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accession-icon GSE38494
Expression data from odontogenic tumours
  • organism-icon Homo sapiens
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The aim of the study was to elucidate the cellular origin of ameloblastoma and keratocystic odontogenic tumour, neoplasms believed to arise from dental epithelial cells, by carrying out a genome-wide expression analysis.

Publication Title

Early dental epithelial transcription factors distinguish ameloblastoma from keratocystic odontogenic tumor.

Sample Metadata Fields

Specimen part

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accession-icon GSE35819
Comparison of hypoxia (4 % O2) cultured human embryonic stem cells (hESCs) to normoxia (21 % O2) cultured
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Human Exon 1.0 ST Array (huex10st)

Description

We compared the transcriptome at gene expression level in hypoxic and normoxic conditions.

Publication Title

Continuous hypoxic culturing of human embryonic stem cells enhances SSEA-3 and MYC levels.

Sample Metadata Fields

Cell line, Treatment, Time

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accession-icon GSE4045
Classification of serrated colorectal tumors
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Serrated adenocarcinomas are morphologically different from conventional adenocarcinomas. The serrated pathway has recently been proposed to represent a novel mechanism of colorectal cancer (CRC) formation. However, whether they are biologically different and truly form a distinct subclass of CRC, is not known. This study shows that the gene expression profile of serrated and conventional CRCs differs from each others and that serrated CRCs are not only morphologically novel, but also biologically distinct subclass of CRC.

Publication Title

Serrated carcinomas form a subclass of colorectal cancer with distinct molecular basis.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE2152
The effect of FH mutations on fibroid expression profile
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

A series of gene expression measurements of uterine fibroids with mutated or wild-type fumarate hydratase (FH) gene.

Publication Title

Distinct expression profile in fumarate-hydratase-deficient uterine fibroids.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE2724
The effect of FH mutations on fibroid expression profile, normal myometrium vs. FH-mutant fibroids.
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

A series of gene expression measurements of uterine fibroids with mutated fumarate hydratase (FH) gene and normal myometrium.

Publication Title

Distinct expression profile in fumarate-hydratase-deficient uterine fibroids.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE2725
The effect of FH mutations on fibroid expression profile 2.
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

A series of gene expression measurements of normal myometrium and uterine fibroids with mutated or wild-type fumarate hydratase (FH) gene.

Publication Title

Distinct expression profile in fumarate-hydratase-deficient uterine fibroids.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE26900
Effect of Tet1-knockdown on gene expression in mouse ES cells cultured in ES and TS cell culture conditions
  • organism-icon Mus musculus
  • sample-icon 27 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

TET-family enzymes convert 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) in DNA. Tet1 and Tet2 are Oct4-regulated enzymes that together sustain 5hmC in mouse embryonic stem (ES) cells. ES cells depleted of Tet1 by RNAi show diminished expression of the Nodal antagonist Lefty1, and display hyperactive Nodal signalling and skewed differentiation into the endoderm-mesoderm lineage in embryoid bodies in vitro. In Fgf4- and heparin-supplemented culture conditions that favor derivation of trophoblast stem (TS) cells, Tet1-depleted ES cells activate the trophoblast stem cell lineage determinant Elf5 and can colonize the placenta in mid-gestation embryo chimeras. Consistent with these findings, Tet1-depleted ES cells form aggressive hemorrhagic teratomas with increased endoderm, reduced neuroectoderm and ectopic appearance of trophoblastic giant cells. Thus Tet1 functions to regulate the lineage differentiation potential of ES cells. Here, we performed whole-genome transcriptome profiling of ES cells stably depleted of Tet1 by shRNA knockdown (Tet1-kd) cultured in either standard ES cell or in TS cell culture conditions. Gene expression changes in Tet1-kd ES cells were fairly modest compared to control (GFP-kd) cells, although gene ontology (GO) analysis of differentially expressed genes yielded many terms related to embryonic development and cell cycle regulation. In TS cell culture conditions, a core set of genes defining trophectodermal cell differentiation, including Cdx2, Eomes and Tead4, was enriched in Tet1-kd compared to GFP-kd cells.

Publication Title

Tet1 and Tet2 regulate 5-hydroxymethylcytosine production and cell lineage specification in mouse embryonic stem cells.

