Fig. 2

Loss of CAMKIV decreases MLL-AF9 AML development. a Mice transplanted with MLL-AF9-infected WT hematopoietic progenitors had significantly reduced survival compared to mice transplanted with MLL-AF9-infected Camk4-null hematopoietic progenitors in both primary (p = 0.0019) and secondary (p = 0.0021) transplantation (n = 16). b Comparison of the sizes of spleens and livers and numbers of peripheral blood cells of the mice transplanted with WT MLL-AF9 cells and those with camk4-null MLL-AF9 cells at 41 days after first transplantation and 23 days after second transplantation. c Histological analysis of AML infiltration in the livers of mice transplanted with control or CAMKIV-transduced PirBTM AML cells (hematoxylin/eosin staining). Significant differences in AML infiltration to the liver in samples are indicated by arrows. d, e Representative Wright-Giemsa-stained cytospin preparation of the BM, spleen, and peripheral blood cells from leukemic mice. f Representative flow cytometry plots show that camk4-null AML mice have more differentiated cells in BM and peripheral blood (PB) compared to mice transplanted with WT cells, at 23 days after transplantation. *p < 0.05, scale bar is 100 μM