Different NUP98-fusion proteins induce a phenotypically similar AML-like disease in mice. (A) Schematic outline of the experimental strategy for the generation of transplantation models for Dox-repressible expression of NUP98-fusion proteins. (B-D) Representative bone marrow histology (B), bone marrow cytospin, ×400 original magnification (C), and flow cytometric analysis (D) from a moribund mouse transplanted with NUP98/DDX10-transformed murine HSPCs. (E) Relative abundance of indicated cell populations in the bone marrow from moribund mice expressing indicated NUP98-fusion proteins (mean ± standard deviation [SD]; n ≥ 4). (F) Kaplan-Meier survival curves of mice transplanted with murine HSPCs expressing indicated NUP98-fusion proteins (n ≥ 4). (G) Principal component analysis of the distances between steady-state gene expression data of NUP98-fusion–protein-driven leukemia cells (n ≥ 3). (H) Venn diagram illustrating the overlap of overexpressed genes of NUP98-fusion–protein-driven leukemia cells vs cells expressing NUP98-5′ (>threefold upregulated, P < .01; n ≥ 3). (I) Gene Set Enrichment Analysis (GSEA) indicating conservation of the gene signature found in murine NUP98-fusion–protein-driven leukemia with AML patients harboring NUP98 rearrangements. FDR, false discovery rate; NES, normalized enrichment score.