Overcoming resistance to tyrosine kinase inhibitors Lessons learned from cancer cells treated with EGFR antagonists

被引：62

作者：

Rexer, Brent N.

Engelman, Jeffrey A.

Arteaga, Carlos L. ^{[1
]}

机构：

[1] Vanderbilt Univ, Sch Med, Breast Canc Res Program, Vanderbilt Ingram Comprehens Canc Ctr,Dept Med, Nashville, TN 37232 USA

来源：

CELL CYCLE | 2009年 / 8卷 / 01期

关键词：

breast cancer; HER2; EGFR; tyrosine kinase inhibitors; TKI resistance; PI3K; GROWTH-FACTOR RECEPTOR; LUNG-CANCER; TRASTUZUMAB RESISTANCE; BREAST-CANCER; ADJUVANT CHEMOTHERAPY; ACTIVATING MUTATIONS; ACQUIRED-RESISTANCE; SOMATIC MUTATIONS; GEFITINIB; GENE;

D O I：

10.4161/cc.8.1.7324

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Tyrosine kinase inhibitors (TKIs) are effective anti-cancer therapies but resistance to these agents eventually develops. Several models of resistance to TKIs have been studied including resistance to EGFR inhibitors. Recent studies in EGFR-dependent A431 cells found upregulation of the IGF1R pathway as a mechanism to overcome blockade of EGFR. This was associated with amplification of IGF1R signaling and recovery of downstream PI3K-AKT activation. This work adds to a growing body of cell lines in culture that have provided insights into mechanisms of resistance that can be interrogated in primary tumors in patients. In this review, these model systems and their applicability to human cancers, as well as strategies to identify and overcome resistance to TKIs, are discussed.

引用

页码：18 / 22

页数：5

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