期刊
SEMINARS IN CANCER BIOLOGY
卷 61, 期 -, 页码 180-198出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.semcancer.2019.09.018
关键词
mSWI/SNF complexes; Epigenetic vulnerabilities; Synthetic lethality; Mechanism-based therapeutic strategies; Molecular biomarkers
类别
资金
- ATIP-Avenir
- Integrated Cancer Research Site (SIRIC) [SOCRATE-2 INCa-DGOS-INSERM_12551]
- Fondation Philanthropia
- Institut Servier
- Fondation des Treilles
- Canceropole Ile-de-France
- INSERM ITMO Cancer grant
Mammalian switch/sucrose non-fermentable (mSWI/SNF) family complexes are pivotal elements of the chromatin remodeling machinery, which contribute to the regulation of several major cellular functions. Large-scale exome-wide sequencing studies have identified mutations in genes encoding mSWI/SNF subunits in 20% of all human cancers, establishing mSWI/SNF deficiency as a recurrent oncogenic alteration. Accumulating evidence now supports that several mSWI/SNF defects represent targetable vulnerabilities in cancer; notably, recent research advances have unveiled unexpected synthetic lethal opportunities that foster the development of novel biomarker-driven and mechanism-based therapeutic approaches for the treatment of mSWI/SNF-deficient tumors. Here, we review the latest breakthroughs and discoveries that inform our understanding of the mSWI/SNF complexes biology in carcinogenesis, and discuss the most promising therapeutic strategies to target mSWI/SNF defects in human solid malignancies.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据