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accession-icon GSE8607
Gene expression profiling of testicular seminoma
  • organism-icon Homo sapiens
  • sample-icon 43 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U95 Version 2 Array (hgu95av2)

Description

Gene expression patterns of testicular seminoma were analysed applying oligonucleotide microarrays in 40 specimens of different tumour stages (pT1, pT2, pT3) and in 3 normal testes.

Publication Title

Gene signatures of testicular seminoma with emphasis on expression of ets variant gene 4.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE71121
Expression data (micro-array and RNA-seq, frozen tumors and FFPE blocks) from various sarcomas
  • organism-icon Homo sapiens
  • sample-icon 259 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

RNA sequencing validation of the Complexity INdex in SARComas prognostic signature.

Sample Metadata Fields

Time

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accession-icon GSE71118
Expression data (micro-array, frozen tumors) from various sarcomas
  • organism-icon Homo sapiens
  • sample-icon 259 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We validated the technological and material transfers of the CINSARC signature.

Publication Title

RNA sequencing validation of the Complexity INdex in SARComas prognostic signature.

Sample Metadata Fields

Time

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accession-icon GSE58697
Expression data from 128 Desmoids
  • organism-icon Homo sapiens
  • sample-icon 123 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

One of the main problems in managing desmoids tumors is their locoregional aggressiveness and their high ability to recur after initial treatment. In our work, with the goal to identify molecular markers that can predict Progression-Free Survival, gene-expression screening was conducted on 128 available independent untreated primary desmoid tumors using cDNA microarray. By analyzing expression profiles, we have identified, for the first time, a gene expression signature that is able to predict Progression-Free Survival. This molecular signature identified two groups with clearly distinct Progression-Free Survival in the two sets of subjects. Patients in good prognostic group had achieved a progression-free 2-year survival rate of 86% while patients in poor prognostic group had a progression-free 2-year survival rate of 44%.

Publication Title

Gene Expression Profiling of Desmoid Tumors by cDNA Microarrays and Correlation with Progression-Free Survival.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon SRP100979
HSF1-dependent and -independent regulation of the mammalian in vivo heat shock response and its impairment in Huntington's disease
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The heat shock response (HSR) is a mechanism to cope with proteotoxic stress by inducing the expression of molecular chaperones and other heat shock response genes. The HSR is evolutionarily well conserved and has been widely studied in bacteria, cell lines and lower eukaryotic model organisms. However, mechanistic insights into the HSR in higher eukaryotes, in particular in mammals, are limited. We have developed an in vivo heat shock protocol to analyze the HSR in mice and dissected heat shock factor 1 (HSF1)-dependent and -independent pathways. Whilst the induction of proteostasis-related genes was dependent on HSF1, the regulation of circadian function related genes, indicating that the circadian clock oscillators have been reset, was independent of its presence. Furthermore, we demonstrate that the in vivo HSR is impaired in mouse models of Huntington's disease but we were unable to corroborate the general repression of transcription after a heat shock found in lower eukaryotes. Overall design: RNA-Seq was performed on mRNA isolated from quadriceps femoris muscle of 24 mice. These mice were of wild type, R6/2, and Hsf1-/- genotypes. Two mice of each genotype were tested in four conditions: (1) heat shock, (2) control heat shock, (3) HSP90 inhibition (NVP-HSP990), and (4) HSP90 inhibition vehicle.

Publication Title

HSF1-dependent and -independent regulation of the mammalian in vivo heat shock response and its impairment in Huntington's disease mouse models.

Sample Metadata Fields

Age, Specimen part, Treatment, Subject

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accession-icon SRP057793
RNA-seq performed on sarcomas to identify various alterations
  • organism-icon Homo sapiens
  • sample-icon 149 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

No description.

Publication Title

Genomic and transcriptomic comparison of post-radiation versus sporadic sarcomas.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP113755
Transcriptome characterization of radiation-induced sarcomas
  • organism-icon Homo sapiens
  • sample-icon 73 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

No description.

Publication Title

Genomic and transcriptomic comparison of post-radiation versus sporadic sarcomas.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage

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accession-icon GSE30873
Effects of caspase-8 deletion in the intestinal epithelium
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Caspase-8 is a cystein protease involved in regulating apoptosis. The function of caspase-8 was studied in the intestinal epithelium, using mice with an intestinal epithelial cell specific deletion of caspase-8.

Publication Title

Caspase-8 regulates TNF-α-induced epithelial necroptosis and terminal ileitis.

Sample Metadata Fields

Specimen part

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accession-icon SRP043967
The CNS-Heart Axis is a Source of Cardiac Dysfunction in Mouse Models of Huntington’s Disease
  • organism-icon Mus musculus
  • sample-icon 30 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Purpose: Transcriptome profiling (RNA-seq) to microarray to evaluate transcriptional changes in the heart of HD mouse models Methods: Heart mRNA profiles of 4-weeks-old wild-type (WT) and R6/2 transgenic; 15-weeks-old WT and R6/2 transgenic mice; 8-month-old WT and HdhQ150 knock-in mice; 22-month-old WT and HdhQ150 knock-in mice were generated by deep sequencing, in triplicate, using Illumina Hi-seq 2000. Conclusions: Our study showed that there is no major transcriptional deregulation in the heart of mouse models of HD. Overall design: Heart mRNA profiles of 4-weeks-old wild-type (WT) and R6/2 transgenic; 15-weeks-old WT and R6/2 transgenic mice; 8-month-old WT and HdhQ150 knock-in mice; 22-month-old WT and HdhQ150 knock-in mice were generated by deep sequencing, in triplicate, using Illumina Hi-seq 2000.

Publication Title

Dysfunction of the CNS-heart axis in mouse models of Huntington's disease.

Sample Metadata Fields

No sample metadata fields

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accession-icon E-TABM-585
Transcription profiling by array of human lung cancer cells after treatment with dasatinib, imatinib, nilotinib or PD0325901
  • organism-icon Homo sapiens
  • sample-icon 111 Downloadable Samples
  • Technology Badge Icon Affymetrix HT Human Genome U133A Array (hthgu133a)

Description

Cell Line: This experiment was designed to measure the transcriptional responses to four kinase inhibitors across a five-logarithm dose range. The A549 human lung cancer cell line was treated with dasatinib, imatinib or nilotinib (4 hours and 20 hours) or PD0325901 (4 hours). Treatments used a 12-point dose range (30 uM with 3-fold dilutions down to 0.17 nM; 0.5% DMSO vehicle for all treatments). Experimental design prevented row or column handling effects being confounded with dose effect.

Publication Title

Transcriptional profiling of the dose response: a more powerful approach for characterizing drug activities.

Sample Metadata Fields

Disease, Cell line, Compound, Time

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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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