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accession-icon GSE37912
Peripheral blood gene expression as a novel genomic biomarker in complicated sarcoidosis
  • organism-icon Homo sapiens
  • sample-icon 73 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Sarcoidosis, a systemic granulomatous syndrome invariably affecting the lung, typically spontaneously remits but in ~20% of cases progresses with severe lung dysfunction or cardiac and neurologic involvement (complicated sarcoidosis). Unfortunately, current biomarkers fail to distinguish patients with remitting (uncomplicated) sarcoidosis from other fibrotic lung disorders, and fail to identify individuals at risk for complicated sarcoidosis.

Publication Title

Peripheral blood gene expression as a novel genomic biomarker in complicated sarcoidosis.

Sample Metadata Fields

Specimen part, Disease, Race

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accession-icon GSE33253
Transcriptional reprogramming of tumor-associated endothelial cells by disruption of TNF- signaling
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Endothelial inflammation contributes to the pathogenesis of numerous human diseases; however, the role of tumor endothelial inflammation in the growth of experimental tumors and its influence on the prognosis of human cancers is less understood. TNF-, an important mediator of tumor stromal inflammation, is known to target the tumor vasculature. In this study, we demonstrate that B16-F1 melanomas grew more rapidly in C57BL/6 wild-type (WT) mice than in syngeneic mice with germline deletions of both TNF- receptors (KO). This enhanced tumor growth was associated with increased COX2 inflammatory expression in WT tumor endothelium compared to endothelium in KO mice. We purified endothelial cells from WT and KO tumors and characterized dysregulated gene expression, which ultimately formed the basis of a 6-gene Inflammation-Related Endothelial-derived Gene (IREG) signature. This inflammatory signature expressed in WT tumor endothelial cells was trained in human cancer datasets and predicted a poor clinical outcome in breast cancer, colon cancer, lung cancer and glioma. Consistent with this observation, conditioned media from human endothelial cells treated with pro-inflammatory cytokines (TNF- and interferons) accelerated the growth of human colon and breast tumors in immune-deprived mice as compared with conditioned media from untreated endothelial cells. These findings demonstrate that activation of endothelial inflammatory pathways contributes to tumor growth and progression in diverse human cancers.

Publication Title

Tumor endothelial inflammation predicts clinical outcome in diverse human cancers.

Sample Metadata Fields

Specimen part

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accession-icon SRP049605
Identification of a Molecular Signature for Acute Lyme Disease by Human Transcriptome Profiling
  • organism-icon Homo sapiens
  • sample-icon 97 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Lyme disease is challenging to diagnose, as clinical manifestations are variable and current tools to detect nucleic acid or antibody responses from Borrelia burgdorferi infection have low sensitivity. Here we conducted the first study of the global transcriptome of patients with Lyme disease to identify potential diagnostic biomarkers. Twenty-nine patients were enrolled and compared to 13 healthy controls at three time points after infection. Fifteen publicly available transcriptome datasets from patients in vivo or infection models in vitro were used to assess specificity of differentially expressed genes (DEGs). We found that Lyme disease results in profound and sustained changes in the patient transcriptomes, with a specific signature that shares =44% DEGs with other infections. Overall design: Gene expression profile from peripheral mononuclear blood cells (PBMC) of Lyme disease patients against healthy controls was undertaken. A total of 29 Lyme disease patients were sampled at 3 time points: acute Lyme pre-treatment (V1), 3 weeks later, immediately following completion of a standard course of antibiotics (V2), and 6 months following treatment completion (V5). 13 healthy controls were also sampled at one time point. Total RNA was extracted from 10e7 PBMC, followed by mRNA purification, paired-end barcode library preparation and sequencing on an Illumina Hiseq 2000.

Publication Title

Longitudinal Transcriptome Analysis Reveals a Sustained Differential Gene Expression Signature in Patients Treated for Acute Lyme Disease.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE55028
CMPF alters expression of genes related to metabolism in isolated mouse islets
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

CMPF is elevated in diabetes and is associated with impaired insulin secretion. We used microarrays to determine the effect of CMPF on gene expression in isolated islets.

