{"title":"RET异常癌症对靶向治疗的适应性抗药性机制。","authors":"Sandra Ortiz-Cuaran, Camille Leonce","doi":"10.1158/1078-0432.CCR-24-3734","DOIUrl":null,"url":null,"abstract":"<p><p>The success of targeted therapies in oncogene-driven cancer is limited by adaptive or acquired treatment resistance, leading to disease progression. A recent study reports that YAP-dependent human epidermal growth factor receptor 3 (HER3) activation constitutes a therapeutic vulnerability of adaptive resistance to RET-targeted therapies in RET-altered cancers, highlighting a promising strategy to improve RET inhibitor tumor responses. See related article by Katayama et al., p. 1127.</p>","PeriodicalId":10279,"journal":{"name":"Clinical Cancer Research","volume":" ","pages":"958-959"},"PeriodicalIF":10.0000,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Mechanisms of Adaptive Resistance to Targeted Therapy in RET-Aberrant Cancers.\",\"authors\":\"Sandra Ortiz-Cuaran, Camille Leonce\",\"doi\":\"10.1158/1078-0432.CCR-24-3734\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The success of targeted therapies in oncogene-driven cancer is limited by adaptive or acquired treatment resistance, leading to disease progression. A recent study reports that YAP-dependent human epidermal growth factor receptor 3 (HER3) activation constitutes a therapeutic vulnerability of adaptive resistance to RET-targeted therapies in RET-altered cancers, highlighting a promising strategy to improve RET inhibitor tumor responses. See related article by Katayama et al., p. 1127.</p>\",\"PeriodicalId\":10279,\"journal\":{\"name\":\"Clinical Cancer Research\",\"volume\":\" \",\"pages\":\"958-959\"},\"PeriodicalIF\":10.0000,\"publicationDate\":\"2025-03-17\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Clinical Cancer Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1158/1078-0432.CCR-24-3734\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical Cancer Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1158/1078-0432.CCR-24-3734","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0
摘要
适应性或获得性抗药性限制了靶向疗法在癌基因驱动的癌症中的成功,导致疾病进展。最近的一项研究报告称,YAP 依赖性 HER3 激活是 RET 改变的癌症对 RET 靶向疗法产生适应性耐药性的一个治疗漏洞,凸显了改善 RET 抑制剂肿瘤反应的一种有前景的策略。
Mechanisms of Adaptive Resistance to Targeted Therapy in RET-Aberrant Cancers.
The success of targeted therapies in oncogene-driven cancer is limited by adaptive or acquired treatment resistance, leading to disease progression. A recent study reports that YAP-dependent human epidermal growth factor receptor 3 (HER3) activation constitutes a therapeutic vulnerability of adaptive resistance to RET-targeted therapies in RET-altered cancers, highlighting a promising strategy to improve RET inhibitor tumor responses. See related article by Katayama et al., p. 1127.
期刊介绍:
Clinical Cancer Research is a journal focusing on groundbreaking research in cancer, specifically in the areas where the laboratory and the clinic intersect. Our primary interest lies in clinical trials that investigate novel treatments, accompanied by research on pharmacology, molecular alterations, and biomarkers that can predict response or resistance to these treatments. Furthermore, we prioritize laboratory and animal studies that explore new drugs and targeted agents with the potential to advance to clinical trials. We also encourage research on targetable mechanisms of cancer development, progression, and metastasis.