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Links from GEO DataSets

Items: 20

1.

ASXL1 Knock Down in Normal CD34+ Cord Blood and UKE1 Cell Lines

(Submitter supplied) Gene expression analysis of Normal CD34+ Cord Blood and UKE1 cell lines treated with hairpins targeting ASXL1.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platforms:
GPL571 GPL570
13 Samples
Download data: CEL
Series
Accession:
GSE38692
ID:
200038692
2.

ASXL1 Mutations Promote Myeloid Transformation Through Loss of PRC2-Mediated Gene Repression

(Submitter supplied) Recurrent somatic ASXL1 mutations occur in patients with myelodysplasia (MDS), myeloproliferative neoplasms (MPN), and acute myeloid leukemia (AML), and are associated with adverse outcome. Despite the genetic and clinical data implicating ASXL1 mutations in myeloid malignancies, the mechanisms of transformation by ASXL1 mutations are not understood. Here we identify that ASXL1 mutations result in loss of PRC2-mediated histone H3 lysine 27 (H3K27) tri-methylation. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL9052
9 Samples
Download data: BW
Series
Accession:
GSE38861
ID:
200038861
3.

Bap1 loss results in EZH2 dependent transformation

(Submitter supplied) Analysis of sorted granulocyte macrophage progenitors (GMPs) in control and Bap1-deficient bone marrow cells. Loss of Bap1 in the hematopoietic compartments results in an MDS-like disease. These data allow for the examination of the genetic underpinnings of Bap1 loss in disease.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18635
6 Samples
Download data: TXT
Series
Accession:
GSE61577
ID:
200061577
4.

Bap1 loss results in EZH2 dependent transformation

(Submitter supplied) BAP1 and ASXL1 interact to form a polycomb deubiquitinase complex that removes monoubiquitin from histone H2A lysine 119 (H2AK119Ub). However, BAP1 and ASXL1 are mutated in distinct cancer types, consistent with independent roles in regulating epigenetic state and malignant transformation. Here we demonstrate that Bap1 loss results in increased trimethylated histone H3 lysine 27 (H3K27me3), elevated Ezh2 expression, and enhanced repression of Polycomb Repressive Complex 2 (PRC2) targets. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
11 Samples
Download data: BW
Series
Accession:
GSE61360
ID:
200061360
5.

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
6.

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
7.

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
8.

Expression analysis of BM cells of ASXL-MT induced MDS mice

(Submitter supplied) Recurrent mutations in ASXL1 are found in various hematological malignancies and are associated with poor prognosis. In particular, ASXL1 mutations are frequently found in patients with hematological malignancies associated with myelodysplasia including myelodysplastic syndromes (MDS), and chronic myelomonocytic leukemia. Although loss-of-function ASXL1 mutations promote myeloid transformation, a large subset of ASXL1 mutations is thought to result in stable truncation of ASXL1. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
6 Samples
Download data: CEL
Series
Accession:
GSE49118
ID:
200049118
9.

Expression analysis of 32Dcl3 cells expressing ASXL-MT in the presence of IL-3 or G-CSF

(Submitter supplied) Recurrent mutations in ASXL1 are found in various hematological malignancies and are associated with poor prognosis. In particular, ASXL1 mutations are frequently found in patients with hematological malignancies associated with myelodysplasia including myelodysplastic syndromes (MDS), and chronic myelomonocytic leukemia. Although loss-of-function ASXL1 mutations promote myeloid transformation, a large subset of ASXL1 mutations is thought to result in stable truncation of ASXL1. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
8 Samples
Download data: CEL
Series
Accession:
GSE49117
ID:
200049117
10.

ChIP-on-chip from acute myeloid leukemia cell lines and clinical samples for H3K4me3, H3K27me3, and EZH2

(Submitter supplied) Histone modifcations at the p15INK4b gene were compared in sample with p15INK4b DNA methylation vs. samples with no DNA methylation AML clinical samples without DNA methylation exhibit bivalent histone modifications at p15INK4b, while clinical samples with DNA methylation display lower H3K4me3 and retain H3K27me3
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by genome tiling array
Platform:
GPL8754
40 Samples
Download data: TXT
Series
Accession:
GSE16730
ID:
200016730
11.

The effects of mutant ASXL1 and BAP1 expression on hematopoietic cells

(Submitter supplied) To identify target genes of mutant ASXL1 and BAP1 in hematopoietic cells, we performed RNA-seq using murine c-kit positive cells transduced with ASXL1-MT (MT) or ASXL1-MT-K351R (KR) together with vector or BAP1. Method:Murine c-kit positive bone marrow cells were transduced with ASXL1-MT (MT) or ASXL1-MT-K351R (KR) (coexpressing blastcidin resistant gene) together with vector or BAP1 (coexpressing puromycin resistant gene). more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
12 Samples
Download data: TXT
Series
Accession:
GSE114861
ID:
200114861
12.

The Polycomb Repressive Complex 2 Is Required For MLL-AF9 Leukemia

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL13112 GPL1261
23 Samples
Download data: CEL, WIG
Series
Accession:
GSE34963
ID:
200034963
13.

