Global mouse gene expression data from NUP98-NSD1/FLT3-ITD  AML samples and Normal Wild Type whole bone marrow and Normal Wild Type lineage negative bone marrow samples assessed by Bulk RNA-Seq.
Acute myeloid leukemia (AML) is a heterogeneous hematologic malignancy driven largely by gene mutations and epigenetic modifications. The Nucleoporin 98kDa (NUP98) gene is a component of the nuclear pore complex that also plays a role as an intranuclear transcription scaffold.  Fusion genes involving NUP98 have been recognized in a wide array of hematologic malignancy, most commonly AML4. Among over 30 partner genes known to be fused to NUP98 in human leukemia, NSD1 (for Nuclear receptor-binding SET Domain protein 1) (NSD1) is the most common. Patients with NUP98::NSD1 gene fusions have a poor prognosis, and the leukemic blasts frequently have an internal tandem duplication (ITD) of the FMS-related tyrosine kinase 3 gene (FLT3) gene accompanying the NUP98::NSD1 fusion. Previous reports have utilized BM transduction with retroviral vectors followed by transplantation into recipient mice to model AML driven by a NUP98::NSD1 fusion.  Given that  genetically engineered mice offer certain advantages over retroviral transduction models, such as consistent transgene expression and integration effects, lack of  ionizing radiation, and transferability between investigators, we generated NUP98::Nsd1 transgenic mice. Overall design: We compared expression profiles of  AML derived from bone marrow tissue of NUP98-NSD1/FLT3-ITD transgenic mouse(N=7) with normal wild type mouse whole bone marrow (N=4) or normal wild type mouse lineage negative bone marrow (N=4).