Abstract:

Gefitinib and erlotinib, which are epidermal growth factor receptor (EGFR) specific tyrosine kinase inhibitors (TKIs), are widely used as molecularly targeted drugs for non-small-cell lung cancer (NSCLC). However, many patients ultimately develop resistance to these drugs. Mechanisms of acquired and primary resistance have been reported in the past few years, such as secondary mutation of the EGFR gene, amplification of the MET gene and mutations of the K-ras gene. Novel pharmaceutical agents are currently being developed to overcome resistance. This review focuses on these mechanisms of resistance to EGFR-TKIs and discusses how can be overcome.

Key words: Resistance, Mutation, Signaling pathway, Therapy