Tuberc Respir Dis.  2013 Nov;75(5):188-198.

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

Affiliations
  • 1Department of Internal Medicine, Wonkwang University College of Medicine, Iksan, Korea. yshpul@wku.ac.kr

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.

Keyword

Drug Resistance; Protein Kinase Inhibitors; Receptor, Epidermal Growth Factor; Receptor Protein-Tyrosine Kinases

MeSH Terms

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*
Epidermal Growth Factor
Hepatocyte Growth Factor
Phosphotransferases
Protein Kinase Inhibitors
Protein-Tyrosine Kinases
Receptor Protein-Tyrosine Kinases
Receptor, Epidermal Growth Factor
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