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J Hematol Oncol. 2016 Jul 22;9(1):59. doi: 10.1186/s13045-016-0290-1.

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

Author information

1
The Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital, Beijing, China.
2
SUNY Stony Brook University, Stony Brook, NY, 11794, USA.
3
Weinberg College of Arts and Sciences, Northwestern University, Evanston, IL, 60208, USA.
4
Henan Cancer Hospital and the affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, China.
5
Henan Cancer Hospital and the affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, China. delong_liu@nymc.edu.

Abstract

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.

PMID:
27448564
PMCID:
PMC4957905
DOI:
10.1186/s13045-016-0290-1
[Indexed for MEDLINE]
Free PMC Article

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