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Links from GEO DataSets

Items: 20

1.

NUP98/HHEX a new oncogenic fusion with acute myeloid leukemia

(Submitter supplied) 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
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL8321
9 Samples
Download data: CEL
Series
Accession:
GSE10909
ID:
200010909
2.

Candidate Genes for Expansion and Transformation of Hematopoietic Stem Cells by NUP98-HOX Fusion Genes

(Submitter supplied) BACKGROUND: Hox genes are implicated in hematopoietic stem cell (HSC) regulation as well as in leukemia development through translocation with the nucleoporin gene NUP98. Interestingly, an engineered NUP98-HOXA10 (NA10) fusion can induce a several hundred-fold expansion of HSCs in vitro and NA10 and the AML-associated fusion gene NUP98-HOXD13 (ND13) have a virtually indistinguishable ability to transform myeloid progenitor cells in vitro and to induce leukemia in collaboration with MEIS1 in vivo. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL339
12 Samples
Download data: CEL, CHP, EXP, RPT
Series
Accession:
GSE9079
ID:
200009079
3.

NUP98-HOXA9 role as oncogenic transcription factor

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL17077 GPL9115
14 Samples
Download data: TXT, WIG
Series
Accession:
GSE62587
ID:
200062587
4.

Evaluation of the NUP98-HOXA9 role as oncogenic transcription factor

(Submitter supplied) To study the oncogenic mechanism triggered by the leukemic fusion protein NUP98-HOXA9, we cloned the cDNA of NUP98-HOXA9 into a retroviral vector (pMSCV-IRES-GFP) and efficiently transduced the HEK293FT human cell line. We performed a ChIP-seq analysis to identify the DNA binding sites of NUP98-HOXA9. These results allowed us to demonstrate that NUP98-HOXA9 regulates the expression of genes involved in the development of Acute Myeloid Leukemia by directly interacting with their enhancer regions. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL9115
5 Samples
Download data: BED, WIG
Series
Accession:
GSE62586
ID:
200062586
5.

Development of NUP98-HOXA9 gene expression signatures

(Submitter supplied) To explore the molecular mechanisms induced by the leukemic fusion protein NUP98-HOXA9, we performed gene expression analysis of human hematopoietic progenitors and primary samples of patients that express NUP98-HOXA9. By combining these data with ChIP-seq results, we observed that the fusion protein is able to both activate and repress the expression of its target genes.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL17077
9 Samples
Download data: TXT
Series
Accession:
GSE62585
ID:
200062585
6.

MLL is essential for NUP98-HOXA9-induced leukemia

(Submitter supplied) Rearrangements involving the NUP98 gene resulting in fusions to several partner genes occur in acute myeloid leukemia and myelodysplastic syndromes. This study demonstrates that the second FG repeat domain of the NUP98 moiety of the NUP98-HOXA9 fusion protein is important for its cell immortalization and leukemogenesis activities. We demonstrate that NUP98-HOXA9 interacts with MLL via this FG repeat domain and that, in the absence of MLL, NUP98-HOXA9-induced cell immortalization and leukemogenesis are severely inhibited. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
8 Samples
Download data: CEL
Series
Accession:
GSE93923
ID:
200093923
7.

NUP98-NSD1 links H3K36 methylation to Hox-A gene activation and leukaemogenesis

(Submitter supplied) Nuclear receptor-binding SET domain protein 1 (NSD1) prototype is a family of mammalian histone methyltransferases (NSD1, NSD2/MMSET/WHSC1, NSD3/WHSC1L1) that are essential in development and are mutated in human acute myeloid leukemia (AML), overgrowth syndromes, multiple myeloma and lung cancers. In AML, the recurring t(5;11)(q35;p15.5) translocation fuses NSD1 to nucleoporin-98 (NUP98). Here, we present the first characterization of the transforming properties and molecular mechanisms of NUP98-NSD1. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
10 Samples
Download data: CHP
Series
Accession:
GSE10071
ID:
200010071
8.

The MLL-Menin interaction is a molecular dependency in NUP98-rearranged AML

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18573 GPL19057
84 Samples
Download data: NARROWPEAK, TXT
Series
Accession:
GSE175597
ID:
200175597
9.

The MLL-Menin interaction is a molecular dependency in NUP98-rearranged AML [RNA-Seq]

(Submitter supplied) Using mouse and human models of NUP98-rearrranged leukemia, we demonstrate that inhibition of MLL-Menin impairs leukemogenic gene expression and disrupts chromatin binding of MLL1 and NUP98 fusion proteins at a critical subset of genes that is essential for sustaining the undifferentiated leukemia phenotype.
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL18573 GPL19057
57 Samples
Download data: TXT
Series
Accession:
GSE175596
ID:
200175596
10.

