Doubling Down on Mutant RAS Can MEK or Break Leukemia

Zuzana Tothova; Benjamin L Ebert

doi:10.1016/j.cell.2017.02.013

Doubling Down on Mutant RAS Can MEK or Break Leukemia

Cell. 2017 Feb 23;168(5):749-750. doi: 10.1016/j.cell.2017.02.013.

Authors

Zuzana Tothova¹, Benjamin L Ebert²

Affiliations

¹ 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.
² 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.

PMID: 28235190
DOI: 10.1016/j.cell.2017.02.013

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 Kras^G12D mutant acute myeloid leukemia and propose its use as a predictive biomarker.

MeSH terms

Genes, ras / drug effects
Humans
Leukemia, Myeloid, Acute
Mutation / drug effects*
Protein Kinase Inhibitors / pharmacology*
ras Proteins / genetics

Substances

Protein Kinase Inhibitors
ras Proteins