KRAS(G12D), pulmonary LCH, and atorvastatin

摘要

In this issue of Blood, Kamata et al(1) elegantly demonstrate in mice that (1) KRAS(G12D) (but not BRAF(V600E)) mutation transfection in pulmonary myeloid cells induces an isolated pulmonary (IP)-Langerhans cell histiocytosis (LCH)-like neoplasm, via phosphatidylinositol 3-kinase (PI3K) activation, and that (2) atorvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A inhibitor that inhibits RAS interaction of PI3K, reduces tumor burden in vivo.