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Links from GEO DataSets

Items: 20

1.

Enhancer invasion shapes MYCN dependent transcriptional amplification in neuroblastoma [ChIP-seq]

(Submitter supplied) In neuroblastoma, amplification of the oncogenic basic helix-loop-helix (bHLH) transcription factor (TF) MYCN is the defining prognosticator of high-risk disease, occurs in one-third of neuroblastoma, and drastically reduces overall survival rates. As a proto-oncogene, targeted MYCN overexpression in peripheral neural crest is sufficient to initiate disease in mouse models. In MYCN amplified neuroblastoma, elevated expression of the factor is crucial to maintain tumor stemness and is associated with increased proliferation and aberrant cell cycle progression, as these tumors lack the ability to arrest in G1 in response to irradiation. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18573 GPL11154
40 Samples
Download data: WIG, XLS
Series
Accession:
GSE80151
ID:
200080151
2.

Enhancer invasion shapes MYCN dependent transcriptional amplification in neuroblastoma [ChIP-seq Th-MYCN]

(Submitter supplied) In neuroblastoma, amplification of the oncogenic basic helix-loop-helix (bHLH) transcription factor (TF) MYCN is the defining prognosticator of high-risk disease, occurs in one-third of neuroblastoma, and drastically reduces overall survival rates. As a proto-oncogene, targeted MYCN overexpression in peripheral neural crest is sufficient to initiate disease in mouse models. In MYCN amplified neuroblastoma, elevated expression of the factor is crucial to maintain tumor stemness and is associated with increased proliferation and aberrant cell cycle progression, as these tumors lack the ability to arrest in G1 in response to irradiation. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
14 Samples
Download data: WIG
Series
Accession:
GSE100538
ID:
200100538
3.

Enhancer invasion shapes MYCN dependent transcriptional amplification in neuroblastoma

(Submitter supplied) Amplification of the locus encoding the oncogenic transcription factor MYCN is a defining feature of high-risk neuroblastoma. Here we present the first dynamic chromatin and transcriptional landscape of MYCN perturbation in neuroblastoma. At oncogenic levels, MYCN associates with E-box binding motifs in an affinity-dependent manner, binding to strong canonical E-boxes at promoters and invading abundant weaker non-canonical E-boxes clustered at enhancers. more...
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing; Other; Expression profiling by high throughput sequencing
4 related Platforms
144 Samples
Download data: BEDGRAPH, CEL, WIG
Series
Accession:
GSE80154
ID:
200080154
4.

Enhancer invasion shapes MYCN dependent transcriptional amplification in neuroblastoma [RNA-seq]

(Submitter supplied) In neuroblastoma, amplification of the oncogenic basic helix-loop-helix (bHLH) transcription factor (TF) MYCN is the defining prognosticator of high-risk disease, occurs in one-third of neuroblastoma, and drastically reduces overall survival rates1,2. As a proto-oncogene, targeted MYCN overexpression in peripheral neural crest is sufficient to initiate disease in mouse models3. In MYCN amplified neuroblastoma, elevated expression of the factor is crucial to maintain tumor stemness4,5 and is associated with increased proliferation and aberrant cell cycle progression, as these tumors lack the ability to arrest in G1 in response to irradiation6-9. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
49 Samples
Download data: TXT
5.

Enhancer invasion shapes MYCN dependent transcriptional amplification in neuroblastoma [ATAC-seq]

(Submitter supplied) In neuroblastoma, amplification of the oncogenic basic helix-loop-helix (bHLH) transcription factor (TF) MYCN is the defining prognosticator of high-risk disease, occurs in one-third of neuroblastoma, and drastically reduces overall survival rates1,2. As a proto-oncogene, targeted MYCN overexpression in peripheral neural crest is sufficient to initiate disease in mouse models3. In MYCN amplified neuroblastoma, elevated expression of the factor is crucial to maintain tumor stemness4,5 and is associated with increased proliferation and aberrant cell cycle progression, as these tumors lack the ability to arrest in G1 in response to irradiation6-9. more...
Organism:
Homo sapiens
Type:
Other
Platform:
GPL18573
5 Samples
Download data: WIG
Series
Accession:
GSE80152
ID:
200080152
6.

