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NUP98-HOXA9 acute myeloid leukemia

ABSTRACT: Mass Spectrometry analysis of the interactome of the oncoprotein NUP98-HOXA9

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture, Early Embryonic Cell

DISEASE(S): Acute Leukemia

SUBMITTER: Fernando Garcia

LAB HEAD: Javier Muñoz

PROVIDER: PXD001828 | Pride | 2017-07-10

REPOSITORIES: Pride

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The molecular pathogenesis of the NUP98-HOXA9 fusion protein in acute myeloid leukemia.

Rio-Machin A A Gómez-López G G Muñoz J J Garcia-Martinez F F Maiques-Diaz A A Alvarez S S Salgado R N RN Shrestha M M Torres-Ruiz R R Haferlach C C Larráyoz M J MJ Calasanz M J MJ Fitzgibbon J J Cigudosa J C JC

Leukemia 20170620 9

PMID: 28630438

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Transcription profiling of mouse bone marrow cells expressing NUP98/HHEX or NUP98/HOXA9 a new oncogenic fusion with acute myeloid leukemia

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2008-06-11 | E-GEOD-10909 | biostudies-arrayexpress

MLL is essential for NUP98-HOXA9-induced leukemia

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Project description:We have cloned and characterized a fusion gene NUP98/HHEX1 resulting from t(7;10) from a patient with acute myeloid leukemia (AML). As NUP98/HHEX acts as an aberrant transcriptional activator, putative targets were searched upon transient expression of the fusion in primary murine bone marrow cells. Keywords: Comparative analysis of NUP98/HHEX, NUP98/HOX vs. MIG (empty virus) in primary bone marrow cells

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Gene expression profiling of Nup98HoxA9 expressing ES cells

Project description:To know whether the Nup98-HoxA9 affects global gene expression, we performed DNA microarray analysis using the following four clones: two independent Nup98-HoxA9 ES clones (clone#1 and clone#9), parental ES cells, and HoxA9-Ct ES clone. Two independent Nup98-HoxA9 ES clones (clone#1 and clone#9), and HoxA9-Ct ES clone, was compared with parental ES cells (reference sample).

2016-01-04 | E-GEOD-67967 | biostudies-arrayexpress

Genome-wide maps of NUP98 fusion and MLL1 co-bound targets and their chromatin state in NUP98 fusion transformed cells.

Project description:By performing biotin-mediated chromatin immunoprecipitation followed by next generation sequencing (ChIP-seq) for two different NUP98 fusions, we defined the genome-wide direct binding sites of NUP98-HOXA9 or NUP98-HOXD13. To test whether NUP98 fusions and Mll1 were recruited to the same region of Hox genes promoters, Mll1 ChIP-seq analysis was carried out in murine NUP98-HOXA9 transformed cells using an anti-Mll1n antibody. In agreement with our results showing that NUP98-HOXA9 interacts with MLL1 in NSL/MLL1 complex, Mll1 binding targets significantly overlap with that of NUP98-HOXA9 at promoter region and gene body region. Given that MOF and MLL1 work in concert to modify H4K16ac and H3K4me3 at promoters, we further test whether H3K4me3 and H4K16ac marks are associated with NUP98-HOXA9-bound targets in murine NUP98-HOXA9 transformed cells by anti-H3K4me3 and anti-H4K16ac ChIP-seq. Our data show that both H3K4me3 and H4K16ac mark presents on NUP98-HOXA9 binding targets at promoters, and this is in line with the coordination role in the activities between MOF-mediated H4K16 acetylation and MLL/SET-mediated H3K4 methylation. In summary, our results confirmed that NUP98-HOXA9 and Mll1 are recruited to the same Hox loci, and this recruitment is associated with activating epigenetic marks, supporting the notion of the association between NUP98 fusions and NSL/Mll1 complex, suggesting that the recruitment of NUP98 fusions to the Hox gene loci maybe through MLL1.

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Frequent derepression of the mesenchymal transcription factor gene in acute myeloid leukemia (mouse)

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