Insulin-like growth factor-1 receptor (IGF-1R) as a biomarker for resistance to the tyrosine kinase inhibitor gefitinib in non-small cell lung cancer.

Date publication

juillet 2013

Journal

Cellular oncology (Dordrecht)

Auteurs

Membres identifiés du Cancéropôle Est :
Pr MASCAUX Céline

Tous les auteurs :
Peled N, Wynes MW, Ikeda N, Ohira T, Yoshida K, Qian J, Ilouze M, Brenner R, Kato Y, Mascaux C, Hirsch FR

Lien Pubmed

https://www.ncbi.nlm.nih.gov/pubmed/23619944

Résumé

The insulin-like growth factor-1 receptor (IGF-1R) pathway is known to play a role in the acquisition of resistance to epidermal growth factor receptor (EGFR)-specific tyrosine kinase inhibitors (TKIs) in non-small cell lung cancer (NSCLC). However, its exact role in TKI resistance has so far remained unclear. Here, we interrogated the hypothesis that the IGF-1R may serve as a biomarker for, and may play a role in, intrinsic resistance to the EGFR-specific TKI gefitinib in NSCLC.

Mots clés

Biomarkers, Tumor, genetics, Carcinoma, Non-Small-Cell Lung, drug therapy, Cell Line, Tumor, Cell Proliferation, drug effects, Cell Survival, drug effects, Drug Resistance, Neoplasm, drug effects, ErbB Receptors, antagonists & inhibitors, Female, Gefitinib, HEK293 Cells, Humans, Immunoblotting, Immunohistochemistry, Inhibitory Concentration 50, Kaplan-Meier Estimate, Lung Neoplasms, drug therapy, Male, Middle Aged, Mutation, Phosphorylation, drug effects, Protein Kinase Inhibitors, pharmacology, Quinazolines, pharmacology, RNA Interference, Receptor, IGF Type 1, genetics, Signal Transduction, drug effects, Tissue Array Analysis

Référence

Cell Oncol (Dordr). 2013 Jul;36(4):277-88