Enhancer invasion shapes MYCN dependent transcriptional amplification in neuroblastoma [ChIP_RX]

(Submitter supplied) In neuroblastoma, amplification of the oncogenic basic helix-loop-helix (bHLH) transcription factor (TF) MYCN is the defining prognosticator of high-risk disease, occurs in one-third of neuroblastoma, and drastically reduces overall survival rates. As a proto-oncogene, targeted MYCN overexpression in peripheral neural crest is sufficient to initiate disease in mouse models. In MYCN amplified neuroblastoma, elevated expression of the factor is crucial to maintain tumor stemness and is associated with increased proliferation and aberrant cell cycle progression, as these tumors lack the ability to arrest in G1 in response to irradiation. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
21 Samples
Download data: BEDGRAPH, TXT
Series
Accession:
GSE80150
ID:
200080150
7.

Enhancer invasion shapes MYCN dependent transcriptional amplification in neuroblastoma [ARRAY]

(Submitter supplied) In neuroblastoma, amplification of the oncogenic basic helix-loop-helix (bHLH) transcription factor (TF) MYCN is the defining prognosticator of high-risk disease, occurs in one-third of neuroblastoma, and drastically reduces overall survival rates1,2. As a proto-oncogene, targeted MYCN overexpression in peripheral neural crest is sufficient to initiate disease in mouse models3. In MYCN amplified neuroblastoma, elevated expression of the factor is crucial to maintain tumor stemness4,5 and is associated with increased proliferation and aberrant cell cycle progression, as these tumors lack the ability to arrest in G1 in response to irradiation6-9. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL16043
15 Samples
Download data: CEL
Series
Accession:
GSE80149
ID:
200080149
8.

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
9.

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:
Homo sapiens; Danio rerio
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
10.

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
11.

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
12.

Differential gene expression in neuroblastoma cells after transfection with control siRNA, MYCN siRNA or TFAP4 siRNA.

(Submitter supplied) We analyed the gene expression profiles after knocking down MYCN or TFAP4. Results showed that transcription factor MYCN and TFAP4 commonly regulats a subset of genes that may contribute to neuroblastoma cells proliferation and migration.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
6 Samples
Download data: CEL
Series
Accession:
GSE74626
ID:
200074626
13.

KDM6B promotes activation of the oncogenic CDK4/6-pRB-E2F pathway by maintaining enhancer activity in MYCN-amplified neuroblastoma [CUT&TAG]

(Submitter supplied) The H3K27me2/me3 histone demethylase KDM6B is over-expressed in neuroblastoma and is essential to neuroblastoma cell survival. While the KDM6B inhibitor, GSK-J4, has shown activity in in vitro and in vivo preclinical models, the mechanism of action remains poorly defined. We demonstrate that genetic and pharmacologic inhibition of KDM6B downregulates the pRB-E2F transcriptome and MYCN expression. Chemical genetic analyses show that high expression of the E2F transcriptome is positively correlated with sensitivity of cancer cells to GSK-J4. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
16 Samples
Download data: BED, BW, NARROWPEAK
Series
Accession:
GSE182884
ID:
200182884
14.

Expression data from BE2C cells treated with GSK-J4 and KDM6B knockdown

(Submitter supplied) KDM6B inhibition shows anticancer activity in neuroblastoma models. However, the acting mechanism of KDM6B inhibition remains poorly understood. We used microarray to detail the global programme of gene expression underlying anticancer activity of KDM6B inhibition in neuroblastoma cells.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL23159
8 Samples
Download data: CEL
Series
Accession:
GSE150045
ID:
200150045
15.

