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Changes in chromatin accessibility when expressing two sets of t(6;11) fusion proteins

ABSTRACT: We have cloned two sets of t(6;11) fusion genes with breakpoints in the majorand minor BCR of the MLL/KMT2A gene. Both setsof fusion genes were stably transfected alone or in combiantion to analyze their molecular power

ORGANISM(S): Homo sapiens

PROVIDER: GSE175558 | GEO | 2021/05/26

REPOSITORIES: GEO

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Changes in gene expression when expressing two sets of t(6;11) fusion proteins

Project description:We have cloned two sets of t(6;11) fusion genes with breakpoints in the majorand minor BCR of the MLL/KMT2A gene. Both setsof fusion genes were stably transfected alone or in combiantion to analyze their molecular power

2021-05-27 | GSE175573 | GEO

MLL-EB1 fusion immortalized murine bone marrow cells

Project description:Background: MLL (KMT2A)-EB1 (MAPRE1) fusion was identified in a patient with de novo pro-B acute lymphoblastic leukemia. To investigate the leukemogenesis of MLL-EB1 fusion, a retroviral transduction of MLL-EB1 to murine bone marrow cells was performed. A frequent MLL fusion, MLL-AF10(OM-LZ), was used as a positive control. Results: Two MLL-EB1 immortalized cell lines (ME1 and ME2G), and a MLL-AF10(OM-LZ) immortalized cell line (12G) were generated. Microarray results showed that many genes including Evi1 and Ets1 were differentially expressed in ME1/ME2G and 12G cell lines.

2017-06-02 | GSE82156 | GEO

Changes in gene expression over time in cells expressing t(4;11) fusion proteins

Project description:We have used a constitutive MLL-AF4 fusion gene together with a inducible AF4-MLL fusion gene to investigate the power of theses fusion proteins. All transgenes were stably or transiently transfected.

2021-06-19 | GSE178465 | GEO

Changes in chromatin accessibility over time in cells expressing t(4;11) fusion proteins [I]

2021-06-22 | GSE178567 | GEO

Non-toxic direct targeted therapy for MLL-fusion driven leukemias

Project description:Improving the poor prognosis of infant leukemias remains an unmet clinical need. This disease is a prototypical fusion oncoprotein-driven pediatric cancer, with MLL (KMT2A)-fusions present in most cases. Direct targeting of these driving oncoproteins represents a unique therapeutic opportunity. This rationale led us to initiate a drug screening with the aim of discovering drugs that can block MLL-fusion oncoproteins. A screen for inhibition of MLL-fusion proteins was developed that overcomes the traditional limitations of targeting transcription factors. This luciferase reporter-based screen, together with a secondary western blot screen, was used to prioritize compounds. We characterized the lead compound, Disulfiram, based on its efficient ablation of MLL fusion proteins. The consequences of drug-induced MLL-fusion inhibition was confirmed by cell proliferation, colony formation, apoptosis assays, RT-qPCR, in vivo assays, RNA-seq and CHIP-qPCR and CHIP-seq analysis. All statistical tests were two-sided. Drug-induced inhibition of MLL-fusion proteins by Disulfiram resulted in a specific block of colony formation in MLL-rearranged cells in vitro, induced differentiation and impeded leukemia progression in vivo. Mechanistically, Disulfiram abrogates MLL-fusion protein binding to DNA, resulting in epigenetic changes and down-regulation of leukemic programs setup by the MLL-fusion protein. Disulfiram can directly inhibit MLL-fusion proteins and demonstrates antitumor activity both in vitro and in vivo, providing, to our knowledge, the first evidence for a therapy that directly target the initiating oncogenic MLL-fusion protein.

2022-08-01 | GSE203203 | GEO

Changes in chromatin accessibility over time in cells expressing t(4;11) fusion proteins [II]

Project description:We have used a combination of constitutive and inducible MLL-AF4 and AF4-MLL fusion genes to investigate the power of theses fusion proteins. All transgenes were stably or transiently transfected. Here, we compared 48 induction of MLL-AF4 or AF4-MLL (day 3) and looked for persistance at days 28. This was compared to the situation with constitutive MLL-AF4 with 48 inductionn of AF4-MLL at day 3 and day 28.

2021-06-22 | GSE178568 | GEO

Protein Interactions of 7 MLL-fusion Proteins

Project description:MLL-fusions represent a large group of leukemia drivers, whose diversity originates from the vast molecular heterogeneity of C-terminal fusion partners of MLL protein. While studies of selected MLL-fusions have revealed critical molecular pathways, unifying mechanisms across all MLL-fusions remain poorly understood. We present the first comprehensive survey of protein-protein interactions of seven distantly related MLL-fusion proteins: MLL-AF1p, MLL-AF4, MLL-AF9, MLL-CBP, MLL-EEN, MLL-ENL and MLL-GAS7.

2018-05-25 | PXD009338 | Pride

Changes in chromatin accessibility when expressing two sets of t(6;11) fusion proteins

Project description:Changes in chromatin accessibility when expressing two sets of t(6;11) fusion proteins

| PRJNA732711 | ENA

Changes in gene expression when expressing two sets of t(6;11) fusion proteins

Project description:Changes in gene expression when expressing two sets of t(6;11) fusion proteins

| PRJNA732920 | ENA

Menin-MLL inhibitors block oncogenic transformation by MLL fusion proteins in a fusion partner independent manner

Project description:Chromosomal rearrangements of the Mixed Lineage Leukemia (MLL) gene result in fusion proteins which retain the N-terminal portion of MLL fused with one of more than 70 different fusion partners. The high diversity of MLL fusion partners raises a question whether it is possible to develop a general therapeutic strategy to block the oncogenic activity of MLL fusion proteins in a fusion partner independent manner. We have demonstrated that blocking the menin-MLL interaction using small molecule inhibitor inhibits oncogenic activity of different MLL fusion proteins according to a mechanism that is independent on the fusion partner.

2018-06-09 | GSE69740 | GEO

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