The mechanism of acquired resistance to irreversible EGFR tyrosine kinase inhibitor-afatinib in lung adenocarcinoma patients
Author(s) -
ShangGin Wu,
Yinan Liu,
MengFeng Tsai,
YihLeong Chang,
ChongJen Yu,
PanChyr Yang,
James ChihHsin Yang,
YuehFeng Wen,
JinYuan Shih
Publication year - 2016
Publication title -
oncotarget
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.373
H-Index - 127
ISSN - 1949-2553
DOI - 10.18632/oncotarget.7189
Subject(s) - afatinib , t790m , medicine , kras , gefitinib , lung cancer , epidermal growth factor receptor , osimertinib , cancer research , lapatinib , neuroblastoma ras viral oncogene homolog , cancer , resistance mutation , oncology , tyrosine kinase inhibitor , erlotinib , biology , colorectal cancer , trastuzumab , breast cancer , gene , reverse transcriptase , rna , biochemistry
Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) are associated with favorable response in EGFR mutant lung cancer. Acquired resistance to reversible EGFR TKIs remains a significant barrier, and acquired EGFR T790M-mutation is the major mechanism. Second-generation irreversible EGFR TKI, afatinib, had also been approved for treating EGFR mutant lung cancer patients, but the mechanism of acquired resistance to afatinib has not been well studied.
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