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Links from GEO DataSets

Items: 20

1.

Transcriptional Amplification in Tumor Cells with Elevated c-Myc

(Submitter supplied) Excessive expression of c-Myc occurs frequently in human cancers, where high levels are associated with tumor aggression and poor clinical outcome, but the effect of high levels of c-Myc on global gene regulation is poorly understood. We report here that in tumor cells expressing high levels of c-Myc, the transcription factor binds to E-box sequences in the core promoters of most actively transcribed genes and, unexpectedly, the enhancers of these active genes. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
56 Samples
Download data: WIG, YLF
Series
Accession:
GSE36354
ID:
200036354
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:
GPL11154 GPL6244
28 Samples
Download data: BED, CEL, XLS
Series
Accession:
GSE76192
ID:
200076192
3.

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
4.

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
5.

Chromosome loop control of oncogenic MYC produces a common vulnerability in diverse cancers [HiChIP]

(Submitter supplied) The majority of human cancers become highly dependent on a deregulated MYC oncogene, thus identifying a common mechanism underlying MYC regulation could provide valuable targets for therapy. We show here that diverse tumor-specific super-enhancers acquired throughout the 3Mb MYC insulated neighborhood functionally interact with a single conserved site occupied by CTCF protein in the MYC promoter. CRISPR-mediated deletion analysis shows that this common CTCF site is required for super-enhancer looping to the MYC promoter, high MYC expression and rapid cell proliferation in multiple cancers. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
1 Sample
Download data: BEDPE
Series
Accession:
GSE112000
ID:
200112000
6.

Chromosome loop control of oncogenic MYC produces a common vulnerability in diverse cancers

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Other
Platform:
GPL11154
24 Samples
Download data: BEDPE, WIG
Series
Accession:
GSE92881
ID:
200092881
7.

Chromosome loop control of oncogenic MYC produces a common vulnerability in diverse cancers [4C-seq]

(Submitter supplied) The majority of human cancers become highly dependent on a deregulated MYC oncogene, thus identifying a common mechanism underlying MYC regulation could provide valuable targets for therapy. We show here that diverse tumor-specific super-enhancers acquired throughout the 3Mb MYC insulated neighborhood functionally interact with a single conserved site occupied by CTCF protein in the MYC promoter. CRISPR-mediated deletion analysis shows that this common CTCF site is required for super-enhancer looping to the MYC promoter, high MYC expression and rapid cell proliferation in multiple cancers. more...
Organism:
Homo sapiens
Type:
Other
Platform:
GPL11154
18 Samples
Download data: WIG
Series
Accession:
GSE92880
ID:
200092880
8.

Chromosome loop control of oncogenic MYC produces a common vulnerability in diverse cancers [ChIP-seq]

(Submitter supplied) The majority of human cancers become highly dependent on a deregulated MYC oncogene, thus identifying a common mechanism underlying MYC regulation could provide valuable targets for therapy. We show here that diverse tumor-specific super-enhancers acquired throughout the 3Mb MYC insulated neighborhood functionally interact with a single conserved site occupied by CTCF protein in the MYC promoter. CRISPR-mediated deletion analysis shows that this common CTCF site is required for super-enhancer looping to the MYC promoter, high MYC expression and rapid cell proliferation in multiple cancers. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
5 Samples
Download data: WIG
Series
Accession:
GSE92879
ID:
200092879
9.

Menin Enhances c-Myc-mediated Transcriptional Activity To Promote Cancer Progression

(Submitter supplied) MYC is a master regulator of transcription in growing cells. Menin is an enigmatic protein that displays unique ability to either suppress or promote tumorigenesis in a context dependent manner. It's interesting to ask is there any relationship between MYC and menin.Here, we used RNA-seq to study global transcriptomic expression of MYC or MEN1 knockdown HT1080 cells to investigate whether there are any correlations between MYC- and menin- regulated gene expression. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL16791 GPL20301
9 Samples
Download data: BED, XLSX
10.

