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Homo sapiens
7 Downloadable Samples
Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)
Description
U1 small nuclear (sn)RNA, required for splicing of pre-mRNA, is encoded by genes on chromosome 1p36. Imperfect copies of these true (t)U1 snRNA genes, located on chromosome 1q12-21, were thought to be pseudogenes. However, many of these variant (v)U1 snRNA genes produce fully-processed transcripts that are packaged into potentially functional particles. Using antisense oligonucleotides, we have achieved functional knockdown of a specific vU1 snRNA in HeLa cells and identified over 400 transcriptome changes following interrogation of the Affymetrix Human Exon ST 1.0 array.
Publication Title
Differentially expressed, variant U1 snRNAs regulate gene expression in human cells.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 70 Downloadable Samples
Illumina HiSeq 2000
Description
Gene expression levels of pancreatic cell lines Overall design: RNA was extracted from cell lines and subjected to 50bp paired-end RNA sequencing
Publication Title
Integrated Patient-Derived Models Delineate Individualized Therapeutic Vulnerabilities of Pancreatic Cancer.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 260 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Master regulators of FGFR2 signalling and breast cancer risk.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 125 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Genome-wide association studies for breast cancer have identified over 80 different risk regions in the genome, with the FGFR2 locus consistently identified as the most strongly associated locus. However, we know little about the mechanisms by which the FGFR2 locus mediates risk or the pathways in which multiple risk loci may combine to cause disease. Here we use a systems biology approach to elucidate the regulatory networks operating in breast cancer and examine the role of FGFR2 in mediating risk. Using model systems we identify FGFR2-regulated genes and, combining variant set enrichment and eQTL analysis, show that these are preferentially linked to breast cancer risk loci. Our results support the concept that cancer-risk associated genes cluster in pathways
Publication Title
Master regulators of FGFR2 signalling and breast cancer risk.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 71 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Genome-wide association studies for breast cancer have identified over 80 different risk regions in the genome, with the FGFR2 locus consistently identified as the most strongly associated locus. However, we know little about the mechanisms by which the FGFR2 locus mediates risk or the pathways in which multiple risk loci may combine to cause disease. Here we use a systems biology approach to elucidate the regulatory networks operating in breast cancer and examine the role of FGFR2 in mediating risk. Using model systems we identify FGFR2-regulated genes and, combining variant set enrichment and eQTL analysis, show that these are preferentially linked to breast cancer risk loci. Our results support the concept that cancer-risk associated genes cluster in pathways
Publication Title
Master regulators of FGFR2 signalling and breast cancer risk.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 46 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Genome-wide association studies for breast cancer have identified over 80 different risk regions in the genome, with the FGFR2 locus consistently identified as the most strongly associated locus. However, we know little about the mechanisms by which the FGFR2 locus mediates risk or the pathways in which multiple risk loci may combine to cause disease. Here we use a systems biology approach to elucidate the regulatory networks operating in breast cancer and examine the role of FGFR2 in mediating risk. Using model systems we identify FGFR2-regulated genes and, combining variant set enrichment and eQTL analysis, show that these are preferentially linked to breast cancer risk loci. Our results support the concept that cancer-risk associated genes cluster in pathways
Publication Title
Master regulators of FGFR2 signalling and breast cancer risk.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 18 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Genome-wide association studies for breast cancer have identified over 80 different risk regions in the genome, with the FGFR2 locus consistently identified as the most strongly associated locus. However, we know little about the mechanisms by which the FGFR2 locus mediates risk or the pathways in which multiple risk loci may combine to cause disease. Here we use a systems biology approach to elucidate the regulatory networks operating in breast cancer and examine the role of FGFR2 in mediating risk. Using model systems we identify FGFR2-regulated genes and, combining variant set enrichment and eQTL analysis, show that these are preferentially linked to breast cancer risk loci. Our results support the concept that cancer-risk associated genes cluster in pathways
Publication Title
Master regulators of FGFR2 signalling and breast cancer risk.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 131 Downloadable Samples
- Illumina HiSeq 2000
Description
Mutations in TRP53, prevalent in human cancers, reportedly drive tumorigenesis through dominant-negative-effects (DNE) over wt TRP53 and neomorphic gain-of-function (GOF) effects. We show that five TRP53 mutants do not accelerate lymphomagenesis on a TRP53-deficient background but strongly synergize with c-MYC over-expression. RNA-seq analysis revealed that mutant TRP53 does not globally repress wt TRP53 function but exerts a DNE with disproportionate impact on subsets of wt TRP53 target genes, particularly those involved in DNA repair, proliferation and metabolism. This reveals that the mutant TRP53 DNE drives tumorigenesis by modulating wt TRP53 function in a manner that is advantageous for neoplastic transformation. Overall design: Each of 5 mutant human TRP53 proteins, and a negative control, was expressed in 3 mouse lymphoma cell lines, both before and after activation of WT TRP53 with nutlin-3a.
Publication Title
Mutant TRP53 exerts a target gene-selective dominant-negative effect to drive tumor development.
Sample Metadata Fields
Cell line, Subject
View Samples- Homo sapiens
- 33 Downloadable Samples
- IonTorrentProton
Description
The type I JAK inhibitor ruxolitinib is approved for therapy of MPN patients but evokes resistance with longer exposure. Several novel type I JAK inhibitors were studied and we show that they uniformly induce resistance via a shared mechanism of JAK family heterodimer formation.Here we studied the expression profiles of SET2 cell lines persistent to several different type I JAK inhibitors in comparison to naive SET2 cells or in comparison to SET2 cells with acute exposure to ruxolitinib. Overall design: Analysis of RNA isolated from several type I JAK inhibitor SET2 cell lines in comparison to naïve SET2 cells
Publication Title
CHZ868, a Type II JAK2 Inhibitor, Reverses Type I JAK Inhibitor Persistence and Demonstrates Efficacy in Myeloproliferative Neoplasms.
Sample Metadata Fields
No sample metadata fields
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GSE2815- Homo sapiens
- 7 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
The transcriptional activities of c-Myb and its oncogenic variant v-Myb were compared by expressing them in human MCF7 cells using recombinant adenovirus vectors. A hybrid construct, 3Mutc, which is a variant of c-Myb harboring three v-Myb-derived DNA binding domain mutations was also analyzed. All the samples were compared to cells infected with a control adenovirus. The results showed that v-Myb, which differs from c-Myb only by N- and C-terminal deletions and eleven amino acid substitutions, has a qualitatively different transcriptional activity.
Publication Title
Oncogenic mutations cause dramatic, qualitative changes in the transcriptional activity of c-Myb.
Sample Metadata Fields
No sample metadata fields
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