title: Doubling Down on Mutant RAS Can MEK or Break Leukemia.
abstract: Targeting of the RAS pathway has long been a critical therapeutic challenge in oncology. Burgess et al. examine how the relative expression of mutant and wild-type KRAS modulates clonal fitness and sensitivity to MEK inhibitors in a model of KrasG12Dmutant acute myeloid leukemia and propose its use as a predictive biomarker.
authors.affiliation: Brigham and Women's Hospital, Division of Hematology, Boston, MA 02115, USA; Dana Farber Cancer Institute, Department of Medical Oncology, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
authors.forename: Zuzana
authors.initials: Z
authors.lastname: Tothova
authors.affiliation: Brigham and Women's Hospital, Division of Hematology, Boston, MA 02115, USA; Dana Farber Cancer Institute, Department of Medical Oncology, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Electronic address: bebert@partners.org.
authors.forename: Benjamin L
authors.initials: BL
authors.lastname: Ebert
mesh_terms: D011905:Genes, ras / Q000187:drug effects; D006801:Humans; D015470:Leukemia, Myeloid, Acute; D009154:Mutation / Q000187:drug effects*; D047428:Protein Kinase Inhibitors / Q000494:pharmacology*; D018631:ras Proteins / Q000235:genetics
chemical_list: D047428:Protein Kinase Inhibitors; D018631:ras Proteins