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Links from GEO DataSets

Items: 20

1.

ChIPSeq data from melanoma cancer cell line CHL-1 after Bromodomain and extra terminal (Bet) domain inhibitor treatment

(Submitter supplied) Bromodomain and extra terminal domain (BET) inhibition reduces occupancy of BET-family proteins at promoter and enhancer sites finally leading to genome wide changes in gene transcription. We used ChIPSeq profiling to investigate genome wide changes in promoter and enhancer occupancy induced by BET inhibitors BAY 1238097 and OTX-015, respectively.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
18 Samples
Download data: BW
Series
Accession:
GSE95585
ID:
200095585
2.

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
3.

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
Series
Accession:
GSE63582
ID:
200063582
4.

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
5.

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
6.

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
7.

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
8.

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:
GPL11154 GPL16043
31 Samples
Download data: CEL, WIG
Series
Accession:
GSE44931
ID:
200044931
9.

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
10.

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
11.

Defining the Triple Negative Breast Cancer Kinome Response to GSK1120212 (RNA-Seq)

(Submitter supplied) LCCC1122 is a window trial in stage I-IV TNBC patients scheduled to undergo definitive surgery (either lumpectomy, mastectomy or surgical resection of oligometastatic disease). Enrolled patients will receive 1.5 -2.0 mg of the MEK1/MEK2 inhibitor GSK1120212 (trametinib; Mekinist®) orally once daily for 7 days (with treatment initiation dependent on surgical schedule) prior to their surgery, with pre- and post- treatment tissue analyzed for kinome response and resistant signatures. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
28 Samples
Download data: TXT
Series
Accession:
GSE107502
ID:
200107502
12.

Enhancer Remodeling During Adaptive Bypass to MEK Inhibition Is Attenuated by Pharmacological Targeting of the P-TEFb Complex

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Methylation profiling by genome tiling array; Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing; Genome variation profiling by high throughput sequencing
5 related Platforms
167 Samples
Download data: BED, CSV, IDAT, TXT, XLSX
Series
Accession:
GSE87424
ID:
200087424
13.

Enhancer Remodeling During Adaptive Bypass to MEK Inhibition Is Attenuated by Pharmacological Targeting of the P-TEFb Complex (Exome-seq)

(Submitter supplied) Targeting the dysregulated BRaf-MEK-ERK pathway in cancer has increasingly emerged in clinical trial design. Despite clinical responses in specific cancers using inhibitors targeting BRaf and MEK, resistance develops often involving non-genomic adaptive bypass mechanisms. Inhibition of MEK1/2 by trametinib in triple negative breast cancer (TNBC) patients induced dramatic transcriptional responses, including upregulation of receptor tyrosine kinases (RTKs) comparing tumor samples before and after one week of treatment. more...
Organism:
Homo sapiens
Type:
Genome variation profiling by high throughput sequencing
Platform:
GPL16791
2 Samples
Download data: XLSX
Series
Accession:
GSE87423
ID:
200087423
14.

Enhancer Remodeling During Adaptive Bypass to MEK Inhibition Is Attenuated by Pharmacological Targeting of the P-TEFb Complex (RNA-seq)

(Submitter supplied) Targeting the dysregulated BRaf-MEK-ERK pathway in cancer has increasingly emerged in clinical trial design. Despite clinical responses in specific cancers using inhibitors targeting BRaf and MEK, resistance develops often involving non-genomic adaptive bypass mechanisms. Inhibition of MEK1/2 by trametinib in triple negative breast cancer (TNBC) patients induced dramatic transcriptional responses, including upregulation of receptor tyrosine kinases (RTKs) comparing tumor samples before and after one week of treatment. more...
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL13112 GPL11154 GPL18573
64 Samples
Download data: CSV, TXT, XLSX
Series
Accession:
GSE87419
ID:
200087419
15.

Enhancer Remodeling During Adaptive Bypass to MEK Inhibition Is Attenuated by Pharmacological Targeting of the P-TEFb Complex (ChIP-seq)

(Submitter supplied) Targeting the dysregulated BRaf-MEK-ERK pathway in cancer has increasingly emerged in clinical trial design. Despite clinical responses in specific cancers using inhibitors targeting BRaf and MEK, resistance develops often involving non-genomic adaptive bypass mechanisms. Inhibition of MEK1/2 by trametinib in triple negative breast cancer (TNBC) patients induced dramatic transcriptional responses, including upregulation of receptor tyrosine kinases (RTKs) comparing tumor samples before and after one week of treatment. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18573 GPL11154
61 Samples
Download data: BED, XLSX
Series
Accession:
GSE87418
ID:
200087418
16.

Enhancer Remodeling During Adaptive Bypass to MEK Inhibition Is Attenuated by Pharmacological Targeting of the P-TEFb Complex (DNA methylation)

(Submitter supplied) Targeting the dysregulated BRaf-MEK-ERK pathway in cancer has increasingly emerged in clinical trial design. Despite clinical responses in specific cancers using inhibitors targeting BRaf and MEK, resistance develops often involving non-genomic adaptive bypass mechanisms. Inhibition of MEK1/2 by trametinib in triple negative breast cancer (TNBC) patients induced dramatic transcriptional responses, including upregulation of receptor tyrosine kinases (RTKs) comparing tumor samples before and after one week of treatment. more...
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL13534
12 Samples
Download data: CSV, IDAT
Series
Accession:
GSE87154
ID:
200087154
17.

Enhancer Remodeling during Adaptive Bypass to MEK Inhibition Is Attenuated by Pharmacologic Targeting of the P-TEFb Complex

(Submitter supplied) Triple negative breast cancer (TNBC) is heterogeneous with patients exhibiting at least two molecular subtypes, basal-like (BL) and claudin-low (CL). MEK inhibitor (MEKi) treatment of BL and CL cell lines and mouse model tumors induced subtype-specific alterations in overall kinome activity referred to as protein kinase reprogramming. BL- and CL-specific reprogramming involving increases in receptor tyrosine kinases was also seen in TNBC patients comparing tumor samples before and after a one week treatment with the MEKi, trametinib. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10481
10 Samples
Download data
Series
Accession:
GSE50550
ID:
200050550
18.

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
19.

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
20.

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
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