Open Access<p>FGFR1 Induces Acquired Resistance Against Gefitinib By Activating AKT/mTOR Pathway In NSCLC</p>
Author(s) -
Dan Zhang,
Lili Han,
Fei Du,
Xiaomeng Liu,
Jin Li,
Huihui Wang,
Minghui Song,
Li Zeng,
Guo-yin Li
Publication year - 2019
Publication title -
oncotargets and therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.054
H-Index - 60
ISSN - 1178-6930
DOI - 10.2147/ott.s220462
Subject(s) - gefitinib , fibroblast growth factor receptor 1 , cancer research , protein kinase b , pi3k/akt/mtor pathway , epidermal growth factor receptor , lung cancer , cell growth , receptor tyrosine kinase , medicine , signal transduction , fibroblast growth factor , biology , cancer , oncology , receptor , microbiology and biotechnology , biochemistry
As an epidermal growth factor, receptor-tyrosine kinase inhibitor (EGFR-TKI), gefitinib demonstrates a good therapeutic effect in patients with EGFR-mutant non-small-cell lung cancer (NSCLC). However, an overwhelming majority of these patients inevitably develop resistance against gefitinib. Unfortunately, the mechanism underlying this phenomenon is still not fully understood. Here we aim to reveal the mechanism of gefitinib resistance in NSCLC induced by FGFR1.