Mechanisms of resistance to EGFR tyrosine kinase inhibitors
Acta Pharmaceutica Sinica B
; (6): 390-401, 2015.
Article
em En
| WPRIM
| ID: wpr-310012
Biblioteca responsável:
WPRO
ABSTRACT
Since the discovery that non-small cell lung cancer (NSCLC) is driven by epidermal growth factor receptor (EGFR) mutations, the EGFR tyrosine kinase inhibitors (EGFR-TKIs, e.g., gefitinib and elrotinib) have been effectively used for clinical treatment. However, patients eventually develop drug resistance. Resistance to EGFR-TKIs is inevitable due to various mechanisms, such as the secondary mutation (T790M), activation of alternative pathways (c-Met, HGF, AXL), aberrance of the downstream pathways (K-RAS mutations, loss of PTEN), impairment of the EGFR-TKIs-mediated apoptosis pathway (BCL2-like 11/BIM deletion polymorphism), histologic transformation, ATP binding cassette (ABC) transporter effusion, etc. Here we review and summarize the known resistant mechanisms to EGFR-TKIs and provide potential targets for development of new therapeutic strategies.
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WPRIM
Idioma:
En
Revista:
Acta Pharmaceutica Sinica B
Ano de publicação:
2015
Tipo de documento:
Article