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accession-icon GSE19605
Specificity for the Nature of Inflammation in Lung Cancer Promotion in Mice
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

A large amount of epidemiologic data supports a role for chronic inflammation in epithelial carcinogenesis. In the lung, several studies have found that smokers with chronic obstructive pulmonary disease (COPD), an inflammatory disease of the airways and alveoli, have an increased risk of lung cancer (1.3 to 4.9 fold) compared to smokers without COPD. We have also shown that COPD-like airway inflammation induced by an aerosolized lysate of non-typeable Hemophilus influenzae (NTHi) promotes lung cancer in a Clara cell-targeted K-ras mutant mouse model (CC-LR) of lung cancer. In contrast, existing epidemiologic data suggest that allergic inflammation of the airways may be protective against lung cancer. We tested this association in a mouse model of allergic airway inflammation. CC-LR mice were sensitized to ovalbumin by intraperitoneal injection weekly for two weeks, then challenged for 30 min to an aerosol of ovalbumin in 0.9% saline weekly for eight weeks. This resulted in eosinophilic lung inflammation associated with increased levels of T helper 2 (Th2) cytokines and mucous metaplasia of airway epithelium, similar to what is seen in asthma patients. However, consistent with epidemiologic data, this type of inflammation did not result in any significant differences in lung surface tumor number (22 3 in OVA exposed vs 26 6 in control mice). We conclude that asthma-like (Th2) inflammation does not promote lung carcinogenesis in a Ras-initiated background, and demonstrate a clear specificity for the nature of inflammation in lung cancer promotion. These findings will assist in determination of the essential cells and signaling events in lung cancer promotion by inflammation.

Publication Title

Interleukin 6, but not T helper 2 cytokines, promotes lung carcinogenesis.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE87330
Influence of Anti-VEGFA and dexamathasone treatments on the early phase of cornea angiogenesis
  • organism-icon Rattus norvegicus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Inflammation is a key component of pathological angiogenesis. Here we monitor gene expression profiles of the pre-sprouting phase of corneal angiogenesis in the rat model, as influenced by topically applied treatments.

Publication Title

Genome-wide expression differences in anti-Vegf and dexamethasone treatment of inflammatory angiogenesis in the rat cornea.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE1017
Acute Quadriplegic Myopathy
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

AQM shows acute muscle wasting and weakness. Key aspects of AQM include muscle atrophy and myofilament loss. Gene expression profiling, using muscle biopsies from AQM, neurogenic atrophy and normal controls, showed that both myogenic and neurogenic atrophy share induction of myofiber-specific ubiquitin/proteosome pathways while only the AQM shows a specific strong induction of transforming growth factor (TGF)-beta/MAPK pathways.

Publication Title

Constitutive activation of MAPK cascade in acute quadriplegic myopathy.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE53957
Transcriptomic profiling of Arabidopsis exposed to E-2-hexenal
  • organism-icon Arabidopsis thaliana
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Plants are known to be responsive to volatiles, but knowledge about the molecular players involved in transducing their perception remain scarce.

Publication Title

WRKY40 and WRKY6 act downstream of the green leaf volatile E-2-hexenal in Arabidopsis.

Sample Metadata Fields

Treatment

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accession-icon GSE6011
Expression data from quadriceps muscle of young DMD patients and age matched controls
  • organism-icon Homo sapiens
  • sample-icon 37 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Albeit increased serum CK level and abnormal muscle histology are always present, boys with DMD are phenotipically indistinguishable from the normal ones at birth and, in their first years of life, acquire early motor milestones at normal times. A clear defect in muscle function becomes generally apparent by the end of the second year. As the disease is typically diagnosed between the ages of 3 and 7, the first two years are often considered and referred to as clinically presymptomatic.

Publication Title

Gene expression profiling in the early phases of DMD: a constant molecular signature characterizes DMD muscle from early postnatal life throughout disease progression.

