Acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors in EGFR-mutant non-small cell lung cancer: A new era begins

J. Remon*, T. Morán, M. Majem, N. Reguart, E. Dalmau, D. Márquez-Medina, P. Lianes

*Autor correspondiente de este trabajo

Producción científica: Contribución a una revistaArtículo de revisiónInvestigaciónrevisión exhaustiva

122 Citas (Scopus)

Resumen

The discovery of mutated oncogenes has opened up a new era for the development of more effective treatments for non-small cell lung cancer patients (NSCLC) harbouring EGFR mutations. However, patients with EGFR-activating mutation ultimately develop acquired resistance (AR). Several studies have identified some of the mechanisms involved in the development of AR to EGFR tyrosine kinase inhibitors (TKI) that can be potential therapeutic strategies, although in up to 30% of cases, the underlying mechanism of AR are still unexplained.In this review we aim to summarize the main mechanisms of AR to EGFR TKI and some clinical strategies that can be used in the daily clinical practice to overcome this resistance and try to prolong the outcomes in this subgroup of patients.
Idioma originalInglés
Páginas (desde-hasta)93-101
Número de páginas9
PublicaciónCancer Treatment Reviews
Volumen40
N.º1
DOI
EstadoPublicada - feb 2014

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