Mechanisms of Resistance to the Third-generation Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitors in Non-small Cell Lung Cancer.
10.3779/j.issn.1009-3419.2018.02.02
- Author:
Lianfang NI
1
;
Ligong NIE
2
Author Information
1. Department of Geriatric Medicine, Peking University First Hospital, 100034 Beijing, China.
2. Department of Respiratory and Critical Care Medicine, Peking University First Hospital, 100034 Beijing, China.
- Publication Type:Journal Article
- Keywords:
Epidermal growth factor receptor;
Lung neoplasms;
Resistance;
Third-generation tyrosine kinase inhibitors
- MeSH:
Carcinoma, Non-Small-Cell Lung;
drug therapy;
genetics;
pathology;
Drug Resistance, Neoplasm;
drug effects;
ErbB Receptors;
antagonists & inhibitors;
genetics;
metabolism;
Humans;
Lung Neoplasms;
drug therapy;
genetics;
pathology;
Protein Kinase Inhibitors;
pharmacology;
therapeutic use;
Signal Transduction;
drug effects
- From:
Chinese Journal of Lung Cancer
2018;21(2):110-115
- CountryChina
- Language:Chinese
-
Abstract:
Targeted therapy of epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKIs) has been the standard modality as first-line treatment of advanced EGFR-mutated non-small cell lung cancer (NSCLC). The third-generation EGFR-TKIs has been approved to overcome the EGFR T790M mutation in patients resistant to the first-or second-generation TKIs, which brings more survival benefits for patients with advanced NSCLC. Unfortunately, acquired resistance inevitably develops after application of approximately 10 months. Heterogeneities of the tumor determines the diversity of resistance. Mechanisms of resistance to the third-generation TKIs includs EGFR-dependent pathway (such as new EGFR mutations, T790M reduction/disappearance and EGFR amplification, etc.) and EGFR-independent pathway (such as bypass pathway activation and histological transformation, etc.). In this paper, we reviewed principle mechanisms of acquired resistance to third-generation EGFR-TKIs.
