{"title":"An unexpected role for cyclin E-CDK2 in regulating responses to cancer immunotherapy","authors":"René Bernards","doi":"10.1016/j.molcel.2026.09.005","DOIUrl":null,"url":null,"abstract":"In this issue of Molecular Cell, Chu et al.1 describe that cancers with increased cyclin E-CDK2 activity suppress responses to immunotherapy through phosphorylation of BRD4, resulting in downregulation of interferon-stimulated genes. Their findings suggest approaches to enhance immunotherapy responses.","PeriodicalId":18950,"journal":{"name":"Molecular Cell","volume":"39 1","pages":"3860-3861"},"PeriodicalIF":16.0000,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular Cell","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1016/j.molcel.2026.09.005","RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
In this issue of Molecular Cell, Chu et al.1 describe that cancers with increased cyclin E-CDK2 activity suppress responses to immunotherapy through phosphorylation of BRD4, resulting in downregulation of interferon-stimulated genes. Their findings suggest approaches to enhance immunotherapy responses.
期刊介绍:
Molecular Cell is a companion to Cell, the leading journal of biology and the highest-impact journal in the world. Launched in December 1997 and published monthly. Molecular Cell is dedicated to publishing cutting-edge research in molecular biology, focusing on fundamental cellular processes. The journal encompasses a wide range of topics, including DNA replication, recombination, and repair; Chromatin biology and genome organization; Transcription; RNA processing and decay; Non-coding RNA function; Translation; Protein folding, modification, and quality control; Signal transduction pathways; Cell cycle and checkpoints; Cell death; Autophagy; Metabolism.