Doubling Down on Mutant RAS Can MEK or Break Leukemia

Publication date: 23 February 2017
Source:Cell, Volume 168, Issue 5
Author(s): Zuzana Tothova, Benjamin L. Ebert
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.

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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.


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