Publication Title

The furan fatty acid metabolite CMPF is elevated in diabetes and induces β cell dysfunction.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

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accession-icon GSE117013
Gene expression array of brain, mandible and maxilla tissues from P0 FoxO6-/- and wildtype mice
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

FoxO6 is expressed in the brain, craniofacial region and somite, but the precise role of FoxO6 in craniofacial development remain unknown. We found that FoxO6 is expressed specifically in craniofacial tissues and FoxO6-/- mice undergo expansion of the face, frontal cortex, olfactory component and skull.

Publication Title

FoxO6 regulates Hippo signaling and growth of the craniofacial complex.

Sample Metadata Fields

Specimen part

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accession-icon GSE86068
Increasing of antitumor effect of decitabine against classical Hodgkin lymphoma (cHL) by targeting decitabine-activated pro-survival pathways
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We found that 5-Aza-dC/decitabine induces various prosurvival pathways (JAK-STAT-, NFkB-, MEK/ERK- and PI3K/AKTpathway) in cHL cell lines. Inhibition of these pathways with specific small molecular weight inhibitors potentiates the antitumor effect of 5-Aza-dC.

Publication Title

Activation of oncogenic pathways in classical Hodgkin lymphoma by decitabine: A rationale for combination with small molecular weight inhibitors.

Sample Metadata Fields

Cell line

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accession-icon GSE66099
Unique Patients from the Genomics of Pediatric SIRS and Septic Shock Investigators (GPSSSI)
  • organism-icon Homo sapiens
  • sample-icon 272 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This dataset is composed of the unique patients (276; at the Day 1 timepoint) that are present in the six other GEO datasets published by Hector Wong and the Genomics of Pediatric SIRS and Septic Shock Investigators. This dataset thus includes all unique patients from GSE4607, GSE8121, GSE9692, GSE13904, GSE26378, and GSE26440. These are only from the Day 1 timepoint.

Publication Title

A comprehensive time-course-based multicohort analysis of sepsis and sterile inflammation reveals a robust diagnostic gene set.

Sample Metadata Fields

Specimen part, Disease

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accession-icon GSE69815
Expression array of glucosamine-fed Drosophila heart/nephrocyte complexes
  • organism-icon Drosophila melanogaster
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Examined the expression effects of supplementing Drosophila food on heart and nephrocyte complexes

Publication Title

Diet-Induced Podocyte Dysfunction in Drosophila and Mammals.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon SRP043544
H2A.Z knockdown RNAseq
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

This experiment seeks to ascertain the transcriptional changes in the adult mouse hippocampus (CA1 subregion) that occur following viral knockdown of the histone variant H2A.Z. We are especially interested in understanding the role of this histone variant in memory formation and memory maintenance in the adult central nervous system. Overall design: This experiment includes 3 groups, each with 3 biological replicates. Samples S108, S109, and S110 are from controls infected with an AAV expressing a scrambled shRNA control. Samples A100, A101, A102, A104, A106, and A107 were infected with an AAV expressing an shRNA against H2A.Z. Samples A100, A101, and A102 were naive animals, whereas samples A104, A106, and A107 were trained in contextual fear conditioning.

Publication Title

Histone H2A.Z subunit exchange controls consolidation of recent and remote memory.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE53509
Drosophila CNS mitochondrial DNA dysfunction microarray
  • organism-icon Drosophila melanogaster
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Drosophila Gene 1.0 ST Array (drogene10st)

Description

Mitochondrial DNA (mtDNA) encodes essential components of the respiratory chain and loss of mtDNA leads to mitochondrial dysfunction and neurodegeneration. Mitochondrial transcription factor A (TFAM) is an essential component of mtDNA replication and a regulator of mitochondrial copy number in cells. Studies have shown that TFAM knockdown leads to mitochondrial dysfunction and respiratory chain deficiencies. ATP synthase is Complex V of the mitochondrial respiratory chain. It is driven by a proton gradient between the intermembrane space and the mitochondrial matrix and generates the majority of cellular ATP. The knockdown of coupling factor 6 (Cf6), one of the components of the proton channel F0, causes dysfunction in the complex, leading to mitochondrial dysfunction and respiratory chain deficiencies. Using gene expression analysis, we aimed to investigate the effects of mtDNA dysfunction in the CNS at the molecular level.

Publication Title

Mitochondrial retrograde signaling regulates neuronal function.

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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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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