The loss of one or two p53 alleles accelerates the development of AML. (A) Representative FACS profiles show Mac-1 and Gr-1, c-Kit and Sca-1, c-Kit and Mac-1, c-Kit and Gr-1staining of BM cells isolated from NHD13⁺, NHD13⁺p53^+/−, and NHD13⁺p53^−/− mice with AML, compared with WT control mice. (B) The frequencies of Mac-1⁺ or Gr-1⁺, c-Kit⁺Sca-1⁻, Mac-1⁺c-Kit⁺, and Gr-1⁺c-Kit⁺ cells in NHD13⁺, NHD13⁺p53^+/−, and NHD13⁺p53^−/− mouse BM with AML, compared with WT control mice (mean ± SD, *P < .05, **P < .01). (C) Representative H&E-stained BM cytospin samples from NHD13⁺, NHD13⁺p53^+/−, and NHD13⁺p53^−/− mice with AML compared with WT control. (D) Representative staining profiles for LSK cells, showing also CD34, Flt3, and CD150 expression within the BM of NHD13⁺, NHD13⁺p53^+/−, and NHD13⁺p53^−/− mice with AML, compared with WT controls. (E) The frequencies of LSK cells, CD150⁺ LT-HSCs, ST-HSCs, and LMPPs in NHD13⁺, NHD13⁺p53^+/−, and NHD13⁺p53^−/− mice with AML, compared with WT control mice (mean ± SD, *P < .05, **P < .01). The mice used for this figure: NHD13⁺ mice with AML (n = 10, age between 9 months to 12 months), NHD13⁺p53^+/− mice with AML (n = 10, age between 5 months to 10 months), NHD13⁺p53^−/− mice with AML (n = 8, age between 4 and 6 months), and WT control (n = 6, age between 4 and 7 months).