Epigenetic profiling of WT and Ezh2-null MLL-AF9 murine leukemic cells

(Submitter supplied) Chromatin immunoprecipitation (ChIP) for H3K27me3 followed by Solexa sequencing in WT and Ezh2-null leukemic cells from primary and secondary recipients.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
4 Samples
Download data: WIG
Series
Accession:
GSE34962
ID:
200034962
14.

Expression profiling of secondary wild type (WT) and Ezh2-null murine MLL-AF9 AML

(Submitter supplied) We evaluated gene expression changes in secondary recipient murine leukemia caused by retroviral overexpression of MLL-AF9. We compared wild-type (WT) leukemia cells with mutant leukemia cells after cre-mediated inactivation of a homozygous conditional allele for Ezh2, a component of the Polycomb Repressive Complex2.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
9 Samples
Download data: CEL, TXT
Series
Accession:
GSE34961
ID:
200034961
15.

Expression profiling of primary wild type (WT), Ezh2-null and Eed-null murine MLL-AF9 AML

(Submitter supplied) We evaluated gene expression changes in murine leukemia caused by retroviral overexpression of MLL-AF9. We compared wild-type (WT) leukemia cells with mutant leukemia cells after cre-mediated inactivation of homozygous conditional alleles for Ezh2 or Eed, both of which are components of the Polycomb Repressive Complex2.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
10 Samples
Download data: CEL, TXT
Series
Accession:
GSE34959
ID:
200034959
16.

Notch1-driven epigenetic changes in a mouse model of T cell Acute Lymphoblastic Leukemia (T-ALL)

(Submitter supplied) T-cell acute lymphoblastic leukemia (T-ALL) is an immature hematopoietic malignancy driven mainly by oncogenic activation of NOTCH1 signaling. In this study we used a mouse model of T-ALL through the overexpression of the intarcellular transcriptionally active part of Notch1 (N1-IC). This model faithfully recapitulates the major characteristics of the human disease. Comparison of the leukemic cells from peripheral tumors(thymoma) of this mouse model to normal thymic cells Double Positive (DP) for the markers CD4 and CD8 that express very low levels of Notch1 showed major expression changes (please see GSE34554) in pathways controlling the transition from physiology to disease. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL9250
18 Samples
Download data: BED
Series
Accession:
GSE34954
ID:
200034954
17.

Notch1-driven transcriptional changes in a mouse model of T-ALL

(Submitter supplied) T-cell acute lymphoblastic leukemia (T-ALL) is an immature hematopoietic malignancy driven mainly by oncogenic activation of NOTCH1 signaling. In this study we used a mouse model of T-ALL through the overexpression of the intarcellular transcriptionally active part of Notch1 (N1-IC). This model faithfully recapitulates the major characteristics of the human disease. Comparison of the leukemic cells from peripheral tumors(thymoma) of this mouse model to normal thymic cells Double Positive (DP) for the markers CD4 and CD8 that express very low levels of Notch1 showed major expression changes in pathways controlling the transition from physiology to disease. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS4303
Platform:
GPL1261
4 Samples
Download data: CEL
Series
Accession:
GSE34554
ID:
200034554
18.
Full record GDS4303

Notch1 overexpression model of T-cell acute lymphoblastic leukemia: double positive CD4+/8+ cells

Analysis of DP (CD4+/8+) cells from an intracellular Notch1 (Notch1-IC)-induced T-ALL model that recapitulates most features of human T-ALL. T-ALL malignancy is driven by oncogenic activation of NOTCH1 signaling. Results provide insight into the molecular basis of Notch1-driven leukemogenesis.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 2 tissue sets
Platform:
GPL1261
Series:
GSE34554
4 Samples
Download data: CEL
19.

Functional study on the cooperation of ASXL1 and RUNX1 mutations for myeloid leukemia transformation

(Submitter supplied) BACKGROUND: Our previous studies showed that RUNX1 and ASXL1 mutations were frequently co-existed in chronic myelomonocytic leukemia (CMML) and clonal evolution of RUNX1 and/or ASXL1 occurred most frequently in chronic myeloid leukemia (CML) with myeloid blastic crisis. The molecular pathogenesis of cooperation of RUNX1 and ASXL1 mutations has not been reported yet. METHODS: Lentiviral-mediated stable transduction of RUNX1-WT/MT (R135T) in K562 cells which harboring ASXL1-MT (Y591X). more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL23126
3 Samples
Download data: CEL
Series
Accession:
GSE99640
ID:
200099640
20.

DMSO control and DZNep treated MOLM-14 cells

(Submitter supplied) We demonstrated that 3-Deazaneplanocin A (DZNep), a histone methyltransferase inhibitor, induce robust apoptosis in AML cells through increased ROS production and ER stress. We identified a core gene signature including TXNIP, a major redox control molecule which is crucial in DZNep-induced apoptosis.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
4 Samples
Download data: CEL
Series
Accession:
GSE30315
ID:
200030315
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