The creatine kinase pathway is a metabolic vulnerability in EVI1-positive acute myeloid leukemia - Fenouille, Nina; Bassil, Christopher F; Ben-Sahra, Issam; Benajiba, Lina; Alexe, Gabriela; Ramos, Azucena; Pikman, Yana; Conway, Amy S; Burgess, Michael R; Li, Qing; Luciano, Frédéric; Auberger, Patrick; et al. (Nature medicine, 2017)
Keywords: 13/31; 59/5; 692/699/67/1990/283/1897; 692/699/67/2327; 96; 96/1; 96/34; 96/35; Acute myelocytic leukemia; Adult; Aged; Aged, 80 and over; Analysis; ATP; Biomedicine; Blotting, Western; Cancer; Cancer Research; Care and treatment; Cell cycle; Cell metabolism; Computer Simulation; Core Binding Factor Alpha 2 Subunit - genetics; Core Binding Factor Alpha 2 Subunit - metabolism; Creatine Kinase - genetics; Creatine Kinase - metabolism; Dehydrogenases; Development and progression; DNA-Binding Proteins - genetics; Female; Flow Cytometry; Gene expression; Gene Expression Profiling; Gene Expression Regulation, Neoplastic - genetics; Genetic aspects; Genome-Wide Association Study; Health aspects; Humans; Infectious Diseases; Kinases; Leukemia; Leukemia, Myeloid, Acute - genetics; Leukemia, Myeloid, Acute - metabolism; Male; MDS1 and EVI1 Complex Locus Protein; Medicine; Metabolic Diseases; Metabolic Networks and Pathways; Metabolism; Metabolites; Metabolomics; Middle Aged; Mitochondria; Molecular Medicine; Mutation; Neurosciences; Oncogenes; Oncology; Physiological aspects; Proteins; Proto-Oncogenes - genetics; RNA, Small Interfering; Transcription factors; Transcription Factors - genetics; New York; San Francisco California; California; United States--US; Massachusetts