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accession-icon GSE104394
The Tumor Suppressor Hic1 Maintains Chromosomal Stability Independent of Tp53
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The tumor suppressor Hic1 maintains chromosomal stability independent of Tp53.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE108345
mRNA expression from three human gastric cancer cell lines (MKN1, NUGC4 and AZ521) following either 10ug/ml Pam3Cys-Ser-(Lys)4 and FSL-1 or no treatment.
  • organism-icon Homo sapiens
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Toll-like receptors (TLRs) are key regulators of innate immune responses, and their dysregulation is observed in numerous inflammation-associated malignancies, including gastric cancer (GC). However, the identity of specific TLRs and their molecular targets which promote the pathogenesis of human GC is ill-defined. Here, we sought to determine the clinical utility of TLR2 in human GC. TLR2 mRNA and protein expression levels were elevated in 50% of GC patient tumors across multiple ethnicities. TLR2 was also widely expressed among human GC cell lines, and DNA microarray-based expression profiling was conducted on RNA from NUGC4 and AZ521 cells either non-stimulated or stimulated with a combination of 10g/ml Pam3Cys-Ser-(Lys)4 and FSL-1.

Publication Title

No associated publication

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE104392
Analysis of gene expression in control, Hic1 KO and p53 KO mouse embrynoic fibroblast (MEF) cell lines I
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

We hypothesised that genetic inactivation of the transcriptional repressor Hic1, would lead to changes in gene expression that may lead to transformation. We assessed changes in gene expression in pre-immortal MEF cell lines in which Hic1 was inactivated compared to controls.

Publication Title

The tumor suppressor Hic1 maintains chromosomal stability independent of Tp53.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE104393
Analysis of gene expression in control, Hic1 KO and p53 KO mouse embrynoic fibroblast (MEF) cell lines II
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

We hypothesised that genetic inactivation of the transcriptional repressor Hic1, would lead to changes in gene expression that may lead to transformation. We assessed changes in gene expression in immortal MEF cell lines in which Hic1 or p53 was inactivated.

Publication Title

The tumor suppressor Hic1 maintains chromosomal stability independent of Tp53.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE75126
L929 vs L929IRF8 following 4hr IFNbeta treatment (1000U/ml)
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

Identify genes like Ifit1 which are induced in L929 cells but not L929 cells expressing ectopic IRF8

Publication Title

Interferon Regulatory Factor 8 (IRF8) Impairs Induction of Interferon Induced with Tetratricopeptide Repeat Motif (IFIT) Gene Family Members.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE37210
The application of nonsense-mediated mRNA decay inhibition to the identification of breast cancer susceptibility genes
  • organism-icon Homo sapiens
  • sample-icon 141 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

Identification of novel, highly penetrant, breast cancer susceptibility genes will require the application of additional strategies beyond that of traditional linkage and candidate gene approaches. Approximately one-third of inherited genetic diseases, including breast cancer susceptibility, are caused by frameshift or nonsense mutations that truncate the protein product [1]. Transcripts harbouring premature termination codons are selectively and rapidly degraded by the nonsense-mediated mRNA decay (NMD) pathway. Blocking the NMD pathway in any given cell will stabilise these mutant transcripts, which can then be detected using gene expression microarrays. This technique, known as gene identification by nonsense-mediated mRNA decay inhibition (GINI), has proved successful in identifying sporadic nonsense mutations involved in many different cancer types. However, the approach has not yet been applied to identify germline mutations involved in breast cancer. We therefore attempted to use GINI on lymphoblastoid cell lines (LCLs) from multiple-case, non-BRCA1/2 breast cancer families in order to identify additional high-risk breast cancer susceptibility genes.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Cell line

View Samples
accession-icon GSE7127
63 Melanoma cell lines
  • organism-icon Homo sapiens
  • sample-icon 57 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

63 melanoma cell lines hybridized to Affymetrix Hu133_Plus 2 oligo arrays. The aim of this study was to identify potential downstream targets of key oncogenes and TSGs in melanoma (including p14ARF, p16INK4A, BRAF etc).

Publication Title

Confirmation of a BRAF mutation-associated gene expression signature in melanoma.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE86260
Cancer Associated Fibroblasts are defined by a core set of epigenome changes that contribute to the tumor phenotype
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Enduring epigenetic landmarks define the cancer microenvironment.

Sample Metadata Fields

Sex, Specimen part, Subject

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accession-icon GSE76337
Novel contribution of acetylated histone variant H2A.Z in activation of neo-enhancers in prostate cancer
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II, Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE7152
Melanoma cell lines involved in the p14ARF genotype analysis
  • organism-icon Homo sapiens
  • sample-icon 33 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

35 Melanoma cell lines hybridized to Affymetrix Hu133_Plus 2 microarrays were analysed for genes differentially expressed between cell lines carrying wild-type p14ARF and those with mutant 14ARF. All of these cell lines contained wild-type p53 (so that the effects of p14ARF mutations could be analysed without contamination from p53).

Publication Title

Gene expression profiling in melanoma identifies novel downstream effectors of p14ARF.

Sample Metadata Fields

No sample metadata fields

View Samples
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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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