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Links from GEO DataSets

Items: 20

1.

Gene expression profiles of MV-4-11 AML cells treated HDAC1/2 -selective inhibitor and Azacitidine

(Submitter supplied) Determine the differences in gene expression profiles of MV-4-11 AML cells treated with HDAC1/2-selective inhibition, azacitidine, or the combination of the two agents. Acute myeloid leukemia (AML) is a heterogeneous group of hematopoietic stem cell disorders characterized by defects in myeloid differentiation and increased proliferation of neoplastic hematopoietic precursor cells. Outcomes for patients with AML remain poor, highlighting the need for novel treatment options. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL15207
4 Samples
Download data: CEL
Series
Accession:
GSE84440
ID:
200084440
2.

Effects of BRD4 inhibition in AML

(Submitter supplied) The BET (bromodomain and extra terminal) protein family members including BRD4 bind to acetylated lysines on histones and regulate the expression of important oncogenes, e.g., MYC and BCL2. Here we demonstrate the sensitizing effects of the histone hyperacetylation inducing pan-histone deacetylase inhibitor (HDI) panobinostat (PS) on human AML blast progenitor cells (BPCs) to the BET protein inhibitor JQ1. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
2 Samples
Download data: CEL
Series
Accession:
GSE51950
ID:
200051950
3.

Differential gene expression analysis of pediatric acute myeloid leukemia cell lines treated with azacytidine and panobinostat alone or in combination and compared to vehicle treated cells.

(Submitter supplied) Pediatric AML cell lines (MV4;11, AML-193 and THP-1) were treated with DNA hypomethylating agent (azacytidine) and a pan histone deactylase inhibitor (panobinostat) alone or in combination. Treatment of AML cell lines with these epigenetic drugs synergistically suppresses cell viability in vitro and in xenograft models in vivo. Data show differential regulation of gene expression in AML cell lines by epigenetic drugs at concentrations which retained cell viability at a minimum of 75% even in the combination treatment.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL16686
60 Samples
Download data: CEL, CHP
Series
Accession:
GSE83983
ID:
200083983
4.

Chemical inhibition of Histone Deacetylases 1 and 2 induces fetal hemoglobin through activation of Gata2

(Submitter supplied) This SuperSeries is composed of the SubSeries GSE60791 and GSE60792.
Organism:
Homo sapiens
Type:
Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL15207 GPL11154
11 Samples
Download data: BW, CEL
Series
Accession:
GSE60793
ID:
200060793
5.

ChIP-seq of erythroid progenitors treated with vehicle or the HDAC1/2-selective inhibitor ACY-957

(Submitter supplied) Establish the DNA binding profiles of HDAC1, HDAC2 and Gata2 in erythroid progenitors derived from human CD34+ bone marrow cells. Determine the effects of HDAC1/2 inhibition on the DNA binding profiles of Gata2.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
5 Samples
Download data: BW
Series
Accession:
GSE60792
ID:
200060792
6.

Gene expression profiles of erythroid progenitors treated with vehicle or the HDAC1/2-selective inhibitor ACY-957

(Submitter supplied) Determine the effects of HDAC1/2-selective chemical inhibtion on the gene expression profiles of erythroid progenitors derived from human CD34+ bone marrow cells.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL15207
6 Samples
Download data: CEL
Series
Accession:
GSE60791
ID:
200060791
7.

Rational targeting of cooperating layers of the epigenome yields enhanced therapeutic efficacy against AML

(Submitter supplied) Disruption of epigenetic regulation is a hallmark of Acute Myeloid Leukemia (AML), but therapeutic interventions are difficult by the interplay of epigenetic mechanisms controlling genomic elements. We hypothesized that concurrent targeting of aberrant promoter and enhancer epigenetic silencing improves efficacy against AML. To test this, we developed an ex vivo culturing system and treated 52 patient-derived AML with low-dose 5-Azacytidine and specific LSD1 inhibitors. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Methylation profiling by high throughput sequencing
Platform:
GPL16791
28 Samples
Download data: TXT
8.

