K-RAS mutation and resistance to epidermal growth factor receptor-tyrosine kinase inhibitor treatment in patients with nonsmall cell lung cancer.

Abstract

The aim of this study was to evaluate the relationship between k-RAS gene mutation and the resistance to epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) treatment in patients with nonsmall-cell lung cancer (NSCLC). Forty-five pathologies confirmed NSCLC patients who received EGFR-TKI (Gefitinib) treatment were retrospectively included in this study. The mutation of codon 12 and 13, located in exon1 and exon 2 of k-RAS gene were examined by polymerase chain reaction (PCR) and DAN sequencing in tumor samples of the included 45 NSCLC patients. The correlation between Gefitinib treatment response and k-RAS mutation status was analyzed in tumor samples of the 45 NSCLC patients. Eight tumor samples of the 45 NSCLC patients were found to be mutated in coden 12 or 13, with an mutation rate of 17.8% (8/45); the objective response rate (ORR) was 29.7%(11/37) with 1 cases of complete response (CR) and 10 cases of partial response in k-RAS mutation negative patients. Furthermore, the ORR was 0.0% in k-RAS mutation positive patients with none CR. The ORR between k-RAS mutation and nonmutation patients were significant different (P < 0.05). k-RAS gene mutation status was associated with the response of Gefitinib treatment in patients with NSCLC.