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Links from GEO DataSets

Items: 20

1.

RNAPol2 accounts for tumor cells liability to JQ1 [ChIP-Seq]

(Submitter supplied) We here use B-cell tumors as a model to address the mechanism of action of JQ1, a widely used BET inhibitor.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
22 Samples
Download data: BED, XLS
Series
Accession:
GSE76191
ID:
200076191
2.

RNAPol2 accounts for tumor cells liability to JQ1

(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:
GPL6244 GPL11154
28 Samples
Download data: BED, CEL, XLS
Series
Accession:
GSE76192
ID:
200076192
3.

RNAPol2 accounts for tumor cells liability to JQ1 [Affymetrix]

(Submitter supplied) We here use B-cell tumors as a model to address the mechanism of action of JQ1, a widely used BET inhibitor.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
6 Samples
Download data: CEL, XLS
Series
Accession:
GSE76188
ID:
200076188
4.

Gene expression profiling of MYC-amplified medulloblastoma cell lines treated by JQ1, a BET bromodomain inhibitor

(Submitter supplied) MYC-amplified medulloblastomas are highly lethal tumors. BET bromodomain inhibition was recently described to downregulate MYC-associated transcriptional activity in various cancer subtypes. To investigate whether JQ1, a BET bromodomain inhibitor is downregulation MYC and MYC-associated transcriptional activity, we performed global gene expression profiling of five medulloblastomas MYC-amplified patient-derived cell lines treated by JQ1 and the inactive form of JQ1.
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS5346
Platform:
GPL6244
10 Samples
Download data: CEL
Series
Accession:
GSE51020
ID:
200051020
5.
Full record GDS5346

BET bromodomain inhibitor JQ1 effect on MYC-amplified medulloblastoma cell lines

Analysis of 5 MYC-amplified medulloblastoma cell lines treated with the BET bromodomain inhibitor JQ1. Cell lines derived from medulloblastoma patients. Results provide insight into the potential use of BET bromodomain inhibitors in the treatment of MYC-amplified medulloblastomas.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 2 agent, 5 cell line sets
Platform:
GPL6244
Series:
GSE51020
10 Samples
Download data: CEL
6.

Differential gene expression in neuroblastoma cells after treatment with vehicle control, JQ1, panobinostat, or combination of JQ1 and panobinostat

(Submitter supplied) The bromodomain inhibitor JQ1 and the histone deacetylase inhibitor panobinostat induce synergistic anticancer effects We analyzed whether JQ1 and panobinostat synergistically modulate gene expression
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL16686
12 Samples
Download data: CEL
Series
Accession:
GSE68690
ID:
200068690
7.

ChIP-Seq and CAGE profiling of cell lines

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
64 Samples
Download data: BED, BROADPEAK, NARROWPEAK
Series
Accession:
GSE113715
ID:
200113715
8.

ChIP-Seq of H4K5acK8ac and BRD2 in H23 NSCLC cell line treated with 500 nM JQ1 for 24h

(Submitter supplied) Changes in acetylation of histone H4 are a common hallmark of cancer cells. In leukemia cells, histone H4 is characterized by loss of K16 mono-acetylation. Bromodomain proteins specifically recognize acetylated lysines and have been used as a target for anti cancer drug, JQ1 and iBET. Although acetylation and de-acetylation of histone H4 have been shown to have big impact in cancer cells, little attention has been focused on histone H4-acetylation at a genome level. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
8 Samples
Download data: BED, BROADPEAK
Series
Accession:
GSE113714
ID:
200113714
9.

CAGE profiling after treatment with JQ1 BET inhibitor in lung cancer cell line.

(Submitter supplied) The bromodomain and extra-terminal domain (BET) proteins are promising drug targets for cancer and immune diseases. However, BET inhibition effects have been studied more in the context of bromodomain-containing protein 4 (BRD4) than BRD2, and the BET protein association to histone H4-hyperacetylated chromatin is not understood at the genome-wide level. Here, we report transcription start site (TSS)-resolution integrative analyses of ChIP-seq and transcriptome profiles in human non-small cell lung cancer (NSCLC) cell line H23. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
27 Samples
Download data: BED, TXT
10.

ChIP-Seq of H4K5acK8ac in GM12878, K562

(Submitter supplied) From: "JQ1 affects BRD2-dependent and independent transcription regulation without disrupting H4-hyperacetylated chromatin states". The bromodomain and extra-terminal domain (BET) proteins are known as drug targets in diseases. However, the BET protein association profile to histone H4 hyperacetylation is not well understood and BET inhibition effects have been studied more in the context of BRD4 than BRD2. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
6 Samples
Download data: NARROWPEAK
Series
Accession:
GSE113635
ID:
200113635
11.

ChIP-Seq of H4K5acK8ac, H3K27ac, H3K4me1, H3K4me3, H3K36me3, H3K9me3, H3K27me3 and BRD2 in H23 NSCLC cell line

(Submitter supplied) The bromodomain and extra-terminal domain (BET) proteins are known as drug targets in diseases. However, the BET protein association profile to histone H4 hyperacetylation is not well understood and BET inhibition effects have been studied more in the context of BRD4 than BRD2. Here, by integrating chromatin and transcriptome analyses of ChIP-seq and Cap Analysis Gene Expression (CAGE) datasets, we show that di-acetylation at K5 and K8 of histone H4 (H4K5acK8ac) co-localizes with H3K27ac and BRD2 in the majority of active enhancers and promoters, where BRD2 has a stronger association with H4K5acK8ac than H3K27ac. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
23 Samples
Download data: NARROWPEAK
Series
Accession:
GSE104481
ID:
200104481
12.

