U.S. flag

An official website of the United States government

Format
Items per page
Sort by

Send to:

Choose Destination

Links from GEO DataSets

Items: 20

1.

PRC2 loss amplifies Ras-driven transcription and confers sensitivity to BRD4-based therapies

(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
15 Samples
Download data: CEL, TXT
Series
Accession:
GSE52777
ID:
200052777
2.

PRC2 loss amplifies Ras-driven transcription and confers sensitivity to BRD4-based therapies [expression array]

(Submitter supplied) The polycomb repressive complex 2 (PRC2) exerts oncogenic effects in many tumour types1. However, loss-of-function mutations in PRC2 components occur in a subset of haematopoietic malignancies, sug- gesting that this complex plays a dichotomous and poorly understood role in cancer2,3. Here we provide genomic, cellular, and mouse mod- elling data demonstrating that the polycomb group gene SUZ12 func- tions as tumour suppressor in PNS tumours, high-grade gliomas and melanomas by cooperating with mutations in NF1. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
9 Samples
Download data: CEL
Series
Accession:
GSE62500
ID:
200062500
3.

PRC2 loss amplifies Ras-driven transcription and confers sensitivity to BRD4-based therapies [ChIP-seq]

(Submitter supplied) The polycomb repressive complex 2 (PRC2) exerts oncogenic effects in many tumour types1. However, loss-of-function mutations in PRC2 components occur in a subset of haematopoietic malignancies, suggesting that this complex plays a dichotomous and poorly understood role in cancer2,3. Here we provide genomic, cellular, and mouse mod- elling data demonstrating that the polycomb group gene SUZ12 func- tions as tumour suppressor in PNS tumours, high-grade gliomas and melanomas by cooperating with mutations in NF1. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
6 Samples
Download data: TXT
Series
Accession:
GSE62499
ID:
200062499
4.

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
5.

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:
GPL11154 GPL18573
28 Samples
Download data: TXT
6.

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
7.

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
8.

Zebrafish Samples for Loss of ATRX cooperates with p53-Deficiency to promote the Development of Sarcomas and other Malignancies

(Submitter supplied) The SWI/SNF-family chromatin remodeling protein ATRX is a tumor suppressor in sarcomas, gliomas and other malignancies. Its loss of function facilitates the alternative lengthening of telomeres (ALT) pathway in tumor cells, while it also affects Polycomb repressive complex 2 (PRC2) silencing of its target genes. To further define the role of inactivating ATRX mutations in carcinogenesis, we knocked out atrx in our previously published p53/nf1-deficient zebrafish line that develops malignant peripheral nerve sheath tumors and gliomas. more...
Organism:
Danio rerio
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20828
10 Samples
Download data: FPKM_TRACKING, TXT
Series
Accession:
GSE125040
ID:
200125040
9.

Epigenomic reprogramming due to PRC2 functional loss induces an aggressive de-differentiated neural crest-like phenotype in MPNST

(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
Platforms:
GPL20301 GPL11154
126 Samples
Download data: BED, BROADPEAK, BW, TAB
Series
Accession:
GSE141439
ID:
200141439
10.

RNA-seq dataset for MPNST patient tissue samples

(Submitter supplied) Comprehensive transcriptomic profiling of PRC2 mutant MPNST patient tissues with adjacent normal tissues and neurofibroma patient tissues was performed to investigate gain of specific transcriptional signature associated with PRC2 loss during transformation to MPNST.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
17 Samples
Download data: TAB, TXT
Series
Accession:
GSE141438
ID:
200141438
11.

RNA-seq dataset for MPNST cell lines

(Submitter supplied) Comprehensive transcriptomic profiling of PRC2 mutant and WT MPNST cell lines were performed to investigate PRC2-dependent transcriptional programs that are activated due to PRC2 loss
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
39 Samples
Download data: TAB, TXT
Series
Accession:
GSE141437
ID:
200141437
12.