VDR/RXR and TCF4/beta-Catenin Cistromes in Colonic Cells of Colorectal Tumor Origin: Impact on c-FOS and c-MYC Gene Expression

(Submitter supplied) Many of the transcriptional and growth regulating activities of 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3) in the intestine and colon are recapitulated in the human colorectal cancer cell LS180. We therefore used this line together with ChIP-seq and gene expression analyses to identify the vitamin D receptor (VDR)/retinoid x receptor (RXR) and TCF7L2(TCF4)/β-catenin cistromes and the genes that they regulate. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by array
Platforms:
GPL10999 GPL11219
19 Samples
Download data: BED, CALLS, PAIR, TIFF, TXT
11.

Myc activation coordinates gene transcription and protein translation responses

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Other
Platform:
GPL11154
20 Samples
Download data
Series
Accession:
GSE66929
ID:
200066929
12.

GRO-seq analysis of control and Myc-induced U2OS cells

(Submitter supplied) We used GRO-seq to examine the effect of Myc activation on RNA transcription in U2OS cells.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Other
Platform:
GPL11154
4 Samples
Download data: TXT
13.

Ribo_seq (aka ribosome profiling) analysis of control and Myc-induced U2OS cells

(Submitter supplied) We used Ribo-seq to examine the effect of Myc activation on protein translation in U2OS cells and correalted these changes with alterations in RNA level measured by RNA-seq on tye same conditions. We also examined these effects in the presence of Torin-1, an inhibitor of mTOR
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Other
Platform:
GPL11154
10 Samples
Download data: TXT
Series
Accession:
GSE66927
ID:
200066927
14.

RNA-seq analysis of control and Myc-induced U2OS cells

(Submitter supplied) We used RNA-seq to examine the effect of Myc activation on U2OS cells transcriptome. We also examined these effects in the presence of Torin-1, an inhibitor of mTOR
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
6 Samples
Download data: TXT
15.

c-MYC drives a subset of high-risk pediatric neuroblastomas and is activated through mechanisms including enhancer hijacking and focal enhancer amplification [RNA-seq]

(Submitter supplied) Childhood neuroblastoma is known for MYCN gene amplification, and here we show that in a separate subset of cases MYC-itself is activated due to enhancer hijacking from chromosomal translocations or duplications, thus defining a unique subset of high-risk disease.
Organism:
Danio rerio
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20828
12 Samples
Download data: TXT
Series
Accession:
GSE107518
ID:
200107518
16.

c-MYC drives a subset of high-risk pediatric neuroblastomas and is activated through mechanisms including enhancer hijacking and focal enhancer amplification

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Danio rerio; Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL20828 GPL18573
27 Samples
Download data: TXT, WIG
Series
Accession:
GSE101297
ID:
200101297
17.

c-MYC drives a subset of high-risk pediatric neuroblastomas and is activated through mechanisms including enhancer hijacking and focal enhancer amplification (ChIP-Seq)

(Submitter supplied) Childhood neuroblastoma is known for MYCN gene amplification, and here we show that in a separate subset of cases MYC-itself is activated due to enhancer hijacking from chromosomal translocations or duplications, thus defining a unique subset of high-risk disease.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
12 Samples
Download data: WIG
Series
Accession:
GSE101295
ID:
200101295
18.

c-MYC drives a subset of high-risk pediatric neuroblastomas and is activated through mechanisms including enhancer hijacking and focal enhancer amplification (ATAC-Seq)

(Submitter supplied) Childhood neuroblastoma is known for MYCN gene amplification, and here we show that in a separate subset of cases MYC-itself is activated due to enhancer hijacking from chromosomal translocations or duplications, thus defining a unique subset of high-risk disease.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
3 Samples
Download data: WIG
Series
Accession:
GSE101294
ID:
200101294
19.

An early Myc-dependent transcriptional program underlies enhanced macromolecular biosynthesis and cell growth during B-cell activation

(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
49 Samples
Download data: BED
Series
Accession:
GSE126340
ID:
200126340
20.

An early Myc-dependent transcriptional program underlies enhanced macromolecular biosynthesis and cell growth during B-cell activation [ChIP-seq]

(Submitter supplied) Upon activation, lymphocytes exit quiescence and undergo substantial increases in cell size and RNA content. A key regulator in this process is the Myc transcription factor, which is directly induced by activating signals and is required for multiple facets of cell activation, including metabolic reprogramming, chromatin decompaction, RNA and protein accumulation, cell growth and proliferation. However, how Myc activity impacts on those diverse cellular processes remains unclear. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
13 Samples
Download data: BED
Series
Accession:
GSE126339
ID:
200126339
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