KDM6B promotes activation of the oncogenic CDK4/6-pRB-E2F pathway by maintaining enhancer activity in MYCN-amplified neuroblastoma

(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 GPL24676
60 Samples
Download data: BED, BW, NARROWPEAK, TXT
Series
Accession:
GSE149539
ID:
200149539
16.

KDM6B promotes activation of the oncogenic CDK4/6-pRB-E2F pathway by maintaining enhancer activity in MYCN-amplified neuroblastoma [RNA-seq]

(Submitter supplied) The H3K27me2/me3 histone demethylase KDM6B is over-expressed in neuroblastoma and is essential to neuroblastoma cell survival. While the KDM6B inhibitor, GSK-J4, has shown activity in in vitro and in vivo preclinical models, the mechanism of action remains poorly defined. We demonstrate that genetic and pharmacologic inhibition of KDM6B downregulates the pRB-E2F transcriptome and MYCN expression. Chemical genetic analyses show that high expression of the E2F transcriptome is positively correlated with sensitivity of cancer cells to GSK-J4. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
38 Samples
Download data: TXT
17.

KDM6B promotes activation of the oncogenic CDK4/6-pRB-E2F pathway by maintaining enhancer activity in MYCN-amplified neuroblastoma [ATAC-Seq]

(Submitter supplied) The H3K27me2/me3 histone demethylase KDM6B is over-expressed in neuroblastoma and is essential to neuroblastoma cell survival. While the KDM6B inhibitor, GSK-J4, has shown activity in in vitro and in vivo preclinical models, the mechanism of action remains poorly defined. We demonstrate that genetic and pharmacologic inhibition of KDM6B downregulates the pRB-E2F transcriptome and MYCN expression. Chemical genetic analyses show that high expression of the E2F transcriptome is positively correlated with sensitivity of cancer cells to GSK-J4. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
6 Samples
Download data: BW
Series
Accession:
GSE149519
ID:
200149519
18.

Gene expression data from primary neuroblastoma tumors

(Submitter supplied) This dataset contains gene expression data from the NRC series (Neuroblastoma Research Consortium) for a total of 283 primary neuroblastoma tumors. All tumor samples are fully annotated including patient age at diagnosis, overall and progresison free survival and MYCN amplification status, enabling subgroup analysis, survival analysis and gene expression network analysis.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL5175
283 Samples
Download data: CEL
Series
Accession:
GSE85047
ID:
200085047
19.

Network-based, cross-cohort discovery of transcriptional mechanisms presiding over maintenance of high-risk neuroblastoma subtype state

(Submitter supplied) Network-based analysis of neuroblastoma samples from two large cohorts identified master regulator proteins controlling the transcriptional state of three high-risk molecular subtypes. In particular, a TEAD4-MYCN positive feedback loop emerged as the core regulatory motif of a small protein module presiding over implementation and stability of the subtype associated with MYCN amplification. Specifically, MYCN transcriptionally activates TEAD4, which in turn activates MYCN both transcriptionally and post-translationally. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18573 GPL16791
16 Samples
Download data: BED, TXT
20.

IGF2BP1 induces neuroblastoma via a druggable feedforward loop with MYCN promoting 17q oncogene expression [mouse miRNA-Seq]

(Submitter supplied) Chromosome 17q gain is an independent prognostic marker in neuroblastoma, harboring several potential oncogenes including IGF2BP1 and BIRC5. IGF2BP1 was shown to be upregulated in unfavorable neuroblastoma and correlates with poor patient survival. Here, we report that overexpression of IGF2BP1 in a transgenic mouse model induces neuroblastoma with all characteristics known for human neuroblastoma, including MYCN upregulation and genomic aberrations. more...
Organism:
Mus musculus
Type:
Non-coding RNA profiling by high throughput sequencing
Platform:
GPL24247
18 Samples
Download data: CSV
Series
Accession:
GSE221848
ID:
200221848
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