Mutation of Runx binding site leads to delayed onset of AML/ETO9a leukemia. (A) Experimental scheme: E14.5 fetal liver cells (lineage depleted) of PU.1-URE-mRunx and WT mice were retrovirally (MigR1) transduced with the fusion oncogene AML/ETO9a (A/E9a) harboring an eGFP signal. After 48 hours, GFP⁺ cells were isolated and transplanted into CD45.2 recipient mice (n = 7). Development of leukemia and survival were monitored. Moribund mice were taken for analysis. (B) Representative immunoblot demonstrating stable A/E9a protein expression in leukemic samples (spleen) of A/E9a recipients. (C) PU.1 mRNA levels of leukemic (c-kit⁺, GFP⁺) cells. Shown are average levels ± SD relative to WT + A/E9a. n = 4; **P < .01. (D) Kaplan-Meier survival analysis of recipients receiving either WT or PU.1-URE-mRunx cells transduced with A/E9a (n = 7; P = .0013).