GSE202137
Next Generation Sequencing of mouse hematopoietic cells retrovirally transfected with MNX1 or empty vector (Ctr) from fetal liver or mouse bone marrow and treated with or without pan-inhibitor against SAM-dependent methyltransferases Sinefungin
Acute myeloid leukemia (AML) results from aberrant hematopoietic processes and these changes are frequently initiated by chromosomal translocations. One particular subtype, AML with translocation t(7;12)(q36;p13), is found in children diagnosed before two years of age. The chromosomal breakage points of the t(7;12) have consistently been found to be located  after exon 1 in the Motor neuron and pancreas homeobox 1 (MNX1) gene in chromosome 7, and after exon 2 in the ETV6 gene in chromosome 12. The aim of this study is the investigation of the leukomogenic potenial of MNX1 overexpression and MNX1-ETV6 fusion using mouse models, in addition to the molecular pathway through which MNX1 is inducing leukemia. Overall design: Fetal liver hematopietic cells from C57BL/6 mice were retrovirally transfected with MNX1 or empty vector and transplanted into 10-12 weeks old NOD.Cg-KitW-41J Tyr + Prkdcscid Il2rgtm1Wjl/ThomJ (NBSGW) mice. After establishment of leukmeia in the NBSGW mice, cells were collected from the bone marrow for mRNA expression profile. Additional controls with fetal liver hematopietic cells from C57BL/6 mice  retrovirally transfected with empty vector were used. For InVitro experiments, fetal liver hematopietic cells were retrovirally transfected with empty vector or MNX1 overexpression and treated with or without 5µM Sinefungin