Figure 2.

Ikaros suppression is critical for maintenance of Ikaros-kd B-ALL. (A) Kaplan-Meier survival analysis of Ikaros-kd B-ALL transplant recipient mice (six independent primary BCR-ABL1;Vav-tTA;TRE-GFP-shIkaros leukemias, two to three recipients per condition) either untreated or Dox-treated upon disease establishment. Median survival 19 d for untreated versus 113 d for Dox treated; P < 0.0001, log-rank test. Censored events represent deaths unrelated to leukemia, including fighting and infection. (B) GFP expression of splenocytes from representative Ikaros-kd B-ALL–recipient mice that were untreated (d0) or Dox treated as indicated upon leukemia onset. (C) Western blot of Ikaros expression in control or Ikaros-kd B-ALL cells isolated from representative leukemic mice that were untreated or Dox treated as indicated. The Ikaros protein isoforms Ik1 and Ik2 are indicated. Actin is a loading control. (D) Western blot of Ikaros protein expression in Ikaros-kd B-ALL cells isolated from representative leukemic recipient mice that were untreated or Dox treated as indicated. (E) Flow cytometry of CD19 and IgM in CD45.2⁺ (donor-derived) peripheral blood cells from representative untreated (upper panels) or Dox-treated (lower panels) leukemic Ikaros-kd B-ALL transplant recipient mice. (F) Spleen histology of representative Ikaros-low B-ALL transplant recipient mice that were untreated or Dox treated for 14 d at disease onset, with arrows indicating follicular structures. (G) Flow cytometry of CD19 and IgM in CD45.2⁺ splenocytes from representative Ikaros-kd B-ALL transplant recipient mice with Dox treatments indicated.