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accession-icon GSE33822
Transcriptome Atlases Of Mouse Brain Reveals Differential Expression Across Brain Regions And Genetic Backgrounds
  • organism-icon Mus musculus
  • sample-icon 96 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Assessed steady-state transcription in whole brain and two more specific brain regions.

Publication Title

Transcriptome atlases of mouse brain reveals differential expression across brain regions and genetic backgrounds.

Sample Metadata Fields

Treatment

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accession-icon GSE57380
Coexistent ARID1A-PIK3CA mutations promote ovarian clear cell tumorigenesis through pro-tumorigenic inflammatory cytokine signaling
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.1 ST Array (mogene21st)

Description

Ovarian clear cell carcinoma (OCCC) is an aggressive form of ovarian cancer with high ARID1A mutation rates. Here we present a genetically engineered mouse model of OCCC. We find that ARID1A inactivation is not sufficient for tumor formation, but requires concurrent activation of the phosphoinositide 3-kinase catalytic subunit, PIK3CA. Remarkably, the mice develop highly penetrant tumors with OCCC-like histopathology, culminating in hemorrhagic ascites and a median survival period of 7.5 weeks. Therapeutic treatment with the pan-PI3K inhibitor, BKM120, prolonged mouse survival by inhibiting tumor cell growth. Cross-species gene expression comparisons support a role for IL-6 inflammatory cytokine signaling in OCCC pathogenesis. We further show that ARID1A-PIK3CA mutations cooperate to promote tumor growth through sustained IL-6 overproduction. Our findings establish an epistatic relationship between SWI/SNF chromatin remodeling and PI3K pathway mutations in OCCC and demonstrate that these pathways converge on pro-tumorigenic cytokine signaling. We propose that ARID1A protects against inflammation-driven tumorigenesis.

Publication Title

Coexistent ARID1A-PIK3CA mutations promote ovarian clear-cell tumorigenesis through pro-tumorigenic inflammatory cytokine signalling.

Sample Metadata Fields

Specimen part

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accession-icon GSE44555
Multiple tissue expression data from inbreds and F1 of CAST, PWK, and WSB
  • organism-icon Mus musculus
  • sample-icon 384 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

We create catalogues of genes showing significant strain, parent-of-origin, dominance, sex effect in inbreds and reciprocal F1 hybrids of three wild-derived strains (CAST, PWK, WSB) across 4 different tissues (brain, kidney, liver, and lung)

Publication Title

Analyses of allele-specific gene expression in highly divergent mouse crosses identifies pervasive allelic imbalance.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE50840
Expression data from activated NK cells
  • organism-icon Homo sapiens
  • sample-icon 32 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

All-trans retinoic acid (ATRA) induces miR-23a expression, decreases CTSC expression and granzyme B activity leading to impaired NK cell cytotoxicity.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE50838
Expression data from activated NK cells [RNA]
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

Natural Killer (NK) cells present natural cytotoxicity against tumor cells, although their activity is increased after activation. NK cell activation depends on a complex intracellular signaling process mediated by activating and inhibitory receptors and the functional outcome depends on the integration of the activating and inhibitory signals received. Soluble cytokines and/or ligands on target cells bind the NK cell receptors, and hence, influence the final NK cell response: attack versus ignorance.

Publication Title

All-trans retinoic acid (ATRA) induces miR-23a expression, decreases CTSC expression and granzyme B activity leading to impaired NK cell cytotoxicity.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP197582
Time-series reveals processes underlying colon inflammation and repair
  • organism-icon Mus musculus
  • sample-icon 26 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

To elucidated through an unbiased manner which genes and pathways are differentially regulated during mouse colonic inflammation followed by a tissue regeneration phase. In particular, we took advantage of the widely used dextran sodium sulfate (DSS)-induced model of colitis. This model is one of the few characterized by a phase of damage followed by a phase of regeneration. Therefore, this model gave the possibility to identify also sets of genes essential in the regeneration phase, a key step towards the resolution of the inflammation. In short, mice were exposed to DSS in the drinking water for 7 days, then allowed to recover for the following 7 days. During this period, we collected colonic tissue samples every second day to then be analyzed by RNA sequencing (RNA-seq). Next, we performed a RNA-seq analysis from colonic samples throughout the experiment and computed differentially expressed genes (DEGs) taking the complete kinetics of expression into consideration for p-value estimation using EdgeR. Overall design: C57BL/6J female mice were treated with 2.5% DSS in order to induce colinic inflammation. 2-3 animals were sacrificed at different time points when the colonic tissue was collected.

