Prise en charge du cancer pulmonaire non à petites cellules avec mutation de KRAS

Abstract

The KRAS^G12C mutation represents the most common genomic alteration in lung adenocarcinomas in non-Asian populations. This genomic alteration leads to constitutive activation of the KRASG12C protein, stimulating signaling cascades involved in proliferation and malignant transformation. Historically considered an undruggable therapeutic target, this mutation has now become actionable through the development of sotorasib and adagrasib, selective inhibitors of KRASG12C in its inactive state. This literature review examines the biology of KRAS mutations, details the mechanisms of action of novel KRASG12C inhibitors along with their clinical benefit, safety profile, associated resistance mechanisms, and development perspectives.