作者: Niki Karachaliou , Jordi Codony-Servat , Cristina Teixidó , Sara Pilotto , Ana Drozdowskyj
DOI: 10.1038/SREP17499
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摘要: BIM is a proapoptotic protein that initiates apoptosis triggered by EGFR tyrosine kinase inhibitors (TKI). mTOR negatively regulates and may influence response to TKI. We examined mRNA expression of MTOR in 57 patients with EGFR-mutant NSCLC from the EURTAC trial. Risk mortality disease progression was lower high compared low/intermediate levels. Analysis further divided into two groups, those having both experiencing shorter overall progression-free survival erlotinib. Validation our results performed an independent cohort 19 treated TKIs. In lung adenocarcinoma cell lines expression, concomitant increased IC50 gefitinib for proliferation. next sought analyse signalling pattern strong activation its substrate P-S6. showed phosphodiesterase 4D (PDE4D) strongly correlate resistant cancer lines. These data suggest combination TKI or PDE4 could be adequate therapy pretreatment levels mTOR.