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

被引:0
作者
Shuhang Wang
Stella T. Tsui
Christina Liu
Yongping Song
Delong Liu
机构
[1] Peking University Cancer Hospital,The Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education)
[2] SUNY Stony Brook University,Weinberg College of Arts and Sciences
[3] Northwestern University,undefined
[4] Henan Cancer Hospital and the affiliated Cancer Hospital of Zhengzhou University,undefined
来源
Journal of Hematology & Oncology | / 9卷
关键词
Epidermal Growth Factor Receptor; Epidermal Growth Factor Receptor Mutant; Anaplastic Lymphoma Kinase; Epidermal Growth Factor Receptor Inhibitor; Epidermal Growth Factor Receptor Gene;
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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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