Effects of Beta Catenin antagonist BC2059 in AML cells

(Submitter supplied) To determine the global transcriptomic changes induced by treatment with the Beta Catenin antagonist BC2059 in AML cells The canonical WNT-β-catenin pathway is essential for self-renewal, growth and survival of AML stem/blast progenitor cells (BPCs). Deregulated WNT signaling inhibits degradation of β-catenin, causing increased nuclear translocation and co-factor activity of β-catenin with the transcriptional regulator TCF4/LEF1 in AML BPCs. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
4 Samples
Download data: CEL
Series
Accession:
GSE61275
ID:
200061275
9.

Azacitidine treated AML cells reveals highly variable cell surface proteome remodeling

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array; Methylation profiling by genome tiling array
Platforms:
GPL570 GPL21145
32 Samples
Download data: CEL, IDAT
Series
Accession:
GSE123211
ID:
200123211
10.

Azacitidine treated AML cells reveals highly variable cell surface proteome remodeling [Affymetrix]

(Submitter supplied) Myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) are diseases of abnormal hematopoietic differentiation with aberrant epigenetic alterations. Azacitidine (AZA) is a DNA methyltransferase inhibitor (DNMTi) widely used to treat MDS and AML, yet the impact of AZA on the cell surface proteome has not been defined. To identify potential therapeutic targets for use in combination with AZA in AML patients, we investigated the effects of AZA treatment on four AML cell lines representing different stages of differentiation. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
16 Samples
Download data: CEL
Series
Accession:
GSE123207
ID:
200123207
11.

Azacitidine treated AML cells reveals highly variable cell surface proteome remodeling [Illumina]

(Submitter supplied) Myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) are diseases of abnormal hematopoietic differentiation with aberrant epigenetic alterations. Azacitidine (AZA) is a DNA methyltransferase inhibitor (DNMTi) widely used to treat MDS and AML, yet the impact of AZA on the cell surface proteome has not been defined. To identify potential therapeutic targets for use in combination with AZA in AML patients, we investigated the effects of AZA treatment on four AML cell lines representing different stages of differentiation. more...
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL21145
16 Samples
Download data: IDAT, TXT
Series
Accession:
GSE123140
ID:
200123140
12.

Romidepsin and azacitidine synergize in their epigenetic modulatory effects to induce apoptosis in CTCL

(Submitter supplied) We demonstrate that the combination of the HDAC inhibitor, romidepsin, and the demethylating agent, azacitidine, exerts synergistic anti-proliferative effects and induction of apoptosis involving activation of the caspase cascade in CTCL cell lines as well as CD4+ T cells derived from patients with Sézary Syndrome (SS) with high tumor burden. We identified genes that were selectively induced by the combination treatment, such the tumor suppressor gene RhoB.
Organism:
Homo sapiens
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL11154
8 Samples
Download data: BED
Series
Accession:
GSE66732
ID:
200066732
13.

OCI/AML2 ATRA AND VPA GENE EXPRESSION

(Submitter supplied) Purpose: Treatment of acute promyelocytic leukemia (APL) with the retinoid, all trans retinoic acid (ATRA), along with standard chemotherapy has significantly improved survival compared to chemotherapy alone1. ATRA mediates its benefit in APL by overcoming the transcriptional block mediated by PML-RAR-alpha fusion oncoprotein, thereby, restoring expression of retinoid response genes2. The therapeutic benefits observed with ATRA treatment in APL have not been achieved in the other more common sub-types of acute myeloblastic leukemia (AML)3. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS1215
Platform:
GPL96
4 Samples
Download data
Series
Accession:
GSE2668
ID:
200002668
14.
Full record GDS1215

Acute myeloblastic leukemia cells response to all trans retinoic acid and valproic acid

Analysis of acute myeloblastic leukemia (AML) cell line, OCI/AML-2, following treatment with valproic acid (VPA) and all trans retinoic acid (ATRA). VPA inhibits histone deacetylase. Results provide insight into the responsiveness of AML cells to ATRA when VPA is present.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 4 agent sets
Platform:
GPL96
Series:
GSE2668
4 Samples
Download data
DataSet
Accession:
GDS1215
ID:
1215
15.

