ARID1A型
癌症研究
生物
肺癌
突变
癌症
受体酪氨酸激酶
基因
医学
激酶
肿瘤科
遗传学
作者
Fukang Jin,Zhiguang Yang,Jingbo Shao,Jianxin Tao,Christoph Reißfelder,Sonja Loges,Lei Zhu,Sebastian Schölch
标识
DOI:10.1016/j.molmed.2023.04.005
摘要
Mutations in the AT-interacting domain-rich protein 1A (ARID1A) gene, a critical component of the switch/sucrose nonfermentable (SWI/SNF) complex, are frequently found in most human cancers. Approximately 5–10% of lung cancers carry ARID1A mutations. ARID1A loss in lung cancer correlates with clinicopathological features and poor prognosis. Co-mutation of ARID1A and epidermal growth factor receptor (EGFR) results in the limited efficacy of EGFR tyrosine kinase inhibitors (EGFR-TKIs) but increases the clinical benefit of immune checkpoint inhibitors (ICIs). ARID1A gene mutation plays a role in cell cycle regulation, metabolic reprogramming, and epithelial–mesenchymal transition. We present the first comprehensive review of the relationship between ARID1A gene mutations and lung cancer and discuss the potential of ARID1A as a new molecular target.
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