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Links from GEO DataSets

Items: 20

1.

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
2.

iBET resistance

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array; Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL13112 GPL6887
35 Samples
Download data: BED
Series
Accession:
GSE63683
ID:
200063683
3.

ChIP of BET proteins in iBET resistance [ChIP-seq]

(Submitter supplied) Bromodomain and Extra Terminal protein (BET) inhibitors are first-in-class targeted therapies that deliver a new therapeutic paradigm by directly targeting epigenetic readers1,2. Early clinical trials have shown significant promise especially in acute myeloid leukaemia (AML)3; therefore the evaluation of resistance mechanisms, an inevitable consequence of cancer therapies, is of utmost importance to optimise the clinical efficacy of these drugs. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
15 Samples
Download data: BED, TXT
Series
Accession:
GSE63682
ID:
200063682
4.

Genome wide expression analysis of BET inhibitor resistance [RNA-seq]

(Submitter supplied) Bromodomain and Extra Terminal protein (BET) inhibitors are first-in-class targeted therapies that deliver a new therapeutic paradigm by directly targeting epigenetic readers1,2. Early clinical trials have shown significant promise especially in acute myeloid leukaemia (AML)3; therefore the evaluation of resistance mechanisms, an inevitable consequence of cancer therapies, is of utmost importance to optimise the clinical efficacy of these drugs. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
6 Samples
Download data: TXT
Series
Accession:
GSE63681
ID:
200063681
5.

Genome wide expression analysis of BET inhibitor resistance

(Submitter supplied) Bromodomain and Extra Terminal protein (BET) inhibitors are first-in-class targeted therapies that deliver a new therapeutic paradigm by directly targeting epigenetic readers. Early clinical trials have shown significant promise especially in acute myeloid leukaemia (AML)3; therefore the evaluation of resistance mechanisms, an inevitable consequence of cancer therapies, is of utmost importance to optimise the clinical efficacy of these drugs. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6887
14 Samples
Download data: TXT
Series
Accession:
GSE63575
ID:
200063575
6.

Response and resistance to BET bromodomain inhibitors in triple negative breast cancer

(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
Platforms:
GPL11154 GPL18573
65 Samples
Download data: WIG
Series
Accession:
GSE63584
ID:
200063584
7.

Response and resistance to BET bromodomain inhibitors in triple negative breast cancer [RNA-Seq]

(Submitter supplied) Triple negative breast cancer (TNBC) is a heterogeneous and clinically aggressive disease for which there is no targeted therapy. Here we report the preferential and high sensitivity of TNBCs to BET bromodomain inhibitors such as JQ1 manifested by cell cycle arrest in early G1, apoptosis, and induction of markers of luminal epithelial differentiation in vitro and in vivo. The sensitivity of TNBC and other tumor types to BET inhibition establishes a rationale for clinical investigation, and a motivation to understand mechanisms of resistance. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL18573 GPL11154
28 Samples
Download data: TXT
8.

Response and resistance to BET bromodomain inhibitors in triple negative breast cancer [ChIP-Seq]

(Submitter supplied) Triple negative breast cancer (TNBC) is a heterogeneous and clinically aggressive disease for which there is no targeted therapy. Here we report the preferential and high sensitivity of TNBCs to BET bromodomain inhibitors such as JQ1 manifested by cell cycle arrest in early G1, apoptosis, and induction of markers of luminal epithelial differentiation in vitro and in vivo. The sensitivity of TNBC and other tumor types to BET inhibition establishes a rationale for clinical investigation, and a motivation to understand mechanisms of resistance. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL11154 GPL18573
35 Samples
Download data: WIG
Series
Accession:
GSE63581
ID:
200063581
9.