The MLL-Menin interaction is a molecular dependency in NUP98-rearranged AML [ChIP-Seq]

(Submitter supplied) Using mouse and human models of NUP98-rearrranged leukemia, we demonstrate that inhibition of MLL-Menin impairs leukemogenic gene expression and disrupts chromatin binding of MLL1 and NUP98 fusion proteins at a critical subset of genes that is essential for sustaining the undifferentiated leukemia phenotype.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
24 Samples
Download data: NARROWPEAK
Series
Accession:
GSE175595
ID:
200175595
11.

The MLL-Menin interaction is a molecular dependency in NUP98-rearranged AML [BioChIP-seq]

(Submitter supplied) Using mouse and human models of NUP98-rearrranged leukemia, we demonstrate that inhibition of MLL-Menin impairs leukemogenic gene expression and disrupts chromatin binding of MLL1 and NUP98 fusion proteins at a critical subset of genes that is essential for sustaining the undifferentiated leukemia phenotype.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
3 Samples
Download data: NARROWPEAK
Series
Accession:
GSE175594
ID:
200175594
12.

CDK6 is an essential direct transcriptional target of NUP98-fusion-protein-driven acute myeloid leukemia

(Submitter supplied) Fusion proteins involving Nucleoporin 98 (NUP98) are recurrently found in Acute Myeloid Leukemia (AML) with poor prognosis. Lack of mechanistic insight into NUP98-fusion-dependent oncogenic transformation has precluded the identification of efficient targeting strategies. We reasoned that shared transcriptional programs of direct NUP98-fusion-protein-mediated gene control converge on actionable targets. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
35 Samples
Download data: BW, TXT
Series
Accession:
GSE134784
ID:
200134784
13.

Gene expression profile of thymic AML generated by NP23 and NHD13 transgenes

(Submitter supplied) Gene expression profile of AML generated via 3 related transgenes is compared.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
12 Samples
Download data: TXT
Series
Accession:
GSE137674
ID:
200137674
14.

Role of HHEX in hematopoietic cells

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platform:
GPL16791
15 Samples
Download data: TDF, TXT
Series
Accession:
GSE147656
ID:
200147656
15.

The effects of expression of mutant ASXL1 and HHEX on hematopoietic cells

(Submitter supplied) To identify target genes of mutant ASXL1 (ASXL1-MT) and HHEX in hematopoietic cells, we performed RNA-seq using RUNX1-ETO expressing cord blood cells transduced with vector or ASXL1-MT together with vector or HHEX.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
12 Samples
Download data: TXT
Series
Accession:
GSE147654
ID:
200147654
16.

Genome-wide maps of HHEX binding

(Submitter supplied) The identification of the binding sites of HHEX.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
3 Samples
Download data: TDF
Series
Accession:
GSE147653
ID:
200147653
17.

Mechanistic insights into chromatin targeting by leukemic NUP98-PHF23 fusion

(Submitter supplied) The dysregulation of plant homeodomain (PHD) fingers has been implicated in several human diseases, including cancer. In a subset of aggressive acute myeloid leukemia (AML), chromosomal translocations that involve nucleoporin 98 (NUP98), a component of the nuclear pore complex, and a PHD finger-containing protein, such as KDM5A/JARID1A, PHF23 and BPTF, generate potent oncoproteins (namely NUP98-KDM5A, NUP98-PHF23 and NUP98-BPTF; or together termed as NUP98-PHD fusions) that are able to arrest hematopoietic differentiation and induce acute myeloid leukemia in murine models. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL9185
5 Samples
Download data: BW
Series
Accession:
GSE146693
ID:
200146693
18.

Acute myeloid leukemia requires Hhex to enable PRC2-mediated epigenetic repression of Cdkn2a

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL17021 GPL19057
17 Samples
Download data: TXT
Series
Accession:
GSE74019
ID:
200074019
19.

Acute myeloid leukemia requires Hhex to enable PRC2-mediated epigenetic repression of Cdkn2a (RNA-Seq)

(Submitter supplied) Unlike clustered HOX genes, the role of non-clustered homeobox gene family members in hematopoiesis and leukemogenesis has not been extensively studied. Here we find that the Hematopoietically-expressed Homeobox gene, Hhex, is overexpressed in acute myeloid leukemia (AML) and is essential for the initiation and propagation of MLL-ENL induced AML, but dispensable for normal myelopoiesis, indicating a specific requirement for Hhex for leukemic growth. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
8 Samples
Download data: TXT
Series
Accession:
GSE74018
ID:
200074018
20.

Acute myeloid leukemia requires Hhex to enable PRC2-mediated epigenetic repression of Cdkn2a (ChIP-Seq)

(Submitter supplied) Unlike clustered HOX genes, the role of non-clustered homeobox gene family members in hematopoiesis and leukemogenesis has not been extensively studied. Here we find that the Hematopoietically-expressed Homeobox gene, Hhex, is overexpressed in acute myeloid leukemia (AML) and is essential for the initiation and propagation of MLL-ENL induced AML, but dispensable for normal myelopoiesis, indicating a specific requirement for Hhex for leukemic growth. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
9 Samples
Download data: TXT
Series
Accession:
GSE74017
ID:
200074017
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