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accession-icon GSE101114
Detailed Longitudinal Sampling of Glioma Stem Cells In Situ Reveals Chr7 Gain and Chr10 Loss As Repeated Events in Primary Tumor Formation and Recurrence
  • organism-icon Homo sapiens
  • sample-icon 54 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

Detailed longitudinal sampling of glioma stem cells in situ reveals Chr7 gain and Chr10 loss as repeated events in primary tumor formation and recurrence.

Sample Metadata Fields

Specimen part, Disease

View Samples
accession-icon GSE101113
Detailed Longitudinal Sampling of Glioma Stem Cells In Situ Reveals Chr7 Gain and Chr10 Loss As Repeated Events in Primary Tumor Formation and Recurrence (expression)
  • organism-icon Homo sapiens
  • sample-icon 54 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

In this study, we developed an extensive dataset for a GBM case via the generation of polyclonal and monoclonal glioma stem cell lines from initial diagnosis, as well as from multiple sections of distant tumor locations of the deceased patients brain following tumor recurrence. Our analyses revealed the tissue-wide expansion of a new clone in the recurrent tumor as well as chromosome 7 gain and chromosome 10 loss as repeated genomic events in primary and recurrent disease. Moreover, chromosome 7 gain and chromosome 10 loss produced similar alterations in mRNA expression profiles in primary and recurrent tumors despite possessing other highly heterogeneous and divergent genomic alterations between the tumors. We identified ETV1 and CDK6 as putative candidate genes, and NFKB (complex), IL1B, IL6, Akt and VEGF as potential signaling regulators, as potentially central downstream effectors of chr7 gain and chr10 loss. Finally, the differences caused by the transcriptomic shift following gain of chromosome 7 and loss of chromosome 10 were consistent with those generally seen in GBM samples compared to normal brain in large-scale patient-tumor data sets.

Publication Title

Detailed longitudinal sampling of glioma stem cells in situ reveals Chr7 gain and Chr10 loss as repeated events in primary tumor formation and recurrence.

Sample Metadata Fields

Specimen part, Disease

View Samples
accession-icon GSE53717
Identification of Molecular Pathways Facilitating Glioma Cell Invasion In Situ
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 32 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Gliomas are mostly incurable secondary to their diffuse infiltrative nature. Thus, specific therapeutic targeting of invasive glioma cells is an attractive concept. As cells exit the tumor mass and infiltrate brain parenchyma, they closely interact with a changing micro-environmental landscape that sustains tumor cell invasion.

Publication Title

Identification of molecular pathways facilitating glioma cell invasion in situ.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE52363
Expression data from glioblastoma cells after ZFHX4 or CHD4 suppression.
  • organism-icon Homo sapiens
  • sample-icon 45 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

ZFHX4 and CHD4 suppression independently shift tumor initiating cells out of a stem like state and toward a differentiated morphology.

Publication Title

ZFHX4 interacts with the NuRD core member CHD4 and regulates the glioblastoma tumor-initiating cell state.

Sample Metadata Fields

Cell line

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accession-icon GSE73667
Expression data from sorted monoyctes/macrophages
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Tissue injury, such as incisional wound, results in an inflammatory response as well as acute to chronic mechanical and thermal pain. It is now understood that there is a strong contribution of these immune cells to the pain phenotype.

Publication Title

CD11b+Ly6G- myeloid cells mediate mechanical inflammatory pain hypersensitivity.

Sample Metadata Fields

Sex, Age

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accession-icon GSE13604
8 hours BMP6 treated vs untreated human mesenchymal stem cells (hMSC)
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We have established that BMP6 is an important endogenous regulator of human osteoblast differentiation. Our preliminary experiment showed that 8 hour BMP6 treatment induced early osteoblast markers in hMSC.

Publication Title

GAGE: generally applicable gene set enrichment for pathway analysis.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE30550
Temporal expression data from 17 health human subjects before and after they were challenged with live influenza (H3N2/Wisconsin) viruses
  • organism-icon Homo sapiens
  • sample-icon 268 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

The transcriptional responses of human hosts towards influenza viral pathogens are important for understanding virus-mediated immunopathology. Despite great advances gained through studies using model organisms, the complete temporal host transcriptional responses in a natural human system are poorly understood. In a human challenge study using live influenza (H3N2/Wisconsin) viruses, we conducted a clinically uninformed (unsupervised) factor analysis on gene expression profiles and established an ab initio molecular signature that strongly correlates to symptomatic clinical disease. This is followed by the identification of 42 biomarkers whose expression patterns best differentiate early from late phases of infection. In parallel, a clinically informed (supervised) analysis revealed over-stimulation of multiple viral sensing pathways in symptomatic hosts and linked their temporal trajectory with development of diverse clinical signs and symptoms. The resultant inflammatory cytokine profiles were shown to contribute to the pathogenesis because their significant increase preceded disease manifestation by 36 hours. In subclinical asymptomatic hosts, we discovered strong transcriptional regulation of genes involved in inflammasome activation, genes encoding virus interacting proteins, and evidence of active anti-oxidant and cell-mediated innate immune response. Taken together, our findings offer insights into influenza virus-induced pathogenesis and provide a valuable tool for disease monitoring and management in natural environments.

Publication Title

Temporal dynamics of host molecular responses differentiate symptomatic and asymptomatic influenza a infection.

Sample Metadata Fields

Specimen part

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accession-icon GSE135524
Gene expression and pathway enrichment associated with psychomotor slowing in patients with depression
  • organism-icon Homo sapiens
  • sample-icon 88 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Analysis of genes and pathways related to psychomotor retardation symptoms in patients with major depressive disorder. Results indicate that psychomotor slowing is associated with enrichment of inflammatory and metabolic pathways in unmedicated patients with depression.

Publication Title

Protein and gene markers of metabolic dysfunction and inflammation together associate with functional connectivity in reward and motor circuits in depression.

Sample Metadata Fields

Sex, Age, Specimen part, Race, Subject

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accession-icon GSE4870
Expression data from T65H translocation mice
  • organism-icon Mus musculus
  • sample-icon 45 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Tissue-specific comparison of gene expression levels in T65H translocation mice, either with or without uniparental duplications of Chrs 7 & 11. Identification of highly differentially expressed transcripts.

Publication Title

Chromosome-wide identification of novel imprinted genes using microarrays and uniparental disomies.

Sample Metadata Fields

Specimen part

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accession-icon GSE47632
Expression data from the Arabidopsis root epidermis mutants
  • organism-icon Arabidopsis thaliana
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

The root epidermis of Arabidopsis provides a simple and experimentally useful model for studying the molecular basis of cell fate and differentiation. The goal of this study was to define the transcript changes in the root epidermis of mutants associated with root epidermis cell specification, including mutants that lack a visible phenotypic alteration (try, egl3, myb23, and ttg2). Transcript levels were assessed by purifying populations of root epidermal cells using fluorescence-based cell-sorting with the WER::GFP transgene. These microarray results were used to compare the effects of single and double mutants on the gene regulatory network that controls root epidermal cell fate and differentiation in Arabidopsis.

Publication Title

Tissue-specific profiling reveals transcriptome alterations in Arabidopsis mutants lacking morphological phenotypes.

Sample Metadata Fields

Specimen part

View Samples
...

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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