Figure 2.
Figure 2. Chd7 deficiency delays leukemia initiation induced by Cbfb-MYH11. (A-C) The indicated groups of mice were treated with ENU to induce additional mutations and with poly(I:C) to induce the expression of Cbfb-MYH11 and/or Chd7 deficiency. Three weeks after poly(I:C) treatment, mice were euthanized and flow cytometry assays were performed. (A) Leukemia development monitored by measuring the c-Kit+/Sca1– population in peripheral blood (PB). (B) Representative FACS plots of bone marrow cells gated on single cells (upper plots), Lin– cells (middle plots), and LK cells (bottom plots). (C) Bar graph showing the percentages (mean ± standard error of the mean [SEM]) of Lin–, LK, LSK, AMP, CMP, GMP, and MEP compartments in the bone marrow of mice of the indicated genotypes. *P < .05; **P < .01; ***P < .001; ****P < .0001, each compared with the control group except for (#), for which the comparisons were between the Chd7f/fMx1-CreCbfb+/56M group and the Mx1-CreCbfb+/56M group.

Chd7 deficiency delays leukemia initiation induced by Cbfb-MYH11. (A-C) The indicated groups of mice were treated with ENU to induce additional mutations and with poly(I:C) to induce the expression of Cbfb-MYH11 and/or Chd7 deficiency. Three weeks after poly(I:C) treatment, mice were euthanized and flow cytometry assays were performed. (A) Leukemia development monitored by measuring the c-Kit+/Sca1 population in peripheral blood (PB). (B) Representative FACS plots of bone marrow cells gated on single cells (upper plots), Lin cells (middle plots), and LK cells (bottom plots). (C) Bar graph showing the percentages (mean ± standard error of the mean [SEM]) of Lin, LK, LSK, AMP, CMP, GMP, and MEP compartments in the bone marrow of mice of the indicated genotypes. *P < .05; **P < .01; ***P < .001; ****P < .0001, each compared with the control group except for (#), for which the comparisons were between the Chd7f/fMx1-CreCbfb+/56M group and the Mx1-CreCbfb+/56M group.

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