MEIS1 collaborates with NPM1c mutation to induce high-penetrance myeloid leukemia in mice. (A) MEIS1 expression in NPM1c de novo AML patients (n = 107) compared with NPM1^WT AML patients (n = 340) from the Vizome data set.²⁶ (B) MEIS1 expression in NPM1c de novo AML patients (n = 107) compared with CD34⁺ healthy BM (n = 13) from the Vizome data set.²⁶ (C) GSEA analysis of 25% of highest MEIS1 (MEIS1^High) expressing vs 25% lowest MEIS1 expressing (MEIS1^Low) NPM1c de novo AML patients from the TCGA data set.²⁷ (D) Schematic of the experimental design of in vivo experiments with Npm1^cA/+ mouse model. (E) Kaplan-Meier plot of Npm1^cA/+ mice transduced with a YFP empty vector (n = 8), Meis1 (n = 10), and secondary transplants of NPM1c⁺ Meis1 leukemic cells (n = 6). (F) Spleen weight of Npm1^cA/+ mice (n = 7) transduced with an empty YFP control vector compared with Npm1^cA/+ mice with Meis1 overexpression (n = 8). (G) WBC counts for Npm1^cA/+ mice (n = 7) transduced with an empty YFP control vector compared with Npm1^cA/+ mice with Meis1 overexpression (n = 7). (H) Histopathological analysis of a Npm1^cA/+ plus YFP mouse compared with a Npm1^cA/+ plus Meis1 mouse. ∗P < .05; ∗∗P < .001; ∗∗∗P < .0001. GSEA, gene set enrichment analysis; TCGA, the cancer genome atlas; WBC, white blood cell.