Mechanisms of Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor Resistance and Strategies to Overcome Resistance in Lung Adenocarcinoma / 결핵및호흡기질환
Tuberculosis and Respiratory Diseases
; : 248-256, 2016.
Article
in En
| WPRIM
| ID: wpr-125744
Responsible library:
WPRO
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.
Key words
Full text:
1
Index:
WPRIM
Main subject:
Protein-Tyrosine Kinases
/
Drug Resistance
/
Adenocarcinoma
/
Clone Cells
/
Treatment Failure
/
Genes, erbB-1
/
Disease-Free Survival
/
Epidermal Growth Factor
/
Asia, Eastern
/
ErbB Receptors
Type of study:
Prognostic_studies
Limits:
Humans
Country/Region as subject:
Asia
Language:
En
Journal:
Tuberculosis and Respiratory Diseases
Year:
2016
Type:
Article