Deletion of Id1 abrogates the initiation of leukemia in the AE9a fetal liver transplantation model. (A) Lethally irradiated recipient mice were injected with WT or Id1−/− mouse E14.5 fetal liver cells transduced with AE9a. The WBC counts of the transplanted mice in Id1−/− AE9a group are significant lower than the WT AE9a mice group 15 weeks after transplant (P = .0288). (B) Loss of Id1 prolongs the survival time of recipient mice (267 days vs 137 days, n = 15 per group, P < .001). (C) Loss of Id1 decreases the frequency of GFP+CD45/CD45.2−C-Kit+ leukemia blast cells and increases the frequency of normal GFP−Gr1+ myeloid cells in the peripheral blood of recipient mice (compared with the WT group) 15 weeks after transplantation. (D) The peripheral blood shows less leukemia blast cells in the Id1−/− AE9a group compared with the WT AE9a mice group. (E) Pathological sections of the spleen stained with hematoxylin-eosin are shown 15 weeks after transplantation (the scale bar indicates 25 μM). The leukemic blast cells are indicated by black arrows. (F) The columns represent the numbers of colonies in each plating of WT or Id1−/− E14.5 fetal liver cells transduced with AE9a (± standard deviation [SD], n = 3, P < .01). (G) The frequency of donor-derived Id1−/− CD45.2+ cells is significantly lower in the peripheral blood of recipient mice, compared with the WT CD45.2+ cells (P < .01). (H) Loss of Id1 abrogates the repopulating ability of hematopoietic cells isolated from E14.5 fetal liver cells.