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accession-icon GSE69688
Gene expression data from murine myeloid leukemia genomes induced by Sleeping Beauty transposon mutagenesis
  • organism-icon Mus musculus
  • sample-icon 47 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Transcriptome analysis of mRNA samples from a cohort of mice with histopathologically diagnosed Undifferentiated Myeloid Leukemia.

Publication Title

Analyzing tumor heterogeneity and driver genes in single myeloid leukemia cells with SBCapSeq.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage

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accession-icon SRP058917
Transcriptome sequencing of murine myeloid leukemia genome
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

Mus musculus (house mouse) Myeloid Leukemia RNA-Seq

Publication Title

Analyzing tumor heterogeneity and driver genes in single myeloid leukemia cells with SBCapSeq.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE85487
Effects of IFN-a and IFN-b on ex vivo ATL patient pbmcs
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The data contained in this record are used to differentiate between the effects of IFN-a and IFN-b on 48h cultures of the ex vivo pbmcs of ATL patients, using Affymetrix microarrays (HuGene 1.0).

Publication Title

IFN-β induces greater antiproliferative and proapoptotic effects and increased p53 signaling compared with IFN-α in PBMCs of Adult T-cell Leukemia/Lymphoma patients.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE82160
FAS signalling in retroviral neuroinflammation
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

We comprehensively explored Fas expression (protein and mRNA) and function in lymphocyte activation, apoptosis, proliferation and transcriptome, using flow cytometry, [3H]-thymidine incorporation and microarray analysis in PBMC from HTLV-1 Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP) patients.

Publication Title

A Fas<sup>hi</sup> Lymphoproliferative Phenotype Reveals Non-Apoptotic Fas Signaling in HTLV-1-Associated Neuroinflammation.

Sample Metadata Fields

Specimen part, Disease stage, Treatment

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accession-icon GSE80008
Systemic disease signature of human cutaneous leishmaniasis
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

In addition to the recently published in situ transcriptomics of LCL skin lesions (Novais et al., Khouri et al.), we herein present the first systemic disease signature of localized cutaneous leishmaniasis (LCL), using Affymetrix microarrays (HuGene 1.0) followed by systems biology analysis of the PBMC transciptome of LCL patients (n=18), as compared to healthy controls (n=12).

Publication Title

Systems Approach Reveals Nuclear Factor Erythroid 2-Related Factor 2/Protein Kinase R Crosstalk in Human Cutaneous Leishmaniasis.

Sample Metadata Fields

Specimen part, Disease stage

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accession-icon GSE46097
Expression data of Participants of Ornish intervention and Control group
  • organism-icon Homo sapiens
  • sample-icon 377 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Intensive lifestyle modification is believed to mediate cardiovascular disease (CVD) risk through traditional pathways that affect endothelial function and progression of atherosclerosis; however, the extent, persistence, and clinical significance of molecular change during lifestyle modification are not well known. Our study reveals that gene expression signatures are significantly modulated by rigorous lifestyle behaviors and track with CVD risk profiles over time.

Publication Title

Intensive cardiovascular risk reduction induces sustainable changes in expression of genes and pathways important to vascular function.

Sample Metadata Fields

Sex, Age

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accession-icon GSE77919
ALS-causing mutations differentially affect PGC-1alpha expression and function in the brain vs. peripheral tissues
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Amyotrophic later sclerosis is a motor neuron disease accompanied by metabolic changes. PGC (PPAR gamma coactivator)-1alpha is a master regulator of mitochondrial biogenesis and function and of critical importance for all metabolically active tissues. PGC-1alpha is a genetic modifier of ALS.

Publication Title

ALS-causing mutations differentially affect PGC-1α expression and function in the brain vs. peripheral tissues.

