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accession-icon GSE17548
Expression data from cirrhosis and HCC tissue samples
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Hepatocellular carcinoma (HCC) is the fifth most-common cancer worldwide causing nearly 600,000 deaths esch year. Approximately 80% of HCC develops on the background of cirrhosis.It is necessary to identify novel genes involved in HCC to implement new diagnostic and treatment options. However, the molecular pathogenesis of HCC largely remains unsolved. Only a few genetic alterations, namely those affecting p53, -catenin and p16INK4a have been implicated at moderate frequencies of these cancers. Early detection of HCC with appropriate treatment can decrease tumor-related deaths

Publication Title

Genome-wide transcriptional reorganization associated with senescence-to-immortality switch during human hepatocellular carcinogenesis.

Sample Metadata Fields

Specimen part

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accession-icon GSE71363
5-aza treatment of breast cancer and non-tumorigenic breast cells
  • organism-icon Homo sapiens
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

CpG hypermethylation in gene promoters is a frequent mechanism of tumor suppressor gene silencing in various types of cancers. 5-aza-2'-deoxycytidine (AZA) is a DNA demethylating and anti-cancer agent resulting in induction of genes suppressed via DNA hypermethylation.

Publication Title

Transgelin gene is frequently downregulated by promoter DNA hypermethylation in breast cancer.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE17546
Expression data from immortal and senescence-programmed Huh7 clones
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Cellular senescence is a tumor suppressor mechanism, and immortalization facilitates neoplastic transformation. Both mechanisms may be highly relevant to hepatocellular carcinoma (HCC) development and its molecular heterogeneity. Cellular senescence appears to play a major role in liver diseases. Chronic liver diseases are associated with progressive telomere shortening leading senescence that is observed highly in cirrhosis, but also in some HCC. We previously described the generation of immortal and senescence-programmed clones from HCC-derived Huh7 cell line.

Publication Title

Genome-wide transcriptional reorganization associated with senescence-to-immortality switch during human hepatocellular carcinogenesis.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE53086
Effects of rapamycin exposure on zebrafish ZF4 cells
  • organism-icon Danio rerio
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

mTOR inhibitor rapamycin is a well-known anticancer and immunosuppressant agent. Effects of rapamycin on zebrafish cells have not been previously studied using transcriptome analyses.

Publication Title

Functionally conserved effects of rapamycin exposure on zebrafish.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE89333
Downregulation of Cholinergic Receptor Alpha 5 (CHRNA5) in MCF7 breast cancer cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Cholinergic Receptor Nicotinic Alpha 5 (CHRNA5), an important susceptibility locus for nicotine addiction and lung cancer, is not well studied in breast cancer. In our study, CHRNA5 was transiently depleted in MCF7 cells and transcriptomic changes were compared to siRNA controls. We for the first time showed by microarray analysis that silencing of CHRNA5 in MCF7 breast cancer cells, downregulated genes involved in the cell cycle and proliferation while resulting in reduced cell viability, DNA synthesis and G1 growth arrest. In addition, simultaneous treatment of CHRNA5 siRNA and topoisomerase inhibitors showed an important role of CHRNA5 in increased drug sensitivity. Phalloidin stained CHRNA5 siRNA treated cells on the other hand exhibited a distinct cellular morphotype with increased cellular extensions and a transcriptome characterized by mixed expression of epithelial-mesenchymal genes. Through bioinformatics analysis of the public transcriptome data we demonstrated a strong positive association of expression signature of CHRNA5 RNAi with that of a differentiated cell as well as hormone starvation. Hence, our study implicates CHRNA5 as an antiproliferative differentiation marker in breast cancer.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE24427
Expression data of multiple sclerosis patients receiving subcutaneous Interferon-beta-1b therapy [U133 A and B]
  • organism-icon Homo sapiens
  • sample-icon 250 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

The purpose of this study was to characterize the transcriptional effects induced by subcutaneous IFN-beta-1b treatment (Betaferon, 250 g every other day) in patients with relapsing-remitting form of multiple sclerosis (MS).

Publication Title

Long-term genome-wide blood RNA expression profiles yield novel molecular response candidates for IFN-beta-1b treatment in relapsing remitting MS.

Sample Metadata Fields

Sex

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accession-icon GSE86034
MicroRNA miR-92a-2 targets TFPI2 to ameliorate oxidative stress of the hypoxia neuron
  • organism-icon Rattus norvegicus
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina ratRef-12 v1.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE45516
Expression data from human Huntington fibroblasts
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Gene expression profile comparison from fibroblasts of Huntington individuals and normal ones

Publication Title

Gene expression profile in fibroblasts of Huntington's disease patients and controls.

Sample Metadata Fields

Sex, Age, Specimen part, Disease

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accession-icon GSE85825
MicroRNA miR-92a-2 targets TFPI2 to ameliorate oxidative stress of the hypoxia neuron [mRNA]
  • organism-icon Rattus norvegicus
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIllumina ratRef-12 v1.0 expression beadchip

Description

Comparison of the differential expression mRNA profiles from the brain cortex of hypoxia and normaixa rats by silica microarray chip

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE12066
Segregation of genes influencing skeletal phenotypes in congenic P/NP rats
  • organism-icon Rattus norvegicus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Bone mineral density and structure candidate gene analysis in alcohol-non-preferring (NP), alcohol-preferring (P), congenic NP (NP.P) and congenic P (P.NP) rats

Publication Title

Identification of genes influencing skeletal phenotypes in congenic P/NP rats.

Sample Metadata Fields

No sample metadata fields

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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)

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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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