Targeting miR-126 in inv(16) acute myeloid leukemia inhibits leukemia development and leukemia stem cell maintenance

(Submitter supplied) Acute myeloid leukemia (AML) harboring inv(16)(p13q22) expresses high levels of miR-126. Here we show that the CBFB-MYH11 (CM) fusion gene upregulates miR-126 expression through aberrant miR-126 transcription and perturbed miR-126 biogenesis via the HDAC8/RAN-XPO5-RCC1 axis. Aberrant miR-126 upregulation promotes survival of leukemia-initiating progenitors and is critical for initiating and maintaining CM-driven AML. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
10 Samples
Download data: TXT
Series
Accession:
GSE184015
ID:
200184015
16.

State-Transition Analysis of Time-Sequential microRNA Expression Predicts Development of Acute Myeloid Leukemia

(Submitter supplied) We show that the microRNA transcriptome undergoes a global state transition during the initiation and progression of acute myeloid leukemia, and accurately predicts time to disease development.
Organism:
Mus musculus
Type:
Non-coding RNA profiling by high throughput sequencing
Platform:
GPL17021
231 Samples
Download data: TSV
Series
Accession:
GSE173785
ID:
200173785
17.

State-Transition Analysis of Time-Sequential Gene Expression Identifies Critical Points That Predict Leukemia Development

(Submitter supplied) Temporal dynamics of gene expression are informative of changes associated with disease development and evolution. Given the complexity of high-dimensionaltemporal datasets, an analytical framework guided by a robust theory is needed to interpret time-sequential changes and to predict system dynamics. Herein, we use acute myeloid leukemia as a proof-of-principle to model gene expression dynamics in a transcriptome state-space constructed based on time-sequential RNA-sequencing data. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
248 Samples
Download data: TSV, TXT
Series
Accession:
GSE133642
ID:
200133642
18.

In vitro and in vivo monitoring of valproic acid effects on gene expression signatures in adult acute myeloid leukemia

(Submitter supplied) PURPOSE: Inhibitors of histone deacetylases (HDACIs) like valproic acid (VPA) display activity in murine leukemia models, and induce tumor-selective cytoxicity against blasts from patients with acute myeloid leukemia (AML). However, despite of the existing knowledge of the potential function of HDACIs, there remain many unsolved questions especially regarding the factors that determine whether a cancer cell undergoes cell cycle arrest, differentiation, or death in response to HDACIs. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10108
43 Samples
Download data
Series
Accession:
GSE32240
ID:
200032240
19.

Epigenetic therapy as a novel approach for GFI136N-associated AML

(Submitter supplied) Acute myeloid leukemia (AML) is characterized by accumulation of myeloid blast cells in the bone marrow. Despite all efforts, prognosis of AML patients remains poor, warranting new therapeutic approaches. A single nucleotide polymorphism of growth factor independence 1 (GFI1), a hematopoietic transcription factor, generates a protein with an asparagine (GFI136N) instead of a serine at position 36 (GFI136S), which we have previously reported to be associated with de novo AML in humans. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
2 Samples
Download data: XLSX
Series
Accession:
GSE77073
ID:
200077073
20.

Effect of Gfi1 36N variant on genome-wide H3K9 Acetylation patterns

(Submitter supplied) ChIP-Seq Analysis of H3K9Ac in pairs of mouse and human samples carrying either the Gfi136S or the GFi136N variants. The objective of the study was to identify the changes in H3K9 acetylation at gene promoters that occur in samples expressing the 36N variant of the Gfi1 gene.
Organism:
Mus musculus; Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL9250 GPL13112 GPL11154
24 Samples
Download data: TXT
Series
Accession:
GSE71254
ID:
200071254
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