Prise en charge thérapeutique des cancers bronchiques non à petites cellules de stades avancés mutés pour l’EGFR

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, it makes it possible to orient the treatment (T790M), during tumor progression. Until recently, 1st and 2nd line therapeutic strategies were well established, but were disrupted by the arrival of the osimertinib in 2nd, then in 1st line. In the absence of data concerning the impact on overall survival of osimertinib and on the secondary mechanisms of resistance at progression, it is important to update our knowledge about new molecules, but also strategies of already available treatments.