Effects of Dnmt3b-knock-in in MLL-AF9 leukemia model. (A-B) Survival of secondary (P < .001) (A) and tertiary (P < .001) (B) recipients of MLL-AF9–transduced wild-type and Dnmt3b-knock-in c-Kit⁺ LSCs. Dnmt3b expression was induced in all Dnmt3b-knock-in mice (n = 18-24 per group). (C) White blood cell counts of secondary recipients of wild-type and Dnmt3b-knock-in MLL-AF9–transduced cells at end of experiment; n = 3 for wild-type, n = 6 for Dnmt3b-knock-in. (D) Percentage of Gr-1⁺, CD11b⁺, and c-Kit⁺ cells in bone marrow of secondary recipients of wild-type (n = 11) and Dnmt3b-knock-in (n = 4) MLL-AF9 LSCs as determined by fluorescence-activated cell sorter analysis. (E) Expression of HSC markers CD34, CD150, Flt3, and Sca-1 on GFP⁺/c-Kit⁺MLL-AF9 LSCs from bone marrow of recipients of wild-type and Dnmt3b-knock-in leukemias (n = 3 for each genotype). (F-G) Dnmt3b expression suppresses colony growth of c-Kit⁺MLL-AF9 LSCs (top 20% of c-Kit–expressing cells were sorted for wild-type and knock-in mice). C-Kit⁺ cells (F) and total spleen cells (G) from secondary recipients of wild-type and Dnmt3b-knock-in MLL-AF9 LSCs were plated in triplicates in Methocult (n = 3-11 mice). Values in panels C-G are mean ± SD. *P < .05; **P < .01