Acquired C797S Mutation upon Treatment with a T790M-Specific Third-Generation EGFR Inhibitor (HM61713) in Non-Small Cell Lung Cancer

被引:84
|
作者
Song, Haa-Na [1 ,2 ]
Jung, Ki Sun [1 ]
Yoo, Kwai Han [1 ]
Cho, Jinhyun [1 ]
Lee, Ji Yun [1 ]
Lim, Sung Hee [1 ]
Kim, Hae Su [1 ]
Sun, Jong-Mu [1 ]
Lee, Se-Hoon [1 ]
Ahn, Jin Seok [1 ]
Park, Keunchil [1 ]
Choi, Yoon-La [3 ]
Park, Woongyang [4 ,5 ]
Ahn, Myung-Ju [1 ]
机构
[1] Sungkyunkwan Univ, Div Hematol & Oncol, Samsung Med Ctr, Dept Med,Sch Med, Seoul, South Korea
[2] Gyeongsang Natl Univ, Dept Internal Med, Sch Med, Jinju, South Korea
[3] Sungkyunkwan Univ, Samsung Med Ctr, Sch Med, Dept Pathol, Seoul, South Korea
[4] Samsung Genome Inst, Seoul, South Korea
[5] Sungkyunkwan Univ, Sch Med, Dept Mol Cell Biol, Seoul, South Korea
关键词
EGFR; T790M mutation; HM61713; C797S mutation;
D O I
10.1016/j.jtho.2015.12.093
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
T790M mutation is most common resistant mechanism to epidermal growth factor receptor gene (EGFR) tyrosin kinase inhibitor (TKI). Several third-generation EGFR-mutant selective TKI, such as AZD9291 (AstraZeneca), Rociletinib (Clovis), or HM61713 (Hanmi) have been developed. Acquired resistant C797S mutation was known to be one of the resistance mechanisms of AZD9291, which has not been reported for HM61713 yet. This is the first case report of C797S mutation as resistance mechanism of HM61713. (C) 2015 International Association for the Study of Lung Cancer. Published by Elsevier Inc. All rights reserved.
引用
收藏
页码:E45 / E47
页数:5
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