Purpose: Identify new targets in EVI1-Positive Acute Myeloid Leukemia;	Methods: Treatment with cyclocreatine  of EVI1-driven AML cell lines TF-1,  UT-7 and UCSD-AML1. Cyclocreatine was purchased from Sigma-Aldrich (Sigma). TF-1, UT-7 and UCSD-AML1 cells were treated in quadruplicate with either vehicle or 3 mM cyclocreatine for 24 hours. Total RNA was extracted and profiled by RNA sequencing (HiSeq, Illumina) at BioMicroCenter from Massachusetts Institute of Technology (Cambridge, MA, USA).;	Results: Alteration of arginine-creatine metabolism by the small-molecule cyclocreatine selectively decreased the viability, promoted cell cycle arrest and apoptosis of EVI1-positive AML cells.;	Conclusions: Targeting CKMT1 is a promising therapeutic strategy for the EVI1-driven AML subtype that is highly resistant to current treatment regimens. SOURCE: Gabriela Alexe (galexe@broadinstitute.org) -  Broad Institute

Pluto Bioinformatics

GSE86151: Targeting the Creatine Kinase Pathway in EVI1-Positive Acute Myeloid Leukemia