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Links from GEO DataSets

Items: 20

1.

Setd2 deficiency impaired erythroid differentiation and accelerated Myelodysplastic Syndrome(MDS) - associated leukemogenesis through S100A8 and S100A9

(Submitter supplied) Setd2, the histone H3 lysine 36 methyltransferase, plays an important role in the pathogenesis of hematologic malignancies. The research on the role of Setd2 in leukemogenesis has made great progress, but its role in MDS is still unknown. Here, we knock out Setd2 in the NUP98-HOXD13 transgenic (NHD13 Tg) mouse, and demonstrate that loss of Setd2 accelerates the transformation of MDS into AML. The conditional deletion of Setd2 also interferes the differentiation of hematopoietic stem and progenitor cells (HSPCs), and results in the decrease of granulocyte monocyte progenitor (GMP) cells, increase of megakaryocyte erythroid progenitor (MEP) cells and common myeloid progenitor (CMP) cells. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing
Platforms:
GPL21273 GPL17021
18 Samples
Download data: BED, BROADPEAK, BW, COV, TXT, XLSX
Series
Accession:
GSE129691
ID:
200129691
2.

Setd2 deficiency impairs hematopoietic stem cell self-renewal and causes malignant transformation

(Submitter supplied) Purpose: The histone H3 lysine 36 methyltransferase SETD2 is frequently mutated in various cancers, including leukemia. However, there has not been any functional model to show the contribution of SETD2 in hematopoiesis or the causal role of SETD2 mutation in tumorigenesis. In this study, using a conditional Setd2 knock-out (KO) mouse model, we show that Setd2 deficiency skews hematopoietic differentiation and impaired HSC (hematopoietic stem cell) self-renewal. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing
Platform:
GPL17021
6 Samples
Download data: BW, TXT
Series
Accession:
GSE108617
ID:
200108617
3.

The oncoprotein NUP98-HOXD13 (NHD13) induces thymocyte self-renewal via Lmo2/Lyl1

(Submitter supplied) T-cell Acute Lymphoblastic Leukaemia (T-ALL) can be classified into a number of subfamilies, including those that overexpress TAL1/LMO, TLX1/3 and HOXA transcription factors. Whilst it has been previously shown in mouse models that TAL1/LMO transcription factors induce thymocyte self-renewal, whether this is the case for other transcription factor subclasses is currently unknown. To address this, we have studied vav-Nup98-HoxD13-transgenic (NHD13-Tg) mice, a model of HOXA-driven T-ALL, which overexpress HOXA transcription factors throughout haematopoiesis and display features of myelodysplastic syndrome in the bone marrow along with T-cell developmental abnormalities in the thymus and subsequent development of T-ALL in approximately 15% of mice. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6887
12 Samples
Download data: TXT
Series
Accession:
GSE121641
ID:
200121641
4.

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
5.

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
6.

NHD13 vs wild type LK cells

(Submitter supplied) Investigation of differences in gene expression between NHD13 mice with myelodysplastic syndrome and wild type littermates.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6887
6 Samples
Download data: TXT
Series
Accession:
GSE39692
ID:
200039692
7.

Myelodysplastic syndrome: NUP98-HoxD13 (NHD13) expression effect on hematopoietic stem cells

(Submitter supplied) Analysis of Lin-c-Kit+Sca-1- haematopoietic stem cells (HSCs) expressing the Nup98-HoxD13 (NHD13) fusion gene. NHD13 induces myelodysplastic syndrome (MDS) in mice. Results provide insight into the molecular basis of the myelodysplastic phenotype
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
6 Samples
Download data: TSV
Series
Accession:
GSE66264
ID:
200066264
8.

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
9.

Age-related epigenetic drift in the pathogenesis of MDS and AML

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus; Homo sapiens
Type:
Methylation profiling by array
Platforms:
GPL9886 GPL17019
25 Samples
Download data: TXT
Series
Accession:
GSE46067
ID:
200046067
10.

Age-related epigenetic drift in the pathogenesis of MDS and AML part 2

(Submitter supplied) Genomic DNA is isolated from spleen (RUNX1 model and normal control) and bone marrow (NHD13 model and normal control). We used MCAM to identify genes that have methylation changes.
Organism:
Mus musculus
Type:
Methylation profiling by array
Platform:
GPL17019
6 Samples
Download data: TXT
Series
Accession:
GSE46065
ID:
200046065
11.