Response and resistance to BET bromodomain inhibitors in triple negative breast cancer [Chem-Seq]

(Submitter supplied) Triple negative breast cancer (TNBC) is a heterogeneous and clinically aggressive disease for which there is no targeted therapy. Here we report the preferential and high sensitivity of TNBCs to BET bromodomain inhibitors such as JQ1 manifested by cell cycle arrest in early G1, apoptosis, and induction of markers of luminal epithelial differentiation in vitro and in vivo. The sensitivity of TNBC and other tumor types to BET inhibition establishes a rationale for clinical investigation, and a motivation to understand mechanisms of resistance. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
2 Samples
Download data: WIG
Series
Accession:
GSE63284
ID:
200063284
10.

RNAi screen identifies Brd4 as a therapeutic target in acute myeloid leukemia

(Submitter supplied) Epigenetic pathways regulate gene expression by controlling and interpreting chromatin modifications. Cancer cells are characterized by altered epigenetic landscapes and commonly exploit the chromatin regulatory machinery to enforce oncogenic gene expression programs. While chromatin alterations are, in principle, reversible and often amendable to drug intervention, the promise of targeting such pathways therapeutically has been hampered by our limited understanding of cancer-specific epigenetic dependencies. more...
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by array
Platforms:
GPL6244 GPL6246
30 Samples
Download data: CEL
Series
Accession:
GSE29799
ID:
200029799
11.

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:
GPL11154 GPL6244
28 Samples
Download data: BED, CEL, XLS
Series
Accession:
GSE76192
ID:
200076192
12.

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
13.

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
14.

BET Bromodomain Inhibition Blocks the Function of a Critical AR-Independent Master Regulator Network in Lethal Prostate Cancer

(Submitter supplied) BET bromodomain inhibitors are known to block prostate cancer cell survival through suppression of c-Myc and androgen receptor (AR) function. However, little is known about other transcriptional modulators whose function is blocked by these drugs and the anti-tumor activity of BET bromodomain inhibition in AR-independent castration-resistant prostate cancers (CRPC), whose frequency may be increasing. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
34 Samples
Download data: BED, TXT
15.

High Resolution Mapping of RNA Polymerases Identifies Mechanisms of Sensitivity and Resistance to BET Inhibitors in t(8;21) AML

(Submitter supplied) Bromodomain and extra-terminal domain (BET) family inhibitors offer a new approach to treating hematological malignancies. We used precision nuclear run-on transcription sequencing (PRO-seq) to create high-resolution maps of active RNA polymerases across the genome in t(8;21) acute myeloid leukemia (AML) that are exceptionally sensitive to BET inhibitors. PRO-seq identified over 1400 genes showing impaired release of promoter-proximal paused RNA polymerases, including the stem cell factor receptor tyrosine kinase KIT that is mutated in t(8;21) AML. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Other
Platforms:
GPL11154 GPL18573
22 Samples
Download data: BEDGRAPH, TXT
16.

BET inhibition releases the Mediator complex from specific cis elements in acute myeloid leukemia cells (RNA-Seq II)

(Submitter supplied) Genome occupancy profiling by high throughput sequencing
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
4 Samples
Download data: TXT
Series
Accession:
GSE78224
ID:
200078224
17.

BET inhibition releases the Mediator complex from specific cis elements in acute myeloid leukemia cells (ChIP-Seq II)

(Submitter supplied) Genome occupancy profiling by high throughput sequencing
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
8 Samples
Download data: TXT
Series
Accession:
GSE78221
ID:
200078221
18.

BET inhibition releases the Mediator complex from specific cis elements in acute myeloid leukemia cells

(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:
GPL13112
21 Samples
Download data: BIGWIG, TXT
Series
Accession:
GSE74651
ID:
200074651
19.

BET inhibition releases the Mediator complex from specific cis elements in acute myeloid leukemia cells (RNA-Seq I)

(Submitter supplied) Genome occupancy profiling by high throughput sequencing
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
6 Samples
Download data: TXT
Series
Accession:
GSE74650
ID:
200074650
20.

BET inhibition releases the Mediator complex from specific cis elements in acute myeloid leukemia cells (ChIP-Seq I)

(Submitter supplied) Genome occupancy profiling by high throughput sequencing
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
9 Samples
Download data: BIGWIG
Series
Accession:
GSE74536
ID:
200074536
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