z-logo
open-access-imgOpen Access
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.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here
Accelerating Research

Address

John Eccles House
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom