{"database":"ENA","file_versions":[],"scores":null,"additional":{"omics_type":["Genomics"],"center_name":["Biochemistry and Molecular Genetics, University of Colorado School of Medicine"],"full_dataset_link":["https://www.ebi.ac.uk/ena/browser/view/PRJNA362638"],"scientific_name":["Mus musculus"],"tag":["xref:PubMed:28609655"],"long_description":["The MLL1 histone methyltransferase gene undergoes many distinct chromosomal rearrangements to yield poor-prognosis leukemia. The remaining wild-type allele is most commonly, but not always, retained. To what extent the wild-type allele contributes to leukemogenesis is unclear. Here we show using rigorous, independent animal models that endogenous MLL1 is dispensable for MLL-rearranged leukemia. Potential redundancy was addressed by co-deleting the closest paralog, Mll2. Surprisingly, Mll2 deletion alone had a significant impact on survival of MLL-AF9-transformed cells and additional Mll1 loss further reduced viability and proliferation. We show that MLL1/MLL2 collaboration is not through redundancy but regulation of distinct pathways. These findings highlight the relevance of MLL2 as a drug target in MLL-rearranged leukemia and suggest its broader significance in AML. We used microarray to investigate the effect of Mll1 deletion on gene expression in LSC-enriched MLL-AF9 leukemia cells. Overall design: Primary MLL-AF9 leukemia mice transformed from Lin-/Sca1+/c-Kit+ (LSK) cells with the genotype of Cre+ Mll1F/+ or Cre+ Mll1F/F were injected with two doses of tamoxifen (TAM) to induce Mll1 deletion. Three days after the last TAM injection, YFP+/Lin-/c-Kit+ leukemia cells were sorted for RNA extraction and microarray."],"repository":["ENA"],"additional_accession":[]},"is_claimable":false,"name":"Mus musculus","description":"MLL2, but not MLL1, plays a major role to sustain leukemia survival [array]","dates":{"last_updated":"2025-09-24","first_public":"2017-04-19"},"accession":"PRJNA362638","cross_references":{"GEO":["GSE93621"],"taxon":["10090"],"PubMed":["28609655"]}}