Targeting the EWS/ETS transcriptional program by BET bromodomain inhibition in Ewing sarcoma

(Submitter supplied) Ewing sarcomas (ES) are highly malignant, osteolytic bone or soft tissue tumors, which are characterized by early metastasis into lung and bone. Genetically, ES are defined by balanced chromosomal EWS/ETS translocations, which give rise to chimeric proteins (EWS-ETS) that generate an oncogenic transcriptional program associated with altered epigenetic marks throughout the genome. By use of an inhibitor (JQ1) blocking BET bromodomain binding proteins (BRDs) we strikingly observed a strong down-regulation of the predominant EWS-ETS protein EWS/FLI1 in a dose dependent manner. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
4 Samples
Download data: CEL
Series
Accession:
GSE72673
ID:
200072673
13.

Gene expression analysis of B-ALL cells treated with BET inhibitor

(Submitter supplied) Two human acute lymphoblastic leukemia cell lines were treated with a BET bromodomain inhibitor that blocks BET association with chromatin. These cell lines, MHH-CALL4 and MUTZ-5, each carry translocation of the CRLF2 gene into the IgH locus, and their growth was found to be susceptible to BET inhibition. Gene expression changes were analyzed in each cell line versus vehicle control.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL5175
24 Samples
Download data: CEL, CHP
Series
Accession:
GSE39995
ID:
200039995
14.

Transcriptome analysis of dominant-negative Brd4 mutants identifies Brd4-specific target genes of BET inhibitor JQ1

(Submitter supplied) We analyzed anti-proliferative dominant-negative Brd4 mutants that compete with the function of distinct Brd4 domains. We used these Brd4 mutants to compare the Brd4-specific transcriptome with the transcriptome of JQ1 treated cells.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18460
20 Samples
Download data: TXT
15.

Selective Inhibition of Tumor Oncogenes by Disruption of Super-Enhancers

(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:
GPL16043 GPL11154
31 Samples
Download data: CEL, WIG
Series
Accession:
GSE44931
ID:
200044931
16.

Selective Inhibition of Tumor Oncogenes by Disruption of Super-Enhancers [Affymetrix]

(Submitter supplied) Chromatin regulators have become highly attractive targets for cancer therapy, yet many of these regulators are expressed in a broad range of healthy cells and contribute generally to gene expression. An important conundrum has thus emerged: how can inhibition of a general regulator of gene expression produce selective effects at specific oncogenes? Here we investigate how inhibition of the transcriptional coactivator BRD4 (Bromodomain containing 4) leads to selective inhibition of disease-critical oncogenes in a highly malignant blood cancer, multiple myeloma (MM). more...
Organism:
Homo sapiens
Type:
Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16043
18 Samples
Download data: CEL
Series
Accession:
GSE44929
ID:
200044929
17.

Selective Inhibition of Tumor Oncogenes by Disruption of Super-Enhancers [ChIP-seq]

(Submitter supplied) Chromatin regulators have become highly attractive targets for cancer therapy, yet many of these regulators are expressed in a broad range of healthy cells and contribute generally to gene expression. An important conundrum has thus emerged: how can inhibition of a general regulator of gene expression produce selective effects at specific oncogenes? Here we investigate how inhibition of the transcriptional coactivator BRD4 (Bromodomain containing 4) leads to selective inhibition of disease-critical oncogenes in a highly malignant blood cancer, multiple myeloma (MM). more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
13 Samples
Download data: WIG
Series
Accession:
GSE42355
ID:
200042355
18.

RNA Sequencing Quantitative Analysis of cell lines derived from tumours from two mouse models of human osteosarcoma that recapitulate clinically distinct human osteosarcoma subtypes.

(Submitter supplied) Purpose: Osteosarcoma (OS) is the most common primary bone malignancy. OS consists of several subtypes including fibroblastic, osteoblastic and chondroblastic OS. We have developed genetically engineered mouse models of human OS that recapitulate two distinct subtypes, fibroblastic (Osx-CreLox p53-/- Rb-/-) and osteoblastic (Osx-Cre shRNA p53-/-) OS. The goal of this study was to identify transcriptional differences that distinguish the two subtypes. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
6 Samples
Download data: TXT
Series
Accession:
GSE58916
ID:
200058916
19.

Transcriptional plasticity promotes primary and acquired resistance to BET bromodomain inhibition

(Submitter supplied) Following the discovery of BRD4 as a non-oncogene addiction target in acute myeloid leukemia (AML), BET inhibitors are being explored as promising therapeutic avenue in numerous cancers. While clinical trials have reported single-agent activity in advanced hematologic malignancies, mechanisms determining the response to BET inhibition remain poorly understood. To identify factors involved in primary and acquired BET resistance in leukemia, we performed a chromatin-focused shRNAmir screen in a sensitive MLL/AF9; NrasG12D‑driven AML model, and investigated dynamic transcriptional profiles in sensitive and resistant murine and human leukemias. more...
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
6 related Platforms
103 Samples
Download data: BED, BW, GTF, TSV
Series
Accession:
GSE63782
ID:
200063782
20.

Expression data from non-small cell lung cancer cell line DV90 after Bromodomain and extra terminal domain (BET) inhibitor JQ1 treatment

(Submitter supplied) Bromodomain and extra terminal domain (BET) inhibition reduces occupancy of BET-family proteins at promoter and enhancer sites resulting in changes in the transcription of specific genes. We used microarray profiling to investigate the transcriptional changes induced by BET inhibitor JQ1 treatment in DV90 cells to identify the underlying changes of gene regulation that lead to JQ1 sensitivity.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL17692
28 Samples
Download data: CEL
Series
Accession:
GSE75960
ID:
200075960
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