Molecular Basis of Drug Resistance: Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors and Anaplastic Lymphoma Kinase Inhibitors.
10.4046/trd.2013.75.5.188
- Author:
Sei Hoon YANG
1
Author Information
1. Department of Internal Medicine, Wonkwang University College of Medicine, Iksan, Korea. yshpul@wku.ac.kr
- Publication Type:Review
- Keywords:
Drug Resistance;
Protein Kinase Inhibitors;
Receptor, Epidermal Growth Factor;
Receptor Protein-Tyrosine Kinases
- MeSH:
Drug Resistance*;
Epidermal Growth Factor*;
Hepatocyte Growth Factor;
Humans;
Lung;
Lymphoma*;
Phosphotransferases*;
Protein Kinase Inhibitors;
Protein-Tyrosine Kinases;
Receptor Protein-Tyrosine Kinases;
Receptor, Epidermal Growth Factor*
- From:Tuberculosis and Respiratory Diseases
2013;75(5):188-198
- CountryRepublic of Korea
- Language:English
-
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.
