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

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, t...

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Main Authors: Shuhang Wang, Stella T. Tsui, Christina Liu, Yongping Song, Delong Liu
Format: Article
Language:English
Published: BMC 2016-07-01
Series:Journal of Hematology & Oncology
Online Access:http://link.springer.com/article/10.1186/s13045-016-0290-1
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spelling doaj-b3937d45fda240d68c72d0cfbb74565d2020-11-24T22:51:11ZengBMCJournal of Hematology & Oncology1756-87222016-07-01911510.1186/s13045-016-0290-1EGFR C797S mutation mediates resistance to third-generation inhibitors in T790M-positive non-small cell lung cancerShuhang Wang0Stella T. Tsui1Christina Liu2Yongping Song3Delong Liu4The Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer HospitalSUNY Stony Brook UniversityWeinberg College of Arts and Sciences, Northwestern UniversityHenan Cancer Hospital and the affiliated Cancer Hospital of Zhengzhou UniversityHenan Cancer Hospital and the affiliated Cancer Hospital of Zhengzhou UniversityAbstract 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.http://link.springer.com/article/10.1186/s13045-016-0290-1
collection DOAJ
language English
format Article
sources DOAJ
author Shuhang Wang
Stella T. Tsui
Christina Liu
Yongping Song
Delong Liu
spellingShingle Shuhang Wang
Stella T. Tsui
Christina Liu
Yongping Song
Delong Liu
EGFR C797S mutation mediates resistance to third-generation inhibitors in T790M-positive non-small cell lung cancer
Journal of Hematology & Oncology
author_facet Shuhang Wang
Stella T. Tsui
Christina Liu
Yongping Song
Delong Liu
author_sort Shuhang Wang
title EGFR C797S mutation mediates resistance to third-generation inhibitors in T790M-positive non-small cell lung cancer
title_short EGFR C797S mutation mediates resistance to third-generation inhibitors in T790M-positive non-small cell lung cancer
title_full EGFR C797S mutation mediates resistance to third-generation inhibitors in T790M-positive non-small cell lung cancer
title_fullStr EGFR C797S mutation mediates resistance to third-generation inhibitors in T790M-positive non-small cell lung cancer
title_full_unstemmed EGFR C797S mutation mediates resistance to third-generation inhibitors in T790M-positive non-small cell lung cancer
title_sort egfr c797s mutation mediates resistance to third-generation inhibitors in t790m-positive non-small cell lung cancer
publisher BMC
series Journal of Hematology & Oncology
issn 1756-8722
publishDate 2016-07-01
description 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.
url http://link.springer.com/article/10.1186/s13045-016-0290-1
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AT stellattsui egfrc797smutationmediatesresistancetothirdgenerationinhibitorsint790mpositivenonsmallcelllungcancer
AT christinaliu egfrc797smutationmediatesresistancetothirdgenerationinhibitorsint790mpositivenonsmallcelllungcancer
AT yongpingsong egfrc797smutationmediatesresistancetothirdgenerationinhibitorsint790mpositivenonsmallcelllungcancer
AT delongliu egfrc797smutationmediatesresistancetothirdgenerationinhibitorsint790mpositivenonsmallcelllungcancer
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