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Links from GEO DataSets

Items: 20

1.

Combination of HDAC inhibitors and Azacytidine for Cancer Cell Selective Targeting of Esophageal Cancer Cells

(Submitter supplied) Esophageal cancers (ECs) are highly aggressive tumors with poor prognosis and few treatment options. This study investigated the possibility of treating esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC) cells by inhibitors of broad and specific histone deacetylases (HDACi; SAHA, MS-275, FK228) and/or of DNMT (Azacytidine, AZA). Drug targets (HDAC1,2,3 and DNMT1) were present in non-neoplastic (HET-1A), ESCC (OE21) and EAC (OE33) cell lines. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
36 Samples
Download data: TXT
Series
Accession:
GSE57130
ID:
200057130
2.

Distal regulation mediated Core Transcriptional Regulatory Circuitry in Esophageal Squamous Cell Carcinoma

(Submitter supplied) In esophageal squamous cell carcinoma (ESCC), the core regulatory circuitry is ill-defined and the limited clinical approaches are available currently for the treatment of ESCC. Here, using enhancer profiling and CRC programme, we generated ESCC-dependent epigenomic-transcriptional regulatory circuitry, elaborated the exquisite work model mediated by core TFs and SEs through physical interaction between enhancers and promoter, and identified the crucial target of ESCC regulatory network.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
4 Samples
Download data: BW
Series
Accession:
GSE148920
ID:
200148920
3.

Distal regulation mediated Core Transcriptional Regulatory Circuitry in Esophageal Squamous Cell Carcinoma [ChIP-Seq Drug]

(Submitter supplied) In esophageal squamous cell carcinoma (ESCC), the core regulatory circuitry is ill-defined and the limited clinical approaches are available currently for the treatment of ESCC. Here, using enhancer profiling and CRC programme, we generated ESCC-dependent epigenomic-transcriptional regulatory circuitry, elaborated the exquisite work model mediated by core TFs and SEs through physical interaction between enhancers and promoter, and identified the crucial target of ESCC regulatory network.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
6 Samples
Download data: BW
Series
Accession:
GSE131661
ID:
200131661
4.

Distal regulation mediated Core Transcriptional Regulatory Circuitry in Esophageal Squamous Cell Carcinoma

(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:
GPL20301
35 Samples
Download data: BW, TSV
Series
Accession:
GSE131493
ID:
200131493
5.

Distal regulation mediated Core Transcriptional Regulatory Circuitry in Esophageal Squamous Cell Carcinoma [RNA-seq]

(Submitter supplied) In esophageal squamous cell carcinoma (ESCC), the core regulatory circuitry is ill-defined and the limited clinical approaches are available currently for the treatment of ESCC. Here, using enhancer profiling and CRC programme, we generated ESCC-dependent epigenomic-transcriptional regulatory circuitry, elaborated the exquisite work model mediated by core TFs and SEs through physical interaction between enhancers and promoter, and identified the crucial target of ESCC regulatory network.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
3 Samples
Download data: TSV
Series
Accession:
GSE131492
ID:
200131492
6.

Distal regulation mediated Core Transcriptional Regulatory Circuitry in Esophageal Squamous Cell Carcinoma [ChIP-seq]

(Submitter supplied) In esophageal squamous cell carcinoma (ESCC), the core regulatory circuitry is ill-defined and the limited clinical approaches are available currently for the treatment of ESCC. Here, using enhancer profiling and CRC programme, we generated ESCC-dependent epigenomic-transcriptional regulatory circuitry, elaborated the exquisite work model mediated by core TFs and SEs through physical interaction between enhancers and promoter, and identified the crucial target of ESCC regulatory network.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
14 Samples
Download data: BW
Series
Accession:
GSE131490
ID:
200131490
7.

Distal regulation mediated Core Transcriptional Regulatory Circuitry in Esophageal Squamous Cell Carcinoma [ATAC-seq]

(Submitter supplied) In esophageal squamous cell carcinoma (ESCC), the core regulatory circuitry is ill-defined and the limited clinical approaches are available currently for the treatment of ESCC. Here, using enhancer profiling and CRC programme, we generated ESCC-dependent epigenomic-transcriptional regulatory circuitry, elaborated the exquisite work model mediated by core TFs and SEs through physical interaction between enhancers and promoter, and identified the crucial target of ESCC regulatory network.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
12 Samples
Download data: BW
Series
Accession:
GSE131489
ID:
200131489
8.

