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本文引用的文献

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卵巢透明细胞癌中的表观遗传合成致死性:EZH2和ARID1A突变

Epigenetic synthetic lethality in ovarian clear cell carcinoma: EZH2 and ARID1A mutations.

作者信息

Bitler Benjamin G, Aird Katherine M, Zhang Rugang

机构信息

Gene Expression and Regulation, The Wistar Institute ; Philadelphia, PA USA.

出版信息

Mol Cell Oncol. 2015 Apr 14;3(1):e1032476. doi: 10.1080/23723556.2015.1032476. eCollection 2016 Jan.

DOI:10.1080/23723556.2015.1032476
PMID:27308548
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4845188/
Abstract

The components of the Switch/Sucrose non-fermentable (SWI/SNF) complex are mutated in approximately 20% of human cancers. The A/T-rich interacting domain 1A (ARID1A) subunit has one of the highest mutation rates. Most notably, ARID1A is mutated in over 50% of ovarian clear cell carcinomas (OCCCs). We reported that inhibition of enhancer of zeste homology 2 (EZH2) is synthetically lethal in ARID1A-mutated OCCC.

摘要

在大约20%的人类癌症中,开关/蔗糖非发酵(SWI/SNF)复合体的组件发生了突变。富含A/T的相互作用结构域1A(ARID1A)亚基的突变率最高。最值得注意的是,超过50%的卵巢透明细胞癌(OCCC)中ARID1A发生了突变。我们报道,在ARID1A突变的OCCC中,抑制zeste同源物2(EZH2)增强子具有合成致死性。