Molecular Basis of Drug Resistance: Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors and Anaplastic Lymphoma Kinase Inhibitors

Overview

Journal Tuberc Respir Dis (Seoul)

Specialty Pulmonary Medicine

Date 2013 Dec 19

PMID 24348666

Citations 7

Authors

Sei-Hoon Yang

Affiliations

Soon will be listed here.

Abstract

Over the past decade, several kinase inhibitors have been approved based on their clinical benefit in cancer patients. Unfortunately, in many cases, patients develop resistance to these agents via secondary mutations and alternative mechanisms. To date, several major mechanisms of acquired resistance, such as secondary mutation of the epidermal growth factor receptor (EGFR) gene, amplification of the MET gene and overexpression of hepatocyte growth factor, have been reported. This review describes the recent findings on the mechanisms of primary and acquired resistance to EGFR tyrosine kinase inhibitors and acquired resistance to anaplastic lymphoma kinase inhibitors, primarily focusing on non-small cell lung carcinoma.

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