EGFR exon 18 DelE709_T710insD as an Acquired Resistance Mechanism to Afatinib in an Advanced EGFR exon 18 E709H Lung Adenocarcinoma

J Thorac Oncol. 2018 Jun;13(6):e93-e95. doi: 10.1016/j.jtho.2018.01.006.

Authors

Liang Zeng¹, Yongchang Zhang², Nong Yang¹

Affiliations

¹ Department of Medical Oncology, Lung Cancer and Gastrointestinal Unit, Hunan Cancer Hospital/The Affiliated Cancer Hospital of Xiangya School of Medicine, Changsha, People's Republic of China.
² Department of Medical Oncology, Lung Cancer and Gastrointestinal Unit, Hunan Cancer Hospital/The Affiliated Cancer Hospital of Xiangya School of Medicine, Changsha, People's Republic of China. Electronic address: zhangyongchang@csu.edu.cn.

PMID: 29793651
DOI: 10.1016/j.jtho.2018.01.006

No abstract available

Publication types

Case Reports
Letter
Research Support, Non-U.S. Gov't

MeSH terms

Adenocarcinoma of Lung / drug therapy*
Adenocarcinoma of Lung / enzymology
Adenocarcinoma of Lung / genetics
Adenocarcinoma of Lung / pathology
Afatinib / therapeutic use*
ErbB Receptors / genetics
Exons
Humans
Lung Neoplasms / drug therapy*
Lung Neoplasms / enzymology
Lung Neoplasms / genetics
Lung Neoplasms / pathology
Male
Middle Aged

Substances

Afatinib
EGFR protein, human
ErbB Receptors