EGFR G796D mutation mediates resistance to osimertinib

摘要: // Di Zheng 1, * , Min Hu 2, Yu Bai 2 Xuehua Zhu Xuesong Lu 3 Chunyan Wu 4 Jiying Wang 1 Li Liu Jian Ni Zhenfan Yang and Jianfang Xu Department of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University School, Shanghai, China IMED Asia, AstraZeneca, Research Development Information, Pathology, These authors contributed equally to this work Correspondence to: Xu, email: xujianfang63@aliyun.com Yang, Pamela.Yang@astrazeneca.com Keywords: EGFR, NSCLC, osimertinib, drug resistance, G796D Received: March 08, 2017      Accepted: May 04, Published: 16, 2017 ABSTRACT Osimertinib is an effective third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) approved in multiple countries regions for patients with EGFR T790M mutation-positive non-small cell lung cancer (NSCLC). Despite impressive initial tumor responses, development resistance ultimately limits the benefit compound. Mechanisms osimertinib are just beginning emerge, such as C797S L718Q mutations, BRAF V600E PIK3CA E545K well ERBB2 MET amplification. However, a comprehensive view still missing. In study, we presented first case Chinese NSCLC patient who developed discovered de novo mutation potential mechanism. Our findings provided insights into mechanisms highlighted heterogeneity clonal evolution during resistance.