Analysis_of_the_chromatin_state_of_mouse_stem_and_progenitor_cell_compartment______-sc-2905
Analysis_of_the_chromatin_state_of_mouse_stem_and_progenitor_cell_compartment______
This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/
AML is an unmet medical need and therapeutic progress will not be made without a greater understanding of this heterogeneous disease. The largest subgroup of AML patients lack a cytogenetic abnormality (AML with normal Karyotype, AML-NK). For this reason, the biology of this subtype have been historically poorly understood. Recently, next generation sequencing efforts in AML-NK genomes has described a number of recurrent abnormalities. In parallel, mouse models have dramatically improved our understanding of disease and due to the great similarities between mouse and human haematopoiesis, have been particularly informative for leukaemia. We aim to model 4 of the most frequent AML-NK mutations using sophisticated mouse models. We will assess the preleukaemic/leukaemic cellular characteristics of these models, particularly their effects on the homeostasis of the haematopoietic stem and progenitor cell (HSPC) compartment. We will also perform integrated genomic analysis to link the mutations and their altered cellular phenotype to aberrant epigenetic control and pre/leukaemic gene expression programmes.