Sample Metadata Fields

Sex, Age

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accession-icon E-MEXP-2740
Transcription profiling by array of yeast wild type and haa1 deletion mutants following acetic acid stress
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome S98 Array (ygs98)

Description

The experiment describes the transcriptional response of Saccharomyces cerevisiae BY4741 and of the deletion mutant Δhaa1 following an incubation in the presence of 50 mM acetic acid (at pH 4.0)

Publication Title

Genomic expression program involving the Haa1p-regulon in Saccharomyces cerevisiae response to acetic acid.

Sample Metadata Fields

Compound

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accession-icon SRP007864
Transcriptome changes in IL-10 treated peritoneal macrophages
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

To try to identify the mechanism of STAT3s indirect action we have used a genomic approach to map the binding sites of STAT3 within the genome and also used RNA-seq technology to map the changes in RNA expression and transcript isoform abundance in response to IL-10. Overall design: Examination of transcriptome changes in peritoneal macrophages when treated with IL-10 for 4 hours. RNA was extracted and sequenced.

Publication Title

Genome-wide analysis of STAT3 binding in vivo predicts effectors of the anti-inflammatory response in macrophages.

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

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accession-icon SRP009895
Systematic RNA-seq analysis of the early events of CD4+ T cell activation
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

RNA-seq was used to look at the transcriptome changes and the early events of T cell receptor stimulation in CD4+ T cells Overall design: CD4+ T cells were stimulated with immobilised anti-CD3/CD28 antibodies for 4 hours and RNA was extracted and subjected to RNA-seq analysis.

Publication Title

Discovery and characterization of new transcripts from RNA-seq data in mouse CD4(+) T cells.

Sample Metadata Fields

Sex, Specimen part, Cell line, Treatment, Subject

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accession-icon GSE66521
Transcriptomic response of Saccharomyces cerevisiae in mixed-culture wine fermentation with Hanseniaspora guilliermondii
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Natural grape-juice fermentations involve the sequential development of different yeast species which strongly influence the chemical and sensorial traits of the final product. In the present study,we aimed to examine the transcriptomic response of Saccharomyces cerevisiae to the presence of Hanseniaspora guilliermondii wine fermentation.

Publication Title

Genomic expression program of Saccharomyces cerevisiae along a mixed-culture wine fermentation with Hanseniaspora guilliermondii.

Sample Metadata Fields

Treatment, Time

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accession-icon SRP070204
TRX-1 Regulates SKN-1 Nuclear Localization Cell Non-Autonomously in Caenorhabditis elegans
  • organism-icon Caenorhabditis elegans
  • sample-icon 53 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The Caenorhabditis elegans oxidative stress response transcription factor, SKN-1, is essential for the maintenance of redox homeostasis and is a functional ortholog of the Nrf family of transcription factors. The numerous levels of regulation that govern these transcription factors underscore their importance. Here, we add a thioredoxin, encoded by trx-1, to the expansive list of SKN-1 regulators. We report that loss of trx-1 promotes nuclear localization of intestinal SKN-1 in a redox-independent, cell non-autonomous fashion from the ASJ neurons. Furthermore, this regulation is not general to the thioredoxin family, as two other C. elegans thioredoxins TRX-2 and TRX-3 do not play a role in this process. Moreover, TRX-1-dependent regulation requires signaling from the p38 MAPK signaling pathway. However, while TRX-1 regulates SKN-1 nuclear localization, SKN-1 transcriptional activity remains largely unaffected. Interestingly, RNA-Seq revealed that loss of trx-1 elicits a general, organism-wide down-regulation of several classes of genes; those encoding for collagens and lipid transport and localization being most prevalent. However, one prominent lipase-related gene, lips-6, is highly up regulated upon loss of trx-1 in a skn-1-dependent manner. Together, these results uncover a novel role for a thioredoxin in regulating intestinal SKN-1 nuclear localization in a cell non-autonomous manner, thereby contributing to the understanding of the processes involved in maintaining redox homeostasis throughout an organism. Overall design: Four samples were analyzed: Two nematode strains were analyzed, each under non-stressed and stressed (10mM NaAs) conditions

Publication Title

TRX-1 Regulates SKN-1 Nuclear Localization Cell Non-autonomously in Caenorhabditis elegans.

Sample Metadata Fields

Disease, Cell line, 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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