HDAC inhibitor kinetic rate constants correlate with cellular histone acetylation but not transcription and cell viability

(Submitter supplied) Histone deacetylases (HDACs) are critical in the control of gene expression and dysregulation of their activity has been implicated in a broad range of diseases including cancer, cardiovascular and neurological diseases. HDAC inhibitors (HDACi) employing different zinc chelating functionalities such as hydroxamic acids and benzamides have shown promising results in cancer therapy. While it has also been suggested that HDACi with increased isozyme-selectivity and potency may broaden their clinical utility and minimize side effects, the translation of this idea to the clinic remains to be investigated. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6480
35 Samples
Download data: TXT
Series
Accession:
GSE49158
ID:
200049158
9.

SAHA Rat Dental Pulp

(Submitter supplied) Transcriptional response of rat dental pulp cells (DPCs) cultured with SAHA at early and late mineralisation time points Transcript profiling of DPC identified several novel genes expression induced and supressed by HDACi at 24 hrs and 14 days under mineralising conditions. SAHA induces several members of the MMP family of endopepsidases (TIMP-1, MMP-9, MMP-13) and other members of the endochondral ossification pathway at 24 h.
Organism:
Rattus norvegicus
Type:
Expression profiling by array
Platform:
GPL14746
8 Samples
Download data: GPR
Series
Accession:
GSE67175
ID:
200067175
10.

Schistosomula exposed to HDAC inhibitor (Trichostatin A)

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Schistosoma mansoni
Type:
Expression profiling by array
Platform:
GPL22001
18 Samples
Download data: TXT
Series
Accession:
GSE83211
ID:
200083211
11.

Schistosomula exposed to HDAC inhibitor (Trichostatin A) [48hrs]

(Submitter supplied) HDACs inhibitors induces mortality in the parasite Schistosoma mansoni (schistosomula and adult worms), and became an interesting drug class for the development of new drugs to treat schistosomiasis. In order to understand the effect of histone hyperacetylation on the parasite, we tested the effect of the HDAC inhibitor Trichostatin A on schistosomula gene expression.
Organism:
Schistosoma mansoni
Type:
Expression profiling by array
Platform:
GPL22001
6 Samples
Download data: TXT
Series
Accession:
GSE83210
ID:
200083210
12.

Schistosomula exposed to HDAC inhibitor (Trichostatin A) [24hrs]

(Submitter supplied) HDACs inhibitors induces mortality in the parasite Schistosoma mansoni (schistosomula and adult worms), and became an interesting drug class for the development of new drugs to treat schistosomiasis. In order to understand the effect of histone hyperacetylation on the parasite, we tested the effect of the HDAC inhibitor Trichostatin A on schistosomula gene expression.
Organism:
Schistosoma mansoni
Type:
Expression profiling by array
Platform:
GPL22001
6 Samples
Download data: TXT
Series
Accession:
GSE83209
ID:
200083209
13.

Schistosomula exposed to HDAC inhibitor (Trichostatin A) [12hrs]

(Submitter supplied) HDACs inhibitors induces mortality in the parasite Schistosoma mansoni (schistosomula and adult worms), and became an interesting drug class for the development of new drugs to treat schistosomiasis. In order to understand the effect of histone hyperacetylation on the parasite, we tested the effect of the HDAC inhibitor Trichostatin A on schistosomula gene expression.
Organism:
Schistosoma mansoni
Type:
Expression profiling by array
Platform:
GPL22001
6 Samples
Download data: TXT
Series
Accession:
GSE83208
ID:
200083208
14.

