Figure 6
BCR–ABL cooperates with Evi1 to induce AML (CML-BC-like disease) in vivo. (a) Experimental scheme of BMT mice with BCR–ABL and Evi1 overexpression. 5FU-primed C57BL/6 BM cells with retroviral BCR–ABL and Evi1 were transplanted into lethally irradiated recipient mice. (b) Wright–Giemsa staining of PB, BM and spleen from BCR–ABL and Evi1 overexpressing mice. (c) HE staining of BM (upper) and spleen (lower) from BCR–ABL and Evi1 overexpressing mice with low (left) and high (right) magnitude. (d) The proportion of blasts in PB, BM and spleen from BCR–ABL and Evi1 overexpressing mice (n=3). (e) The weight of spleen and liver from normal (n=13), BCR–ABL (n=27), BCR–ABL+NUP98–HOXA9 (n=29) or BCR–ABL+Evi1 mice (n=3). (f) Kaplan–Meier plot of the survival of primary or secondary recipient mice transplanted with BCR–ABL and Evi1 overexpressing cells (n=7 for primary transplants and n=4 for secondary transplants) and primary recipient mice transplanted with BCR–ABL overexpressing cells (n=24). (g) Representative FCM data of BM cells from BCR–ABL and Evi1 overexpressing mice. In BCR–ABL(+) Evi1(+) BM cells, most cells were Lin– (upper left) and about 40% of Lin– cells had c-kit expression (upper right). Mostly BCR–ABL(+) Evi1(+) BM cells were Gr-1+, B220- and CD4/CD8− (lower). Data are mean±s.d. *P<0.01, **P<0.001.
