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

Doubling Down on Mutant RAS Can MEK or Break Leukemia.

Author information

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.

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 KrasG12D mutant acute myeloid leukemia and propose its use as a predictive biomarker.

PMID:
28235190
DOI:
10.1016/j.cell.2017.02.013
[Indexed for MEDLINE]
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