ERG induces an early progenitor myeloid leukemia in mice. (A) Bar graph depicting expression of human ERG by quantitative RT-PCR in TgERG leukemia and human AML cell lines MEG01 and CMY compared with normal CD34⁺ cells derived from cord blood (mean ± SEM, n = 3; experiment was repeated twice). (B) Kaplan-Meier survival curve showing that all transgenic ERG mice die by the age of 22 weeks (WT mice, n = 14; TgERG mice, n = 26). (C) Hematoxylin and eosin–stained sections of spleens and livers and Giemsa-stained cytospin samples from the bone marrow of TgERG mice and WT littermates (original magnification ×200 for sections, ×600 for cytospin samples). (D) Immunophenotype of TgERG leukemias. Typical dot plots showing that most of the bone marrow cells found in sick TgERG mice are lin^–, cKit⁺ Sca-1^– CD150⁺. (E) Validation of CD150 expression by quantitative RT-PCR normalized to β-actin (mean ± SEM, n = 3 for WT and WT lin^–. N = 5 for TgERG leukemia). (F) Heat map depicting hierarchical clustering of TgERG leukemias and WT controls (see supplemental Methods). (G) GSEA showing enrichment of the TgERG leukemia signature in MEPs compared with CMPs.¹⁹  (H) GSEA showing enrichment of high ERG–expressing human AML signature⁹  in the TgERG leukemia compared with WT mice. (I) GSEA showing enrichment of TgERG leukemia signature in human AML progenitors compared with normal hematopoietic progenitors.²⁰  (J) GSEA showing enrichment of the promoter-stem cell enhancer signature²¹  in TgERG leukemia compared with WT mice.