Epidermal growth factor receptor mutation in combination with expression of MIG6 alters gefitinib sensitivity.

ABSTRACT:

Background

Epidermal growth factor receptor (EGFR) signaling plays an important role in the regulation of cell proliferation, survival, metastasis, and invasion in various tumors. Earlier studies showed that the EGFR is frequently overexpressed in non-small-cell lung cancer (NSCLC) and EGFR mutations at specific amino acid residues in the kinase domain induce altered responsiveness to gefitinib, a small molecule EGFR tyrosine kinase inhibitor. However, the mechanism underlying the drug response modulated by EGFR mutation is still largely unknown. To elucidate drug response in EGFR signal transduction pathway in which complex dynamics of multiple molecules involved, a systematic approach is necessary. In this paper, we performed experimental and computational analyses to clarify the

SUBMITTER: Naruo Y 

PROVIDER: S-EPMC3224393 | biostudies-literature | 2011 Feb

REPOSITORIES: biostudies-literature