Sample Metadata Fields

Specimen part

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accession-icon SRP049593
7q11.23 dosage-dependent dysregulation in the human pluripotent state primes aberrant transcriptional programs in disease-relevant lineages (RNAseq)
  • organism-icon Homo sapiens
  • sample-icon 406 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

We apply the cellular reprogramming experimental paradigm to two disorders caused by symmetrical copy number variations (CNV) of 7q11.23 and displaying a striking combination of shared as well as symmetrically opposite phenotypes: Williams Beuren syndrome (WBS) and 7q microduplication syndrome (7dupASD). Through a uniquely large and informative cohort of transgene-free patient-derived induced pluripotent stem cells (iPSC), along with their differentiated derivatives, we find that 7q11.23 CNV disrupt transcriptional circuits in disease-relevant pathways already at the pluripotent state. These alterations are then selectively amplified upon differentiation into disease-relevant lineages, thereby establishing the value of large iPSC cohorts in the elucidation of disease-relevant developmental pathways. In addition, we functionally define the quota of transcriptional dysregulation specifically caused by dosage imbalances in GTF2I (also known as TFII-I), a transcription factor in 7q11.23 thought to play a critical role in the two conditions, which we found associated to key repressive chromatin modifiers. Finally, we created an open-access web-based platform (accessible at http://bio.ieo.eu/wbs/ ) to make accessible our multi-layered datasets and integrate contributions by the entire community working on the molecular dissection of the 7q11.23 syndromes. Overall design: We reprogrammed skin fibroblasts from patients harbouring a 7q11.23 hemi-deletion (WBS, 4 patients; +1 atypical deletion, AtWBS) or microduplication (7dupASD; 2 patients), as well as from one unaffected relative and two unrelated controls, using integration-free mRNA-reprogramming, leading to the establishment of a total of 27 characterized iPSC clones. We profiled these by RNAseq (either polyA or ribo-zero). To isolate the contribution of GTF2I to the transcriptional dysregulation, we created stable lines expressing a short hairpin against GTF2I from a representative subset of these iPSC clones, and profiled by RNAseq 7 such lines along with their respective scramble controls. Finally, we also profiled by RNAseq mesenchymal stem cells (MSC) derived from a representative subset of the lines.

Publication Title

RNAontheBENCH: computational and empirical resources for benchmarking RNAseq quantification and differential expression methods.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP067737
Polycomb dysregulation in gliomagenesis targets a Zfp423-dependent differentiation network [RNA-Seq]
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Malignant gliomas constitute one of the most significant areas of unmet medical need, due to the invariable failure of surgical eradication and their marked molecular heterogeneity. Accumulating evidence has revealed a critical contribution by the Polycomb axis of epigenetic repression. However, a coherent understanding of the regulatory networks affected by Polycomb during gliomagenesis is still lacking. Here we integrate transcriptomic and epigenomic analyses to define Polycomb-dependent networks that promote gliomagenesis, validating them both in two independent mouse models and in a large cohort of human samples. We found that Polycomb dysregulation in gliomagenesis affects transcriptional networks associated to invasiveness and de-differentiation. The dissection of these networks uncovers Zfp423 as a crtitical Polycomb-dependent transcription factor whose silencing negatively impacts survival. The anti-gliomagenic activity of Zfp423 requires interaction with the SMAD proteins within the BMP signaling pathway, pointing to a novel synergic circuit through which Polycomb inhibits BMP signaling. Overall design: Transcriptomic analysis of two different stages of gliomagenesis

Publication Title

Polycomb dysregulation in gliomagenesis targets a Zfp423-dependent differentiation network.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE140988
Epigenetic changes of pericytes after ischemia-reperfusion renal injury
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

Analysis of epigenetic changes of pericytes after ischemia-reperfusion renal injury. The hypothesis tested in the present study was that epigenetic change develope in pericytes after acute kidney injury. This phenotype change would cause pericyte to be more proliferative and profibrotic. Results provide important information of the epigenetic change of pericytes, such as specific mechano-responsive genes, up-regulated specific proliferative and profibrotic functions.

Publication Title

Methylation in pericytes after acute injury promotes chronic kidney disease.

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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