and complex structural variants as an additional class of tumor driver alterations. Notably, the identification of FGFR2 exon 18 truncations and the demonstration of their potent oncogenic competence have refined our understanding of FGFR-driven tumorigenesis and have impacted clinical trial design for FGFR-targeted agents. This review explores the biological and clinical implications of FGFR rearrangements. It covers their mechanisms in driving cancer, their potential as biomarkers to predict treatment response, and the emerging challenges and opportunities for FGFR-targeted therapy. Ultimately, a deeper understanding of FGFR rearrangements is critical for advancing precision oncology and improving patient benefit.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"461-476"},"PeriodicalIF":21.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147356622","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
Epigenetic dysregulation and microenvironment remodeling in pancreatic cancer. 胰腺癌的表观遗传失调和微环境重塑。
IF 21.6 1区 医学
Trends in cancer Pub Date : 2026-05-01 Epub Date: 2026-03-16 DOI: 10.1016/j.trecan.2026.01.011
Ningning Niu, Mo Chen, Jing Xue
{"title":"Epigenetic dysregulation and microenvironment remodeling in pancreatic cancer.","authors":"Ningning Niu, Mo Chen, Jing Xue","doi":"10.1016/j.trecan.2026.01.011","DOIUrl":"10.1016/j.trecan.2026.01.011","url":null,"abstract":"<p><p>Epigenetic dysregulation including frequent mutations in epigenetic regulators alongside nonmutational reprogramming driven by oncogenic and metabolic stresses represents a hallmark of pancreatic ductal adenocarcinoma (PDAC). Recent advances using low-input epigenomics and single-cell technologies have revealed their role in fostering cellular plasticity, stromal reprogramming, immune evasion, and therapy resistance. This review synthesizes current knowledge of epigenetic mechanisms in PDAC pathogenesis, highlighting their stage- and context-dependent roles in tumor progression, tumor microenvironment crosstalk, and metabolic adaptation. We further highlight emerging therapeutic strategies that target epigenetic vulnerabilities. By integrating cutting-edge epigenomic profiling with functional studies, we outline a roadmap for translating epigenetic discoveries into clinical strategies against this lethal malignancy.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"447-460"},"PeriodicalIF":21.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147475436","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
In vivo CAR T cell engineering: design principles and open questions. 体内CAR - T细胞工程：设计原则和悬而未决的问题。
IF 21.6 1区 医学
Trends in cancer Pub Date : 2026-05-01 Epub Date: 2026-03-25 DOI: 10.1016/j.trecan.2026.01.007
Amin Aalipour, Ariana Barreiro, Andrea Garmilla, Michael E Birnbaum
{"title":"In vivo CAR T cell engineering: design principles and open questions.","authors":"Amin Aalipour, Ariana Barreiro, Andrea Garmilla, Michael E Birnbaum","doi":"10.1016/j.trecan.2026.01.007","DOIUrl":"10.1016/j.trecan.2026.01.007","url":null,"abstract":"<p><p>Chimeric antigen receptor (CAR) T cell therapy has transformed the treatment of hematologic malignancies, leading to seven FDA-approved products, but widespread adoption has been limited by costly and complex manufacturing and administration. Several methods have emerged to directly reprogram T cells within patients, with the potential to simultaneously improve potency, reduce costs, and broaden accessibility. While early clinical studies demonstrate safety and therapeutic activity, critical questions remain regarding long-term efficacy, the interplay between means of delivery and host biology, and optimal disease indications for each delivery approach. This review summarizes the preclinical and clinical data for state-of-the-art viral and nonviral approaches for in vivo CAR-T engineering, discusses their opportunities and limitations, and highlights key open questions that will shape the maturation of this emerging field.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"434-446"},"PeriodicalIF":21.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147521458","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 role of the integrated stress response in cancer immune evasion. 综合应激反应在癌症免疫逃避中的意外作用。
IF 21.6 1区 医学
Trends in cancer Pub Date : 2026-05-01 Epub Date: 2026-04-01 DOI: 10.1016/j.trecan.2026.03.001
Lucia Borriello, Lorenzo Galluzzi
{"title":"Unexpected role of the integrated stress response in cancer immune evasion.","authors":"Lucia Borriello, Lorenzo Galluzzi","doi":"10.1016/j.trecan.2026.03.001","DOIUrl":"10.1016/j.trecan.2026.03.001","url":null,"abstract":"<p><p>Viral mimicry, i.e., the ability of uninfected cancer cells to emit molecular signals normally associated with infection, is paramount for anticancer immunity. Recent findings from Bossowski et al. indicate that the integrated stress response (a crucial component of cellular responses against infection) can unexpectedly promote immune evasion via an LCN2-driven, macrophage-dependent mechanism.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"383-385"},"PeriodicalIF":21.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147609991","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
The redox paradox in HGGs: ROS as drivers and destroyers. 温室气体中的氧化还原悖论：活性氧作为驱动者和破坏者。
IF 21.6 1区 医学
Trends in cancer Pub Date : 2026-05-01 Epub Date: 2026-03-10 DOI: 10.1016/j.trecan.2026.01.005
Pooja Kumari, Zacary P Germon, Evangeline R Jackson, Tuan Vo, Matthew D Dun
{"title":"The redox paradox in HGGs: ROS as drivers and destroyers.","authors":"Pooja Kumari, Zacary P Germon, Evangeline R Jackson, Tuan Vo, Matthew D Dun","doi":"10.1016/j.trecan.2026.01.005","DOIUrl":"10.1016/j.trecan.2026.01.005","url":null,"abstract":"<p><p>Reactive oxygen species (ROS) are essential second-messenger molecules, yet when deregulated, they fuel cancer growth and therapeutic resistance. In high-grade gliomas, including glioblastoma, diffuse hemispheric glioma, and diffuse midline glioma (DMG), genetic, epigenetic, and metabolic alterations drive chronic ROS production and redox imbalance. This oxidative stress promotes DNA damage, epigenetic reprogramming, tumor growth, and immune escape. In DMG, global DNA and histone hypomethylation are amplified by oxidative stress, while ROS-dependent Ras/Raf/mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling pathways reinforce tumor survival. Paradoxically, the same ROS create an intrinsic vulnerability as excess ROS can overwhelm defenses and trigger cytotoxicity. Targeting ROS is challenging; however, new strategies, including NADPH oxidase inhibition, metabolic modulation, and ROS-inducing therapies, reveal vulnerabilities. Understanding this redox paradox is critical to exposing therapeutic vulnerabilities and improving outcomes for patients with these deadly cancers.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"420-433"},"PeriodicalIF":21.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147435801","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
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