De novo MET amplification promotes intrinsic resistance to first-generation EGFR tyrosine kinase inhibitors

被引：1

作者：

Li, Jing-Wen ^{[1
]}

Cao, Shu-Hui ^{[1
]}

Xu, Jian-Lin ^{[1
]}

Zhong, Hua ^{[1
]}

机构：

[1] Shanghai Jiao Tong Univ, Shanghai Chest Hosp, Dept Pulm, Shanghai, Peoples R China

来源：

CANCER BIOLOGY & THERAPY | 2019年 / 20卷 / 09期

关键词：

De novo MET amplification; intrinsic resistance; EGFR-TKI; NSCLC; EGFR mutation; LUNG-CANCER; GEFITINIB; TKI;

D O I：

10.1080/15384047.2019.1617568

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

First-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) could induce dramatic tumor responses in non-small-cell lung cancer patients with EGFR-activating mutations. However, a small proportion of patients have no tumor response on initial EGFR TKI treatment with an activating EGFR mutation and the primary resistance mechanism is not well understood. Here, we report the patient with primary dual MET/EGFR mutation treated with icotinib shows a disease progression, but the chest computed tomography shows the mass has significantly shrunk after 3 weeks of single-agent crizotinib. These suggest that de novo MET amplification could be a potential mechanism of intrinsic resistance to first-generation EGFR TKI.

引用

页码：1183 / 1186

页数：4

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