Figure 5
Evi1-high CML-BC cells possess leukemogenic potential and TKI resistance in vivo. (a) Kaplan–Meier plot of the survival of sublethally irradiated recipient mice receiving Evi1-high or Evi1-low CML-BC BM cells (n=8 mice per group) or mice with Evi1-high or Evi1-low LK cells of CML-BC (n=15 for Evi1-high CML-BC LK cells, n=9 for Evi1-low CML-BC LK cells). (b) Vehicle or nilotinib (75 mg/kg daily) were administered orally to Evi1-reporter CML-BC mice for a week from day 10 after BMT and the number of residual Evi1-high or Evi1-low CML-BC LK cells per femur were calculated (n=5). (c) Experimental scheme of generating Evi1+/+ or Evi1+/− CML-BC mice. 5FU-primed Evi1+/+ or Evi1+/− BM cells with retroviral BCR–ABL and NUP98–HOXA9 were transplanted into lethally irradiated recipient mice (1st BMT). BM cells from primary transplants were inoculated into sublethally irradiated recipient mice (2nd BMT). (d) Kaplan–Meier plot of the survival of primary transplants receiving 5FU-primed Evi1+/+ or Evi1+/− BM cells transduced with BCR–ABL and NUP98–HOXA9 (n=6 mice per group). (e) Kaplan–Meier plot of the survival of secondary transplants with Evi1+/+ or Evi1+/− CML-BC BM cells (n=8 mice per group). Data are mean±s.d. *P<0.01, **P<0.001.
