Exome_sequencing_of_Utx_mouse_haemopoietic_tumours

The H3K27 lysine-specific demethylase UTX is targeted by loss-of-function mutations in multiple cancers. Using mouse models, we demonstrate that UTX suppresses myeloid leukaemogenesis through non-catalytic functions, a property it shares with its catalytically inactive Y-chromosome paralogue, UTY. In keeping with this, we demonstrate concomitant loss/mutation of UTX and UTY in multiple human cancers. Spontaneous development of AML in the Utx knockout mice is a long process, most probably due to the necessity of the generation of collaborative mutation. To define the pattern of Utx-collaborative mutation we propose analysis of AML samples form diseased mice and comparison of their exomes to match exomes before gene deletion.