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Items: 1 to 20 of 81

1.

Long noncoding RNA INCA1 regulates tumor interferon signaling [CLIP-seq]

(Submitter supplied) Tumor interferon signaling regulates the expression of immunosuppressive molecules and promotes cancer immune evasion. Although the role of long noncoding RNAs (lncRNAs) in the regulation of gene expression is now emerging, their function in tumor interferon signaling remains unexplored. We have identified the interferon-γ (IFNγ)-stimulated non-coding RNA 1 (INCA1) as a novel lncRNA expressed form the PD-L1 locus. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
4 Samples
Download data: XLSX
Series
Accession:
GSE137526
ID:
200137526
2.

Long noncoding RNA INCA1 regulates tumor interferon signaling.

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL24676 GPL20301
22 Samples
Download data
Series
Accession:
GSE137489
ID:
200137489
3.

Long noncoding RNA INCA1 regulates tumor interferon signaling

(Submitter supplied) Tumor interferon signaling regulates the expression of immunosuppressive molecules and promotes cancer immune evasion. Although the role of long noncoding RNAs (lncRNAs) in the regulation of gene expression is now emerging, their function in tumor interferon signaling remains unexplored. We have identified the interferon-γ (IFNγ)-stimulated non-coding RNA 1 (INCA1) as a novel lncRNA expressed form the PD-L1 locus. more...
Organism:
Homo sapiens
Type:
Non-coding RNA profiling by high throughput sequencing
Platform:
GPL24676
12 Samples
Download data: TXT
Series
Accession:
GSE137454
ID:
200137454
4.

Long noncoding RNA expression profiles analysis in GBM patient-derived cells stimulated with interferon gamma

(Submitter supplied) Long noncoding RNAs (lncRNAs) are key regulators of gene expression both in physiological and pathological conditions. Previous studies showed changes in lncRNA expression during tumorigenesis. To analyze the role of lncRNAs in tumor interferon signaling and cancer-mediated immunosuppression, we used RNA-seq technique to identify lncRNAs that are differentially expressed in GBM patient-derived cells stimulated with interferon gamma compared to unstimulated cells. more...
Organism:
Homo sapiens
Type:
Non-coding RNA profiling by high throughput sequencing
Platform:
GPL20301
6 Samples
Download data: TXT
Series
Accession:
GSE137453
ID:
200137453
5.

Chromatin Folding Domains Disruptions by Somatic Genomic Rearrangements in Human Cancers

(Submitter supplied) Genomic material within the nucleus is folded into successive layers in order to package and organize the long string of linear DNA. This hierarchical level of folding is closely associated with transcriptional regulation and DNA replication. Genes within the same folding domain demonstrate similar expression and histone-modification profiles1. Therefore, boundaries separating different domains have important roles in reinforcing the stability of these domain-wide features. more...
Organism:
Homo sapiens
Type:
Other
Platforms:
GPL20301 GPL18573
6 Samples
Download data: TXT
6.

Treatment-induced tumor dormancy through YAP-mediated transcriptional reprogramming of the apoptotic pathway [scRNASeq]

(Submitter supplied) Eradicating tumor dormancy that develops following oncogene-targeted therapy, including after epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) treatment of EGFR-mutant non-small cell lung cancer (NSCLC), is an attractive therapeutic strategy but the mechanisms governing the establishment of tumor dormancy are poorly understood. We observe that blockade of ERK1/2 reactivation following EGFR TKI treatment by combined EGFR/MEK inhibition uncovers cells that survive by entering a senescence-like dormant state, characterized by extensive epigenetic remodeling and high YAP/TEAD activity. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL11154 GPL18573
5 Samples
Download data: TXT
Series
Accession:
GSE138693
ID:
200138693
7.

Treatment-induced tumor dormancy through YAP-mediated transcriptional reprogramming of the apoptotic pathway [ChIP + ATAC]

(Submitter supplied) Eradicating tumor dormancy that develops following oncogene-targeted therapy, including after epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) treatment of EGFR-mutant non-small cell lung cancer (NSCLC), is an attractive therapeutic strategy but the mechanisms governing the establishment of tumor dormancy are poorly understood. We observe that blockade of ERK1/2 reactivation following EGFR TKI treatment by combined EGFR/MEK inhibition uncovers cells that survive by entering a senescence-like dormant state, characterized by extensive epigenetic remodeling and high YAP/TEAD activity. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
27 Samples
Download data: BW
Series
Accession:
GSE131687
ID:
200131687
8.

Treatment-induced tumor dormancy through YAP-mediated transcriptional reprogramming of the apoptotic pathway

(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:
GPL18573 GPL11154
68 Samples
Download data: BW, TXT
Series
Accession:
GSE131604
ID:
200131604
9.

Treatment-induced tumor dormancy through YAP-mediated transcriptional reprogramming of the apoptotic pathway [YAP1 KO vs CTRL]

(Submitter supplied) Eradicating tumor dormancy that develops following oncogene-targeted therapy, including after epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) treatment of EGFR-mutant non-small cell lung cancer (NSCLC), is an attractive therapeutic strategy but the mechanisms governing the establishment of tumor dormancy are poorly understood. We observe that blockade of ERK1/2 reactivation following EGFR TKI treatment by combined EGFR/MEK inhibition uncovers cells that survive by entering a senescence-like dormant state, characterized by extensive epigenetic remodeling and high YAP/TEAD activity. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
24 Samples
Download data: TXT
Series
Accession:
GSE131601
ID:
200131601
10.

