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).