ChIP-seq dataset for epigenomic landscape of MPNST

(Submitter supplied) In order to comprehensively define the epigenetic patterns specific to MPNST, we generated profiles for 6 histone modification marks, including H3K4me1 (enhancer), H3K27Ac (active enhancer), H3K9me3 (heterochromatin), H3K27me3 (polycomb repression), H3K79me2 (transcription) and H3K4me3 (promoter). Systematic epigenomic profiling of chromatin states in MPNST cells revealed epigenetic subtypes in MPNST based on Polycomb related repressive and bivalent chromatin states. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
70 Samples
Download data: BED, BROADPEAK, BW
Series
Accession:
GSE141435
ID:
200141435
13.

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
14.

Transcriptional dependencies in diffuse intrinsic pontine glioma

(Submitter supplied) Diffuse intrinsic pontine glioma (DIPG) is a fatal pediatric brain tumor with limited therapeutic options. The majority of cases of DIPG exhibit a mutation in histone 3 (H3K27M) that results in oncogenic transcriptional aberrancies. We show here that DIPG is vulnerable to transcriptional disruption using either bromodomain inhibition or CDK7 blockade. We observe that targeting oncogenic transcription through either of these methods synergizes with HDAC inhibition and that DIPG cells resistant to HDAC inhibitor therapy retain sensitivity to CDK7 blockade. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL18573 GPL20301
26 Samples
Download data: BW, TXT
15.

Heterotypic nucleosomes and PRC2 drive DIPG oncogenesis

(Submitter supplied) Diffuse intrinsic pontine gliomas (DIPG) are characterized by a heterozygous lysine-to-methionine mutation of histone H3 (H3K27M) that potently reduces Polycomb Repressive Complex 2 (PRC2) methylation of wild-type histone H3K27 (H3K27wt). The role of H3K27M and reduced H3K27wt methylation in DIPG pathogenesis has yet to be determined. Here, we have performed epigenomic profiling of patient-derived H3K27M mutant DIPG cells and demonstrate that H3K27M resides in nucleosomes with H3K27wt acetylation (H3K27ac), and H3K27M-H3K27ac containing nucleosomes co-localize with bromodomain proteins at actively transcribed genes and that PRC2 is excluded from H3K27M occupied regions. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
100 Samples
Download data: BW
16.

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
17.

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
18.

Dynamic chromatin targeting of BRD4 stimulates cardiac fibroblast activation [RNA-seq_Mm]

(Submitter supplied) Small molecule inhibitors of the acetyl-histone binding protein BRD4 have been shown to block cardiac fibrosis in pre-clinical models of heart failure (HF). However, the mechanisms by which BRD4 promotes pathological myocardial fibrosis remain unclear. Here, we demonstrate that BRD4 functions as an effector of TGF-b signaling to stimulate conversion of quiescent cardiac fibroblasts into Periostin (Postn)-positive cells that express high levels of extracellular matrix. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
10 Samples
Download data: TXT, XLS
Series
Accession:
GSE129265
ID:
200129265
19.

Dynamic chromatin targeting of BRD4 stimulates cardiac fibroblast activation

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus; Rattus norvegicus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18694 GPL21103 GPL14844
25 Samples
Download data: BED, WIG
Series
Accession:
GSE127230
ID:
200127230
20.

Dynamic chromatin targeting of BRD4 stimulates cardiac fibroblast activation [RNA-seq]

(Submitter supplied) Small molecule inhibitors of the acetyl-histone binding protein BRD4 have been shown to block cardiac fibrosis in pre-clinical models of heart failure (HF). However, the mechanisms by which BRD4 promotes pathological myocardial fibrosis remain unclear. Here, we demonstrate that BRD4 functions as an effector of TGF-b signaling to stimulate conversion of quiescent cardiac fibroblasts into Periostin (Postn)-positive cells that express high levels of extracellular matrix. more...
Organism:
Rattus norvegicus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18694
9 Samples
Download data: TXT
Series
Accession:
GSE127229
ID:
200127229
Format
Items per page
Sort by

Send to:

Choose Destination

Supplemental Content

db=gds|term=|query=17|qty=5|blobid=MCID_67266d1ee8de71654a36fc26|ismultiple=true|min_list=5|max_list=20|def_tree=20|def_list=|def_view=|url=/Taxonomy/backend/subset.cgi?|trace_url=/stat?
   Taxonomic Groups  [List]
Tree placeholder
    Top Organisms  [Tree]

Find related data

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Support Center