Chronic myeloid leukemia (CML) results from hematopoietic stem cell transformation by the BCR-ABL tyrosine kinase. We have shown that the SIRT1 deacetylase is overexpressed in CML LSC, and may contribute to their maintenance. Here, using genetic deletion of SIRT1 in transgenic CML mice, we definitively demonstrate that SIRT1 is required for leukemia development, and reveal its critical role in mediating increased mitochondrial respiration in CML LSC. SOURCE: Ravi Bhatia (rbhatia@uabmc.edu) -  University of Alabama at Birmingham

Pluto Bioinformatics

GSE129158: SIRT1 regulates enhanced mitochondrial respiration and leukemogenicity in CML stem cells