Figure 1.

Experimental expression of Evi1 decreases the latency of Flt3-ITD/Npm1c-driven murine AML. (a) Relative Evi1 mRNA levels in normal murine bone marrow cells (nBM) and in leukemic cells from bone marrow (BM) of mice with Flt3-ITD/Npm1c- and MLL-AF9-driven AML (LC^{Flt3-ITD/Npm1c} and LC^MLL-AF9, respectively; n = 3). (b) Schematic of experimental design. Spleen cells from mice terminally ill with Flt3-ITD/Npm1c-driven AML (AML^{Flt3-ITD/Npm1c}) were transduced with pMSCV_FLAG-Evi1_IRES_GFP or with empty vector as a control. GFP-positive cells were sorted and transplanted into sub-lethally irradiated recipient mice. FC, flow cytometry; BM, bone marrow. (c) Kaplan–Meier plot of mice transplanted with Flt3-ITD/Npm1c_vec and Flt3-ITD/Npm1c_Evi1 cells (400,000 cells/mouse). n = 4 (AML^{Flt3-ITD/Npm1c_vec} group), n = 5 (AML^{Flt3-ITD/Npm1c_Evi1} group). (d) Immunoblot analysis of FLAG-EVI1 expression in spleen LC^{Flt3-ITD/Npm1c_Evi1} and LC^{Flt3-ITD/Npm1c_vec} from terminally ill recipient mice. GAPDH was used as a loading control.