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accession-icon GSE34481
Human cancer cells express Slug-based epithelial-mesenchymal transition gene expression signature obtained in vivo
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Background: The biological mechanisms underlying cancer cell motility and invasiveness remain unclear, although it has been hypothesized that they involve some type of epithelial-mesenchymal transition (EMT).

Publication Title

Human cancer cells express Slug-based epithelial-mesenchymal transition gene expression signature obtained in vivo.

Sample Metadata Fields

Specimen part

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accession-icon GSE29458
Expression data from PDGF driven mouse tumors
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Background

Publication Title

Glioblastoma models reveal the connection between adult glial progenitors and the proneural phenotype.

Sample Metadata Fields

Specimen part

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accession-icon GSE101291
Gene expression analysis of IDH1 wild type and IDH1 R132H mutated U87 cells
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

U87 cells were transduced with IDH1 WT or IDH1 R132H and stable clones were selected.

Publication Title

Induction of synthetic lethality in IDH1-mutated gliomas through inhibition of Bcl-xL.

Sample Metadata Fields

Specimen part

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accession-icon GSE64751
Expression comparison of mutant EGFR-driven gliomas with relapse tumors upon mutant EGFR ablation
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

To determine the roles of oncogenic EGFR signaling in gliomagenesis and tumor maintenance, we generated a novel glioma mouse model driven by inducible expression of a mutant EGFR (EGFR*). Genetic suppression of EGFR* induction led to significant tumor regression and prolonged survival. But in spite of the initial response, the tumors relapsed invariably and propagated independent of EGFR*.

Publication Title

Development of Resistance to EGFR-Targeted Therapy in Malignant Glioma Can Occur through EGFR-Dependent and -Independent Mechanisms.

Sample Metadata Fields

Specimen part

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accession-icon SRP073042
Gene expression profiling of retrovirus PDGFB-induced glioma
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We performed gene expression profilings of platelet-derived growth factor subunit B (PDGFB)-induced mouse glioma to compare the differential transcriptome profiles between Ctrl-T tumor cells and Olig2cKO tumor cells. Overall design: Expression profiling of Ctrl-T and Olig2cKO brain tumor (glioma) cells, normal oligodendrocyte progenitor cells (OPCs), normal astrocytes, and normal brain cortex by high-throughput sequencing.

Publication Title

Olig2-Dependent Reciprocal Shift in PDGF and EGF Receptor Signaling Regulates Tumor Phenotype and Mitotic Growth in Malignant Glioma.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP061758
Gene expression profiling of retrovirus PDGFB induced Glioma in control and Olig2cKO tumor
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We performed gene expression pofiling of of Olig2cKO and control glioma tumor and identified significantly changed genes Overall design: RNA-seq of control tumor tissues and Olig2cKO tumor tissues

Publication Title

Olig2-Dependent Reciprocal Shift in PDGF and EGF Receptor Signaling Regulates Tumor Phenotype and Mitotic Growth in Malignant Glioma.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP044668
MRI-localized biopsies reveal subtype-specific differences in molecular and cellular composition at the margins of glioblastoma
  • organism-icon Homo sapiens
  • sample-icon 94 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

We obtained radiographically-localized biopsies during glioma resection surgeries to sample the tumor core and margins from multiple glioma patients. We also procured fresh, non-neoplastic brain tissue specimens from multiple patients having procedures to relieve epilespy symptoms or to place shunts to treat normal pressure hydrocephalus. We then used RNA-Seq to compare expression patterns between geographically distinct regions of gliomas and computational deconvolution to estimate cell type-specific expression patterns in different disease subtypes. Overall design: RNA-Seq analysis in 39 contrast-enhancing glioma core samples, 36 non-enhancing FLAIR glioma margin samples, and 17 non-neoplastic brain tissue samples.

Publication Title

MRI-localized biopsies reveal subtype-specific differences in molecular and cellular composition at the margins of glioblastoma.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE15481
Gene expression data from AP-2 silenced MCF-7 cells
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Overexpression of the AP-2 transcription factor in breast tumours has been identified as an independent predictor of poor outcome and failure of hormone therapy, even in ER positive, ErbB2 negative tumours; markers of a more favourable prognosis. To understand further the role of AP-2 in breast carcinoma, we have used an RNA interference and gene expression profiling strategy using the MCF-7 cell line as a model for ER positive, ErbB2 negative tumours with AP-2 overexpression.

Publication Title

AP-2gamma promotes proliferation in breast tumour cells by direct repression of the CDKN1A gene.

Sample Metadata Fields

Cell line

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accession-icon GSE49107
Oxidative stress induces mitochondrial dysfunction and a protective unfolded protein response in RPE cells
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

How retinal pigmented epithelial (RPE) cells degenerate from oxidative stress in age-related macular degeneration (AMD) is incompletely understood. The study's intent was to identify key cytoprotective pathways activated by oxidative stress, and to determine the extent of their protection. Immunohistochemistry was used to identify the unfolded protein response (UPR) and mitochondria in the RPE of AMD samples. Maculas with early AMD had prominent IRE1, but minimal mitochondrial TOM20 immunolabeling in mildly degenerated RPE. RPE cells treated with cigarette smoke extract (CSE), by microarray analysis, had over-represented genes involved in the antioxidant and unfolded protein response, and mitochondrial location. CSE induced the UPR sensors IRE1, p-PERK, and ATP6, which activated CHOP. CHOP knockdown compromised cell viability after CSE exposure. At the same CSE doses, mitochondria generated superoxide anion and produced less ATP. In mice given intravitreal CSE, the RPE had increased IRE1 and decreased ATP, which elicited RPE epithelial-mesenchymal transition, as suggested by altered ZO1 immunolabeling of RPE flatmounts. Our experiments indicate that RPE cells exposed to oxidative stress respond with a cytoprotective antioxidant and unfolded protein response, but develop mitochondrial impairment that contributed to epithelial mesenchymal transition. With similar responses in the RPE of early AMD samples, these results suggest that mitochondria are vulnerable to oxidative stress while the ER elicits a protective response during early AMD.

Publication Title

Oxidative stress induces mitochondrial dysfunction and a protective unfolded protein response in RPE cells.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon E-MEXP-1414
Transcription profiling of hepatocyes from Zucker fa/fa obese rats vs controls
  • organism-icon Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome U34 Array (rgu34a)

Description

Analysis of the gene signature of steatosis associated to obesity in hepatocytes of Zucker fa/fa obese rats and their controls; identifying target genes linked to steatosis progression. or Obesity and insulin resistance-associated steatosis can be a non-inflammatory condition affecting hepatocytes or progress to steatohepatitis: a condition that can result in end-stage liver disease. Although molecular events leading to accumulation of lipid droplets in the liver have been identified individually, the complexity of the condition suggested that emergent target would be uncovered by a more comprehensive examination. Then, this study was aimed at establishing a gene signature of steatosis in hepatocytes and at identifying target genes linked to steatosis progression. Using Affymetrix oligonucleotide arrays, we compared transcriptomes of hepatocytes isolated from Zucker "fa/fa" obese rats with three different age-related grades of steatosis with those of their counterpart non-steatotic cells.

Publication Title

A subset of dysregulated metabolic and survival genes is associated with severity of hepatic steatosis in obese Zucker rats.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage

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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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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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