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Links from GEO DataSets

Items: 20

1.

Identification of differential expressed genes of JQ1 or JQ1+Bortezomib in colorectal cancer cells

(Submitter supplied) The bromodomain and extra-terminal domain inhibitors (BETi) are promising epigenetic drugs for the treatment of various cancers through suppression of oncogenic transcription factors including MYC. However, only a subset of CRC cells response to BETi, suggesting an intrinsic resistance to BETi in CRC. We investigated the effect of JQ1 on cell proliferation, apoptosis, angiogenesis and MYC expression in a panel of 11 CRC cells in vitro and in vivo. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
12 Samples
Download data: XLSX
2.

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
3.
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
4.

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
5.

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
6.

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
7.

Synergistic activity of BET protein antagonist-based combinations in Mantle Cell Lymphoma cells sensitive or resistant to ibrutinib

(Submitter supplied) To determine the global transcriptome changes in mantle cell lymphoma cells following treatment with the BET bromodomain antagonist, JQ1 Mantle Cell Lymphoma (MCL) cells exhibit increased B cell receptor and NFkB activities. The BET protein BRD4 is essential for the transcriptional activity of NFkB. Here, we demonstrate that treatment with the BET protein bromodomain antagonist (BA) JQ1 attenuates MYC and CDK4/6, inhibits the nuclear RelA levels and the expression of NFκB target genes including Bruton’s Tyrosine Kinase (BTK) in MCL cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
6 Samples
Download data: CEL
Series
Accession:
GSE70651
ID:
200070651
8.

BET Inhibition Enhances TNF Mediated Anti-Tumor Immunity

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
41 Samples
Download data: BW
Series
Accession:
GSE184592
ID:
200184592
9.

Syngergistic Effect of JQ1 and Rapamycin for Treatment of Human Osteosarcoma

(Submitter supplied) Bromodomain and extra terminal domain (BET) proteins are important epigenetic regulators facilitating the transcription of genes in chromatin areas linked to acetylated histones. JQ1, a BET protein inhibitor, has antiproliferative activity against many cancers, mainly through inhibition of c-MYC and upregulation of p21. In this research, we investigated the use of JQ1 for human osteosarcoma (OS) treatment. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
8 Samples
Download data: TXT
Series
Accession:
GSE57203
ID:
200057203
10.

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
11.

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
12.

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
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.

BET-Bromodomain Inhibitors Engage The Host Immune System And Regulate Expression Of The Immune Checkpoint Ligand PD-L1

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL16791 GPL17021 GPL19057
53 Samples
Download data: TXT
Series
Accession:
GSE94134
ID:
200094134
15.

BET-Bromodomain Inhibitors Engage The Host Immune System And Regulate Expression Of The Immune Checkpoint Ligand PD-L1 [EuMyc_RNA-seq]

(Submitter supplied) BET inhibitors (BETi) target bromodomain-containing proteins and are currently being evaluated as anti-cancer agents. We discovered that the maximal therapeutic effects of BETi in a Myc-driven B cell lymphoma model required an intact host immune system. Genome-wide analysis of the BETi induced transcriptional response identified the immune checkpoint ligand Cd274 (Pd-l1) as a Myc-independent, BETi target-gene. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
8 Samples
Download data: TXT
Series
Accession:
GSE94133
ID:
200094133
16.

BET-Bromodomain Inhibitors Engage The Host Immune System And Regulate Expression Of The Immune Checkpoint Ligand PD-L1 [EuMyc_ChIP-seq]

(Submitter supplied) BET inhibitors (BETi) target bromodomain-containing proteins and are currently being evaluated as anti-cancer agents. We discovered that the maximal therapeutic effects of BETi in a Myc-driven B cell lymphoma model required an intact host immune system. Genome-wide analysis of the BETi induced transcriptional response identified the immune checkpoint ligand Cd274 (Pd-l1) as a Myc-independent, BETi target-gene. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL19057 GPL17021
29 Samples
Download data: TXT
Series
Accession:
GSE94130
ID:
200094130
17.

BET-Bromodomain Inhibitors Engage The Host Immune System And Regulate Expression Of The Immune Checkpoint Ligand PD-L1 [3mRNA-seq]

(Submitter supplied) BET inhibitors (BETi) target bromodomain-containing proteins and are currently being evaluated as anti-cancer agents. We discovered that the maximal therapeutic effects of BETi in a Myc-driven B cell lymphoma model required an intact host immune system. Genome-wide analysis of the BETi induced transcriptional response identified the immune checkpoint ligand Cd274 (Pd-l1) as a Myc-independent, BETi target-gene. more...
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL16791 GPL17021
16 Samples
Download data: TXT
Series
Accession:
GSE94057
ID:
200094057
18.

JQ1 treatment of germ cell cancer cells induces differentiation, apoptosis and cell cycle arrest

(Submitter supplied) Type II testicular germ cell cancers (GCC) are the most frequently diagnosed tumors in young men (20 - 40 years) and are classified as seminoma or non-seminoma. GCCs are commonly treated by orchiectomy and chemo- or radiotherapy. However, a subset of metastatic non-seminomas display only incomplete remission or relapse and require novel treatment options. Recent studies have shown effective application of the small-molecule inhibitor JQ1 in tumor therapy, which interferes with the function of bromodomain and extra-terminal (BET)-proteins. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
16 Samples
Download data: TXT
Series
Accession:
GSE87477
ID:
200087477
19.

Treatment of primary effusion lymphoma cell lines with lenalidomide

(Submitter supplied) Technical replicates from BC3 and BCBL1 cell lines were treated with DMSO or 5 micromoles of lenalidomide for 24 hours. NOTE: Detection p-values were neither computed nor used in this experiment. All data was processed directly from IDATs and the proportion of present probes estimated from the negative and positive controls.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
8 Samples
Download data: IDAT, TXT
Series
Accession:
GSE60618
ID:
200060618
20.

BET protein proteolysis targeting chimera (PROTAC) exerts potent lethal activity against Mantle Cell Lymphoma cells

(Submitter supplied) Bromodomain extraterminal protein (BETP) inhibitors transcriptionally repress oncoproteins and NFkB target genes, which undermines the growth and survival of MCL cells. However, BETi treatment causes accumulation of BETPs, associated with reversible binding and incomplete inhibition of BRD4, which potentially compromises the activity of BETi in MCL cells. Unlike BETi, BET-PROTACs (proteolysis-targeting chimera) ARV-825 and ARV-771 (Arvinas, Inc.) recruit and utilize an E3-ubiquitin ligase to effectively degrade BETPs in MCL cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL9115
12 Samples
Download data: XLS
Series
Accession:
GSE98268
ID:
200098268
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