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.
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