Doubling Down on Mutant RAS Can MEK or Break Leukemia.

Tothova, Zuzana; Ebert, Benjamin L

Tothova, Zuzana; Ebert, Benjamin L.

Afiliação

Tothova Z; 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.
Ebert BL; 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.

Cell ; 168(5): 749-750, 2017 02 23.

Article em En | MEDLINE | ID: mdl-28235190

RESUMO

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.

Assuntos

Mutação/efeitos dos fármacos; Inibidores de Proteínas Quinases/farmacologia; Genes ras/efeitos dos fármacos; Humanos; Leucemia Mieloide Aguda; Proteínas ras/genética

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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Inibidores de Proteínas Quinases / Mutação Tipo de estudo: Prognostic_studies Limite: Humans Idioma: En Ano de publicação: 2017 Tipo de documento: Article

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