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.
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.
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。
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