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accession-icon GSE37203
Barrett's esophageal tissues and esophageal adenocarcinoma specimens
  • organism-icon Homo sapiens
  • sample-icon 67 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a), Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Decreased selenium-binding protein 1 in esophageal adenocarcinoma results from posttranscriptional and epigenetic regulation and affects chemosensitivity.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage, Race

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accession-icon GSE37200
Gene expression profiling of Barretts esophageal tissues and esophageal adenocarcinoma specimens
  • organism-icon Homo sapiens
  • sample-icon 46 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Specimens were collected from esophageal adenocarcinoma patients undergoing esophagectomy for adenocarcinoma at the University of Michigan Health System between 1991 and 2004. Written consent was obtained from each patient according to the approval and guidelines of the University of Michigan institutional review board. Patients receiving treatment with chemotherapy and/or radiotherapy prior to surgery were excluded.

Publication Title

Decreased selenium-binding protein 1 in esophageal adenocarcinoma results from posttranscriptional and epigenetic regulation and affects chemosensitivity.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage, Race

View Samples
accession-icon GSE37201
Gene expression profiling of esophageal adenocarcinoma
  • organism-icon Homo sapiens
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2), Affymetrix Human Genome U133A Array (hgu133a)

Description

Specimens were collected from esophageal adenocarcinoma patients undergoing esophagectomy for adenocarcinoma at the University of Michigan Health System between 1991 and 2004. Written consent was obtained from each patient according to the approval and guidelines of the University of Michigan institutional review board. Patients receiving treatment with chemotherapy and/or radiotherapy prior to surgery were excluded.

Publication Title

Decreased selenium-binding protein 1 in esophageal adenocarcinoma results from posttranscriptional and epigenetic regulation and affects chemosensitivity.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage, Race

View Samples
accession-icon SRP075051
microRNAs with an AAGUGC seed motif constitute an integral part of a signaling network driving NSCLC cell proliferation
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

miR-372-3p target identification mRNA level Overall design: Differential expression analysis 30h post transfection with miR-372-3p mimics

Publication Title

microRNAs with AAGUGC seed motif constitute an integral part of an oncogenic signaling network.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

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accession-icon GSE12667
Discovery of somatic mutations in lung adenocarcinomas
  • organism-icon Homo sapiens
  • sample-icon 72 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This was a collaborative study to discover somatic mutations in 188 lung adenocarcinomas. DNA sequencing of 623 genes with known or potential relationships to cancer revealed more than 1,000 somatic mutations across the samples. Our analysis identified 26 genes that are mutated at significantly high frequencies and thus are likely to play a role in carcinogenesis. The observed mutational profiles correlate with clinical features, smoking status, and DNA repair defects. These results are complemented by data integration including SNP array data and gene expression array data (deposited here). Our findings shed further light on several key signaling pathways involved in lung adenocarcinoma, and suggest new molecular targets for treatment.

Publication Title

Somatic mutations affect key pathways in lung adenocarcinoma.

Sample Metadata Fields

Sex, Race

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accession-icon GSE6614
Expression changes in mouse brains following nicotine-induced seizures; the modulation of transcription factor networks
  • organism-icon Mus musculus
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Nicotine, acting through the neuronal nicotinic acetylcholine receptors (nAChR), can induce seizures in mice. We aimed to study brain transcriptional response to seizure and to identify genes whose expression is altered after nicotine-induced seizures. Whole brains of untreated mice were compared to brains one hour after seizure activity, using Affymetrix U74Av2 microaarays. Experimental groups included wild-type mice and both nicotine-induced seizures sensitive and resistant nAChR mutant mice. Each genotype group received different nicotine doses to generate seizures. This approach allowed the identification of significantly changed genes whose expression was dependent on seizure activity, nicotine administration or both, but not on the type of nAChR subunit mutation or the amount of nicotine injected. Significant expression changes were detected in 62 genes (p < 0.05, FDR correction). Among them, GO functional annotation analysis determined that the most significantly over-represented categories were of genes encoding MAP kinase phosphatases, regulators of transcription and nucleosome assembly proteins. In-silico bioinformatic analysis of the promoter regions of the 62 changed genes detected the significant enrichments of 16 transcription regulatory elements (TREs), creating a network of transcriptional regulatory responses to seizures. The TREs for ATF and SRF were most significantly enriched, supporting their association with seizure activity. Our data suggest that nicotine-induced seizure in mice is a useful model to study seizure activity and its global brain transcriptional response. The differentially expressed genes detected here can help understand the molecular mechanisms underlying seizures in animal models, and may also serve as candidate genes to study epilepsy in humans.

