Chd7 deficiency delays leukemogenesis in mice induced by Cbfb-MYH11.

ABSTRACT: Inversion of chromosome 16 is a consistent finding in patients with acute myeloid leukemia subtype M4 with eosinophilia, which generates a CBFB-MYH11 fusion gene. Previous studies showed that the interaction between CBFβ-smooth muscle myosin heavy chain (SMMHC; encoded by CBFB-MYH11) and RUNX1 plays a critical role in the pathogenesis of this leukemia. Recently, it was shown that chromodomain helicase DNA-binding protein-7 (CHD7) interacts with RUNX1 and suppresses RUNX1-induced expansion of hematopoietic stem and progenitor cells. These results suggest that CHD7 is also critical for CBFB-MYH11-induced leukemogenesis. To test this hypothesis, we generated Chd7^f/fMx1-CreCbfb^+/56M mice, which expressed the Cbfb-MYH11

SUBMITTER: Zhen T 

PROVIDER: S-EPMC5709785 | biostudies-literature | 2017 Nov

REPOSITORIES: biostudies-literature