Age-related epigenetic drift in the pathogenesis of MDS and AML part 1

(Submitter supplied) Genomic DNA is isolated from bone marrow (MDS patient) and whole blood (normal control). We used MCAM to identify genes that have methylation changes.
Organism:
Homo sapiens
Type:
Methylation profiling by array
Platform:
GPL9886
19 Samples
Download data: TXT
Series
Accession:
GSE46063
ID:
200046063
12.

Genome-wide maps of N_NUP98 and NUP98-TOP1 and MLL1 co-bound targets and their chromatin state in NUP98 fusion transformed cells.

(Submitter supplied) 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-TOP1 or N-NUP98. 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 (MO435). more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL9185
6 Samples
Download data: BIGWIG
Series
Accession:
GSE83221
ID:
200083221
13.

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

(Submitter supplied) 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. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
10 Samples
Download data: BIGWIG, BW
Series
Accession:
GSE76001
ID:
200076001
14.

Gene expression changes upon Mll1 knockout in NUP98-HOXA9 transformed murine LSKs

(Submitter supplied) We report Illumina next generation RNA sequencing (RNAseq) of NUP98-HOXA9 in vitro transformed murine LSKs upon genetic deletion of Mll1. These gene expression data illustrate that Mll1 regulates Hoxa, Hoxb and Meis1 expression in NUP98-HOXA9 transformed murine BM cells.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
6 Samples
Download data: TXT
Series
Accession:
GSE75997
ID:
200075997
15.

Global mouse gene expression data from Idh2R140Q/NHD13 DN1/DN2 T-ALL, SCL/LMO1 non-DN1/DN2 T-ALL, and Wild Type samples assessed by oligonucleotide microarrays

(Submitter supplied) Mutations in the isocitrate dehydrogenase 1 (IDH1) and IDH2 genes are frequently observed in a wide variety of hematologic malignancies, including myeloid and T-cell leukemias. In this study, we generated Idh2R140Q transgenic mice to examine the role of the Idh2R140Q mutation in leukemia. No leukemia developed in Idh2R140Q transgenic mice, suggesting a need for additional genetic events for leukemia development. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
18 Samples
Download data: CEL, XLSX
Series
Accession:
GSE181007
ID:
200181007
16.

Setd2-dependent H3K36me3 is required for Acrbp1 and protamine transcriptions and spermiogenesis in mice

(Submitter supplied) Spermatogenesis is precisely cotrolled by complex gene expression programs and involves epigenetic reprogramming including histone modification and DNA methylation. Setd2 catalyzes the trimethylation of histone H3 Lys36 (H3K36me3) and plays key roles in embryonic stem cell differentiation and somatic cell development; however, its role in male germ cell development remains elusive. Here we demonstrate an essential role of Setd2 for spermiogenesis. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL21273 GPL17021
14 Samples
Download data: BED, BEDGRAPH, TXT
Series
Accession:
GSE108717
ID:
200108717
17.

HOXBLINC is aberrantly expressed in acute myeloid leukemia and functions as a potent oncogenic long non-coding RNA in leukemogenesis

(Submitter supplied) Dysregulation of HOXA/B genes is a dominant mechanism of leukemic transformation.HOXB locus-associated long non-coding RNA (lncRNAs), HOXBLINC, regulates transcription of the anterior HOXB genes and plays a critical role in hematopoiesis development. Here, we show that HOXBLINC lncRNA is up-regulated in over 60% of patients with AML. Interestingly, AML patients with high HOXBLINC expression have a significantly shortened survival as compared to low HOXBLINC expressing patients. more...
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Other
5 related Platforms
40 Samples
Download data: BED, TXT
Series
Accession:
GSE115096
ID:
200115096
18.

RNA-seq in acute myeloid leukemia (AML) cells with and without knockdown of METTL14

(Submitter supplied) To dissect the mechanism underlying the oncogenic function of METTL14 in AML, we performed deep sequencing for mRNA isolated from MM6 and NB4 cells with and without knockdown of METTL14
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL15433
8 Samples
Download data: TXT
19.

N6-methyladenosine (m6A) sequencing of messenger RNAs in acute myeloid leukemia (AML) cells with and without knockdown of METTL14 [m6A-seq]

(Submitter supplied) To dissect the mechanism underlying the oncogenic function of METTL14 in AML, we performed m6A RNA immunoprecipitation and deep sequencing for mRNA isolated from MM6 and NB4 cells with and without knockdown of METTL14
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
8 Samples
Download data: BW
20.

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
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