Abstract

EGFR mutations remain today the most frequently observed dependence mechanism in extensive non-small cell lung cancer (NSCLC), accounting for 12% of adenocarcinoma and 44% of NSCLC in non-smokers, in France. The “common” mutations of EGFR − deletions of exon 19 and L858R mutation, are observed in 89% of cases. However, the use of new molecular biology techniques confronts us frequently to the identification of “rare” EGFR mutations, but also to the observation of a molecular heterogeneity at diagnosis and during follow-up. This heterogeneity partly explains the variations in efficacy of EGFR tyrosine kinase inhibitors (EGFR-TKI) observed and on the other hand, leads to the emergence of resistant clones that direct the treatment during tumor progression. While 1st and 2nd line therapeutic strategies have been disrupted by the arrival of osimertinib, new evolutions are announced with the development of numerous trials associating different therapeutic classes such as chemotherapy, antiangiogenics but also targeted therapies i.e. small molecules, specific antibodies and conjugated antibodies.© 2021 SPLF. Published by Elsevier Masson SAS. All rights reserved.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call