Sample Metadata Fields

Specimen part

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accession-icon GSE18497
Diagnosis-relapse in ALL
  • organism-icon Homo sapiens
  • sample-icon 81 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Almost a quarter of pediatric patients with Acute Lymphoblastic Leukemia (ALL) suffer from relapses. The biological mechanisms underlying therapy response and development of relapses have remained unclear. In an attempt to better understand this phenomenon, we have analyzed 41 matched diagnosis relapse pairs of ALL patients using genomewide expression arrays (82 arrays) on purified leukemic cells. In roughly half of the patients very few differences between diagnosis and relapse samples were found (stable group), suggesting that mostly extra-leukemic factors (e.g., drug distribution, drug metabolism, compliance) contributed to the relapse. Therefore, we focused our further analysis on 20 samples with clear differences in gene expression (skewed group), reasoning that these would allow us to better study the biological mechanisms underlying relapsed ALL. After finding the differences between diagnosis and relapse pairs in this group, we identified four major gene clusters corresponding to several pathways associated with changes in cell cycle, DNA replication, recombination and repair, as well as B cell developmental genes. We also identified cancer genes commonly associated with colon carcinomas and ubiquitination to be upregulated in relapsed ALL. Thus, about half of relapses are due to selection or emergence of a clone with deregulated expression of a genes involved in pathways that regulate B cell signaling, development, cell cycle, cellular division and replication.

Publication Title

Genome-wide expression analysis of paired diagnosis-relapse samples in ALL indicates involvement of pathways related to DNA replication, cell cycle and DNA repair, independent of immune phenotype.

Sample Metadata Fields

Sex, Specimen part, Disease

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accession-icon GSE72672
Expression data from epidermal and dorsal root ganglion tissues of wild-type and mutant mice with mechanosensory deficit
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

A novel mouse line was found to exhibit prominent mechanosensory deficits both behaviorally and at the primary sensory afferents, and exhibits decreased ATP release from the skin.

Publication Title

Mechanosensory and ATP Release Deficits following Keratin14-Cre-Mediated TRPA1 Deletion Despite Absence of TRPA1 in Murine Keratinocytes.

Sample Metadata Fields

Specimen part

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accession-icon SRP170629
RNA Sequencing Analysis of Intracranial Aneurysm Walls Reveals Involvement of Lysosomes and Immunoglobulins in Rupture
  • organism-icon Homo sapiens
  • sample-icon 60 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Background and Purpose—Analyzing genes involved in development and rupture of intracranial aneurysms can enhance knowledge about the pathogenesis of aneurysms, and identify new treatment strategies. We compared gene expression between ruptured and unruptured aneurysms and control intracranial arteries. Methods—We determined expression levels with RNA sequencing. Applying a multivariate negative binomial model, we identified genes that were differentially expressed between 44 aneurysms and 16 control arteries, and between 22 ruptured and 21 unruptured aneurysms. The differential expression of 8 relevant and highly significant genes was validated using digital polymerase chain reaction. Pathway analysis was used to identify enriched pathways. We also analyzed genes with an extreme pattern of differential expression: only expressed in 1 condition without any expression in the other. Results—We found 229 differentially expressed genes in aneurysms versus controls and 1489 in ruptured versus unruptured aneurysms. The differential expression of all 8 genes selected for digital polymerase chain reaction validation was confirmed. Extracellular matrix pathways were enriched in aneurysms versus controls, whereas pathways involved in immune response and the lysosome pathway were enriched in ruptured versus unruptured aneurysms. Immunoglobulin genes were expressed in aneurysms, but showed no expression in controls. Conclusions—For rupture of intracranial aneurysms, we identified the lysosome pathway as a new pathway and found further evidence for the role of the immune response. Our results also point toward a role for immunoglobulins in the pathogenesis of aneurysms. Immune-modifying drugs are, therefore, interesting candidate treatment strategies in the prevention of aneurysm development and rupture. Overall design: RNA sequencing of 44 intracranial aneurysm samples (including 21 unruptured, 22 ruptured and 1 undetermined) and 16 control samples of the intracranial cortical artery

Publication Title

RNA Sequencing Analysis of Intracranial Aneurysm Walls Reveals Involvement of Lysosomes and Immunoglobulins in Rupture.

Sample Metadata Fields

Sex, Age, Subject

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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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