Mechanisms of Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor Resistance and Strategies to Overcome Resistance in Lung Adenocarcinoma.
10.4046/trd.2016.79.4.248
- Author:
Yoon Soo CHANG
1
;
Chang Min CHOI
;
Jae Cheol LEE
Author Information
1. Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
- Publication Type:Review
- Keywords:
Drug Resistance;
Receptor, Epidermal Growth Factor;
Adenocarcinoma of Lung;
Genes, erbB-1
- MeSH:
Adenocarcinoma*;
Clone Cells;
Disease-Free Survival;
Drug Resistance;
Epidermal Growth Factor*;
Far East;
Genes, erbB-1;
Humans;
Lung*;
Protein-Tyrosine Kinases;
Receptor, Epidermal Growth Factor*;
Treatment Failure
- From:Tuberculosis and Respiratory Diseases
2016;79(4):248-256
- CountryRepublic of Korea
- Language:English
-
Abstract:
Somatic mutations that lead to hyperactivation of epidermal growth factor receptor (EGFR) signaling are detected in approximately 50% of lung adenocarcinoma in people from the Far East population and tyrosine kinase inhibitors are now the standard first line treatment for advanced disease. They have led to a doubling of progression-free survival and an increase in overall survival by more than 2 years. However, emergence of resistant clones has become the primary cause for treatment failure, and has created a new challenge in the daily management of patients with EGFR mutations. Identification of mechanisms leading to inhibitor resistance has led to new therapeutic modalities, some of which have now been adapted for patients with unsuccessful tyrosine kinase inhibitor treatment. In this review, we describe mechanisms of tyrosine kinase inhibitor resistance and the available strategies to overcoming resistance.
