PT  - JOURNAL ARTICLE
AU  - Alexis B. Cortot
AU  - Pasi A. Jänne
TI  - Molecular mechanisms of resistance in epidermal growth factor receptor-mutant lung adenocarcinomas
AID  - 10.1183/09059180.00004614
DP  - 2014 Sep 01
TA  - European Respiratory Review
PG  - 356--366
VI  - 23
IP  - 133
4099  - http://err.ersjournals.com/content/23/133/356.short
4100  - http://err.ersjournals.com/content/23/133/356.full
SO  - EUROPEAN RESPIRATORY REVIEW2014 Sep 01; 23
AB  - The discovery of epidermal growth factor receptor (EGFR) mutations in nonsmall cell lung cancer (NSCLC) has allowed the identification of a subset of patients whose tumours are exquisitely sensitive to EGFR tyrosine kinase inhibitors (TKIs). Despite the efficacy and superiority of EGFR TKIs over chemotherapy as first-line therapy, all patients will ultimately develop progressive disease, with a median of 9–13 months progression-free survival. A better understanding of the molecular mechanisms underlying resistance to EGFR TKIs can help design new drugs and therapeutic strategies to overcome resistance. This has been illustrated by the new generation TKIs that are effective on the T790M mutation, which is the most frequent mechanism of acquired resistance to EGFR TKIs. In this article, we will address the main molecular mechanisms of primary and acquired resistance to EGFR TKIs in EGFR-mutant NSCLC.