Treatment-induced tumor dormancy through YAP-mediated transcriptional reprogramming of the apoptotic pathway [DMSO vs DORMANT]

(Submitter supplied) Eradicating tumor dormancy that develops following oncogene-targeted therapy, including after epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) treatment of EGFR-mutant non-small cell lung cancer (NSCLC), is an attractive therapeutic strategy but the mechanisms governing the establishment of tumor dormancy are poorly understood. We observe that blockade of ERK1/2 reactivation following EGFR TKI treatment by combined EGFR/MEK inhibition uncovers cells that survive by entering a senescence-like dormant state, characterized by extensive epigenetic remodeling and high YAP/TEAD activity. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
12 Samples
Download data: TXT
Series
Accession:
GSE131594
ID:
200131594
11.

Neuronal differentiation and cell-cycle programs mediate response to BET-bromodomain inhibition in MYC-driven medulloblastoma (ChIP-seq)

(Submitter supplied) BET-bromodomain inhibition (BETi) has shown pre-clinical promise for MYC-amplified medulloblastoma. However, the mechanisms for its action, and ultimately for resistance, have not been fully defined. Here, using a combination of expression profiling, genome-scale CRISPR/Cas9-mediated loss of function and ORF/cDNA driven rescue screens, and cell-based models of spontaneous resistance, we identify bHLH/homeobox transcription factors and cell-cycle regulators as key genes mediating BETi’s response and resistance. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
22 Samples
Download data: BED
Series
Accession:
GSE129521
ID:
200129521
12.

Neuronal differentiation and cell-cycle programs mediate response to BET-bromodomain inhibition in MYC-driven medulloblastoma

(Submitter supplied) we used gene expression profiling to determine gene expression changes in sensitive and drug tolerant medulloblastoma cells to reexposure to BET-bromodomain inhibitors
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL16686
20 Samples
Download data: CEL
Series
Accession:
GSE122404
ID:
200122404
13.

Renal medullary carcinomas depend upon SMARCB1 loss and are sensitive to proteasome inhibition

(Submitter supplied) Whole gene expression arrays for primary and metastatic cell lines derived from patients with RMC
Organism:
Homo sapiens
Type:
Expression profiling by array; Third-party reanalysis
Platform:
GPL570
4 Samples
Download data: CEL, TXT
Series
Accession:
GSE111787
ID:
200111787
14.

Analysis of Changes in Gene Expression and Genomewide H3K27 trimethylation Triggered upon C2C12 Myotube Differentiation in Normoxia versus Hypoxia

(Submitter supplied) We report changes in gene expression and corresponding H3K27 trimethylation induced upon myotube differentiation in C2C12 cells that were cultured under Normoxia (21% oxygen) or Hypoxia (2% oxygen)
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
24 Samples
Download data: BW, CSV
Series
Accession:
GSE114086
ID:
200114086
15.

Transcriptional changes and H3K27ac occupancy associated with resistance to JQ1 treatment 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
Platform:
GPL18573
58 Samples
Download data: BW, TXT
Series
Accession:
GSE107708
ID:
200107708
16.

Transcriptional changes associated with resistance to JQ1 treatment in MYCN-amplified neuroblastoma

(Submitter supplied) Drug resistance is a major clinical challenge in achieving durable responses to targeted cancer therapeutics. Resistance mechanisms to new classes of epigenetic-targeted drugs entering the clinic remain largely unexplored. We used BET inhibition in MYCN-amplified neuroblastoma as a prototype to model innate and acquired resistance to chromatin remodeling inhibitors in cancer. Genome-scale, pooled lentiviral ORF and CRISPR knockout rescue screens nominated the PI3K pathway as a key signaling node that mediates resistance to BET inhibition. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
30 Samples
Download data: TXT
Series
Accession:
GSE107707
ID:
200107707
17.

Enhancer remodeling promotes resistance to epigenetic-targeted therapy and engenders tumor cell vulnerabilities

(Submitter supplied) Drug resistance is a major clinical challenge in achieving durable responses to targeted cancer therapeutics. Resistance mechanisms to new classes of epigenetic-targeted drugs entering the clinic remain largely unexplored. We used BET inhibition in MYCN-amplified neuroblastoma as a prototype to model innate and acquired resistance to chromatin remodeling inhibitors in cancer. Genome-scale, pooled lentiviral ORF and CRISPR knockout rescue screens nominated the PI3K pathway as a key signaling node that mediates resistance to BET inhibition.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
28 Samples
Download data: BW
Series
Accession:
GSE107706
ID:
200107706
18.

Genetic and transcriptional variation alters cancer cell line drug response

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
11 Samples
Download data
Series
Accession:
GSE114462
ID:
200114462
19.

Genetic and transcriptional variation alters cancer cell line drug response [MCF7 strain AA]

(Submitter supplied) 10X Genomics single cell RNAseq of MCF7 cells treated with bortezomib. Human cancer cell lines are the workhorse of cancer research. While cell lines are known to evolve in culture, the extent of the resultant genetic and transcriptional heterogeneity and its functional consequences remain understudied. Here, genomic analyses of 106 cell lines grown in two laboratories revealed extensive clonal diversity. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
4 Samples
Download data: CSV
Series
Accession:
GSE114461
ID:
200114461
20.

Genetic and transcriptional variation alters cancer cell line drug response [MCF7 strain L]

(Submitter supplied) 10X Genomics single cell RNAseq of MCF7 cells Human cancer cell lines are the workhorse of cancer research. While cell lines are known to evolve in culture, the extent of the resultant genetic and transcriptional heterogeneity and its functional consequences remain understudied. Here, genomic analyses of 106 cell lines grown in two laboratories revealed extensive clonal diversity. Follow-up comprehensive genomic characterization of 27 strains of the common breast cancer cell line MCF7 uncovered rapid genetic diversification. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
3 Samples
Download data: CSV
Series
Accession:
GSE114460
ID:
200114460
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