HDACI and DAC induce specific epigenetic profile in DLBCL

(Submitter supplied) Diffuse large B-cell lymphoma (DLBCL) is the most common type of lymphoid neoplasm in the world representing 30-40% of all lymphomas. Standard immunochemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisone and rituximab) ensures cure in 60 to 65% of patients, while the rest progress or relapse. While advances have been made in the treatment of DLBCL, especially with the addition of rituximab, it is now apparent that there may be significant differences in prognosis that are related to the cell of origin, and that this disease is heterogeneous and novel treatment options are needed. more...
Organism:
Homo sapiens
Type:
Expression profiling by array; Methylation profiling by array
Dataset:
GDS4006
Platforms:
GPL8490 GPL6947
24 Samples
Download data: TXT
Series
Accession:
GSE27226
ID:
200027226
15.
Full record GDS4006

Histone deacetylase inhibitor and hypomethylating agent effect on diffuse large B-cell lymphoma cell lines

Analysis of three large B-cell lymphoma cell lines treated with the histone deacetylase inhibitor panobinostat, hypomethylating agent decitabine, or both for 48hrs. Panobinostat synergizes with decitabine in DLBCL cells. Results provide insight into the molecular basis for this synergistic effect.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 4 agent, 3 cell line sets
Platform:
GPL6947
Series:
GSE27226
12 Samples
Download data
16.

Gene expression profiles of MM.1S cells after knockdown of HDAC3 or DNMT1

(Submitter supplied) Previous study demonstrated that HDAC3 has a critical role in MM proliferation; however, the underlying mechanism has not yet been elucidated. We identify that HDAC3 inhibition targets DNMT1 through dual regulations. We demonstrate that knockdown of DNMT1 leads to apoptosis and significant growth inhibition in myeloma cells. HDAC3 inhibition by gene silencing or HDAC3 selective inhibitor BG45 downregulates an oncoprotein c-Myc through its acetylation. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
10 Samples
Download data: CEL
Series
Accession:
GSE86147
ID:
200086147
17.

RNA expression in MDA-MB-231 cells treated for 24h with SAHA, Pargyline, or both [HG-U133A_2]

(Submitter supplied) Abnormal activities of histone lysine demethylases (KDMs) and lysine deacetylases (HDACs) are associated with aberrant gene expression in breast cancer development. However, the precise molecular mechanisms underlying the crosstalk between KDMs and HDACs in chromatin remodeling and regulation of gene transcription are still elusive. In this study, we showed that treatment of human breast cancer cells with inhibitors targeting the zinc cofactor dependent class I/II HDACs, but not NAD+ dependent class III HDACs, led to significant increase of H3K4me2 which is a specific substrate of histone lysine-specific demethylase 1 (LSD1) and a key chromatin mark promoting transcriptional activation. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL571
12 Samples
Download data: CEL
Series
Accession:
GSE72688
ID:
200072688
18.

Analysis of differential miRNA expression in mineralising DPCs treated with pharmacological epigenetic inhibitors.

(Submitter supplied) To establish a miRNA expression profile for DPCs undergoing epigenetically-mediated mineralisation, rodent DPCs were induced to mineralise and treated with a HDAC inhibitor, SAHA, and a DNMT inhibitor, 5-AZA-CdR. RNA was then isolated from DPCs at day 4 of culture and subjected to RNA sequencing. Subsequent bioinformatic analysis identified differentially expressed miRNAs compared with untreated mineralising DPCs.
Organism:
Rattus norvegicus
Type:
Non-coding RNA profiling by high throughput sequencing
Platform:
GPL18694
12 Samples
Download data: XLSX
Series
Accession:
GSE229197
ID:
200229197
19.

Gene expression profiles of HCT116 colorectal carcinoma cells treated with HDAC inhibitors

(Submitter supplied) Histone deacetylases (HDACs) regulate gene expression. Inhibition of class I HDACs has been shown to inhibit cancer cell growth. Largazole, a new potent HDAC inhibitor, shows strong antitumor activity, presumably by modulating transcription of cancer relevant genes. We used microarray analysis of human HCT116 colorectal carcinoma cell line to determine the gene expression profile after largazole treatment in comparison with other HDAC inhibitors (FK228 and SAHA). more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
8 Samples
Download data: CEL
Series
Accession:
GSE22061
ID:
200022061
20.

HDAC Inhibitors induce tumor cell-selective pro-apoptotic transcriptional responses.

(Submitter supplied) The identification of recurrent somatic mutations in genes encoding epigenetic enzymes, coupled with biochemical studies demonstrating aberrant recruitment of epigenetic enzymes such as histone deacetylases (HDACs) and histone methyltransferases (HMTs) to promoter regions through association with oncogenic fusion proteins such as PML-RARα and AML1-ETO has provided a strong rationale for the development compounds that target the epigenome for the treatment of cancer. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
42 Samples
Download data: CEL
Series
Accession:
GSE43010
ID:
200043010
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