Transcriptomic differences in murine AML bone marrow samples with different Gab2 genotypes

Internal tandem duplications (ITD) of FLT3 predict poor prognosis in acute myeloid leukemia (AML) and often co-exist with inactivating DNMT3A mutations. In a genetically modified mouse model harboring these genetic aberrations, we analyzed the role of the adaptor protein Gab2 in this disease. We observed Gab2 to be essential for the development of Flt3-ITD driven AML in vivo, which was corroborated by RNA sequencing data of whole murine bone marrow with different Gab2 genotypes Overall design: Whole bone marrow was isolated from AML mice (Mx1-Cre; Dnmt3a+/-; Flt3ITD/ITD) with different Gab2 genotypes. Three of these donor mice were Gab2 WT, three Gab2 KO and two mice were Gab2 HET. After RNA isolation, samples were sequenced on an Illumina HiSeq4000.