Novel mechanism of resistance to targeted therapies in lung cancer

被引：3

作者：

Wang, Walter ^{[1
]}

Carbone, David P. ^{[1
]}

Arasada, Rajeswara Rao ^{[1
]}

机构：

[1] Ohio State Univ, Med Ctr, Dept Internal Med, Div Med Oncol, Columbus, OH 43210 USA

来源：

MOLECULAR & CELLULAR ONCOLOGY | 2019年 / 6卷 / 01期

关键词：

EGFR; Notch3; EGFR TKI; drug persister cells; cancer stem cells; PATHWAY; NOTCH;

D O I：

10.1080/23723556.2018.1551015

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

We have identified a non-canonical role of0 Notch3 in response to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) therapy, whereby Notch3 associates with beta-catenin, resulting in increased catenin beta-1 (CTNNB1, best known as beta-catenin) stability and increased survival of drug persister cells (DPCs). Furthermore, combined treatment of an EGFR TKI with a beta-catenin inhibitor demonstrated improved therapeutic outcomes in xenograft models.

引用

页数：2

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