Publication Title

Expression changes in mouse brains following nicotine-induced seizures: the modulation of transcription factor networks.

Sample Metadata Fields

Sex, Age, Treatment

View Samples
accession-icon GSE20411
The effects of aging vs. alpha7 nAChR subunit deficiency on the mouse brain transcriptome
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Aging is accompanied by expression changes in multiple genes and the brain is one of the tissues most vulnerable to aging. Since the alpha7 nicotinic acetylcholine receptor (nAChR) subunit has been associated with neurodevelopmental disorders and cognitive decline during aging, we hypothesized that its absence might affect gene expression profiles in aged brains. To study whether transcriptional changes occur due to aging, alpha7 deficiency or both, we analyzed whole brain transcriptomes of young (8 week) and aged (2 year) alpha7 deficient and wild-type control mice, using Mouse Genome 430 2.0 microarray. Highly significant expression changes were detected in 47 and 1543 genes (after Bonferroni and FDR correction) in the brains of aged mice compared to young mice, regardless of their genotype. These included genes involved in immune system function and ribosome structure, as well as genes that were previously demonstrated as differentially expressed in aging human brains. Genotype-dependent changes were detected in only 3 genes, Chrna7 which encodes the alpha7 nAChR subunit, and two closely linked genes, likely due to a mouse background effect. Expression changes dependent on age-genotype interaction were detected in 207 genes (with a low significance threshold). Age-dependent differential expression levels were approved in all nine genes that were chosen for validation by real-time RT-PCR. Our results suggest that the robust effect of aging on brain transcription clearly overcomes the almost negligible effect of alpha7 nAChR subunit deletion, and that germline deficiency of this subunit has a minor effect on brain expression profile in aged mice.

Publication Title

The effects of aging vs. α7 nAChR subunit deficiency on the mouse brain transcriptome: aging beats the deficiency.

Sample Metadata Fields

Age

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accession-icon SRP181857
Early genome activation in Drosophila is extensive with an initial tendency for aborted transcripts and retained introns
  • organism-icon Drosophila melanogaster
  • sample-icon 41 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Control of metazoan embryogenesis shifts from maternal to zygotic gene products as the zygotic genome becomes transcriptionally activated. In Drosophila, zygotic genome activation (ZGA) begins with a minor wave, but technical challenges have hampered the identification of early transcripts or obscured the onset of their transcription. Here, we develop an approach to isolate transcribed mRNAs and apply it over the course of the minor wave and the start of the major wave of Drosophila ZGA. Our results increase known genes of the minor wave by 10 fold and show that this wave is continuous and gradual. Transposable-element mRNAs are also produced, but discontinuously. Genes in the early and middle part of the minor wave are short with few if any introns, and their transcripts are frequently aborted and tend to have retained introns, suggesting that inefficient splicing as well as rapid cell divisions constrain the lengths of early transcripts. Overall design: The goal of this study is to use NGS to identify zygotic transcripts produced during early zygotic genome activation in Drosophila.

Publication Title

Early genome activation in <i>Drosophila</i> is extensive with an initial tendency for aborted transcripts and retained introns.

Sample Metadata Fields

Subject

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accession-icon GSE7360
Equine Laminitis vs Control.
  • organism-icon Equus caballus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Bovine Genome Array (bovine)

Description

Equine lameller tissues were collected to compare normal vs laminitis generated differences in transcriptom level.

Publication Title

Gene expression in the lamellar dermis-epidermis during the developmental phase of carbohydrate overload-induced laminitis in the horse.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE102037
Novel MYC-driven medulloblastoma models generated by CRISPR activation of endogenous Myc
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Myc-driven Group 3 medulloblastoma (MB) is the most aggressive tumor among the four subgroups classified by transcriptome, genomic landscape and clinical outcomes. So far in all available mouse Group 3 models, the constitutive ectopic Myc expression was under control of LTR element or other exogenous promoters within the vectors, which were randomly inserted into the genome with multiple copies. Here we are deploying nuclease deficient CRISPR/dCas9-based transactivator that is targeted to promoter DNA sequences by specific guide RNA to force the transcriptional activation of endogenous Myc in p53-/-;cdkn2c-/- neurospheres cells. A combination of three sgRNAs together with dCas9-VP64 induced the highest expression of endogenous Myc. When the targeted cells were transplanted to the cortex of recipients, tumors arose fully recapitulate the Group 3 MB in human. This novel mouse model should significantly strengthen our understanding and treatment of the Myc-driven Group 3 medulloblastoma.

Publication Title

Mouse medulloblastoma driven by CRISPR activation of cellular Myc.

Sample Metadata Fields

Specimen part

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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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