EGFR C797S mutation mediates resistance to third-generation inhibitors in T790M-positive non-small cell lung cancer

被引：120
|
作者：
Wang, Shuhang [1 ]
Tsui, Stella T. [2 ]
Liu, Christina [3 ]
Song, Yongping [4 ,5 ]
Liu, Delong [4 ,5 ]
机构：
[1] Peking Univ, Canc Hosp, Key Lab Carcinogenesis & Translat Res, Minist Educ, Beijing, Peoples R China
[2] SUNY Stony Brook, Stony Brook, NY 11794 USA
[3] Northwestern Univ, Weinberg Coll Arts & Sci, Evanston, IL 60208 USA
[4] Zhengzhou Univ, Henan Canc Hosp, Zhengzhou, Peoples R China
[5] Zhengzhou Univ, Affiliated Canc Hosp, Zhengzhou, Peoples R China
来源：
JOURNAL OF HEMATOLOGY & ONCOLOGY | 2016年 / 9卷
基金：
中国国家自然科学基金;
关键词：
TYROSINE KINASE INHIBITORS; ALK INHIBITORS; NIVOLUMAB; AZD9291; CHEMOTHERAPY; MONOTHERAPY; ROCILETINIB; ACTIVATION; MECHANISMS; STRATEGIES;
D O I：
10.1186/s13045-016-0290-1
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
T790M mutation is the most common mechanism for resistance to first-and second-generation tyrosine kinase inhibitors (TKI) for epidermal growth factor receptor (EGFR). Several third-generation EGFR mutant selective TKIs are being explored to conquer this resistance. AZD9291 (osimertinib, tagrisso) has been approved for treatment of the metastatic EGFR T790M mutation-positive non-small cell lung cancer. Resistance to AZD9291 has been described. C797S mutation was reported to be a major mechanism for resistance to T790M-targeting EGFR inhibitors. This review summarizes the latest development in identifying the C797S mutation and EAI045, the novel selective inhibitor overcoming the C797S mutant.
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页数：5
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