Publication Title

Conserved transcriptomic profile between mouse and human colitis allows unsupervised patient stratification.

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

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accession-icon SRP124262
IL-7-dependent STAT1 activation limits homeostatic CD4+ T cell expansion
  • organism-icon Mus musculus
  • sample-icon 75 Downloadable Samples
  • Technology Badge IconNextSeq 500, Illumina HiSeq 2500

Description

IL-7 regulates homeostatic mechanisms that maintain the overall size of the T cell pool throughout life. We show that, under steady-state conditions, IL-7 signaling is principally mediated by activation of signal transducers and activators of transcription 5 (STAT5). In contrast, under lymphopenic conditions, there is a modulation of STAT1 expression resulting in an IL-7-dependent STAT1 and STAT5 activation. Consequently, the IL-7-induced transcriptome is altered with enrichment of IFN-stimulated genes (ISGs). Moreover, STAT1 overexpression was associated with reduced survival in CD4+ T cells undergoing lymphopenia-induced proliferation (LIP). We propose a model in which T cells undergoing LIP upregulate STAT1 protein, "switching on" an alternate IL-7-dependent program. This mechanism could be a physiological process to regulate the expansion and size of the CD4+ T cell pool. During HIV infection, the virus could exploit this pathway, leading to the homeostatic dysregulation of the T cell pools observed in these patients. Overall design: Sorted naive CD4 T and CD8 T cells from WT or STAT1 transgenic mice were stimulated for 90 minutes with IL-7 or IFNg. Additonally CD4 T cells from WT or STAT1 trangenic or IL7Ra449F transgenic mice were stimulated for overnight with IL-7 or IFNg or IFNa4. Up to four biological replicates tested for each condition.

Publication Title

IL-7-dependent STAT1 activation limits homeostatic CD4+ T cell expansion.

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP063363
Transcriptomes of peripheral blood mononuclear cells from a Guillain-Barre Syndrome patient and her healthy twin sampled at three different points of the disease evolution
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzerIIx

Description

Guillain-Barré syndrome (GBS) is an immune-mediated peripheral neuropathy that debilitates the voluntary and autonomous response of the patient. In this study the transcriptome of peripheral blood mononuclear cells from a GBS patient and her healthy twin were compared to discover possible correlates of disease progression and recovery. Overall design: Blood samples were collected simultaneously from the Guillain-Barré patient (A) and from her control healthy twin (B) at three different time points during disease progression from hospitalization in the intensive care unit (T1), passing to intermediate care (T2), and at conclusion of locomotion rehabilitation program when the patient was close to abandon the hospital (T3).

Publication Title

Expression of Early Growth Response Gene-2 and Regulated Cytokines Correlates with Recovery from Guillain-Barré Syndrome.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE37485
Expression data of pre-stasis cultured HMEC
  • organism-icon Homo sapiens
  • sample-icon 52 Downloadable Samples
  • Technology Badge Icon Affymetrix HT Human Genome U133A Array (hthgu133a)

Description

We have generated a large collection of normal human mammary epithelial cell strains from women aged 16 to 91 years, derived from primary tissues, to enable functional and molecular interrogation of aging. We demonstrate in finite-lifespan cultured and uncultured epithelial cells that aging is associated with reduction of myoepithelial cells and with increases in luminal cells expressing keratin 14 and integrin 6, traits that are expressed exclusively in myoepithelial cells in women under 30. We find that changes to the luminal lineage result from age-dependent expansion of multipotent progenitors that bear defects resulting in incompletely differentiated luminal cells. These findings were verified in vivo in normal breast tissues. Myoepithelial cells have been suggested to act as tumor suppressors, and progenitor cells are implicated as the etiological roots of mammary carcinomas. Thus with aging there is a shift in the balance of luminal/myoepithelial lineages, and changes in the functional spectrum of multipotent progenitors, which presages increased potential for malignant transformation.

Publication Title

Accumulation of multipotent progenitors with a basal differentiation bias during aging of human mammary epithelia.

Sample Metadata Fields

Age, Specimen part

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accession-icon SRP075478
Targeting Taxane-Platin Resistant Lung Cancers with JumonjiC Lysine Demethylase Inhibitors (RNA-Seq)
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Characterization of gene expression changes upon development of taxane-platin drug resistance in NSCLC cells and further, upon treatment of these resistant cells with the Jumonji KDM inhibitor, GSK-J4. Overall design: Comparison of gene expression changes between H1299 Parental cells (chemo-sensitive) and H1299 T18 cells (taxane-platin resistant), and comparison of H1299 T18: GSK-J4 treated vs. H1299 T18: DMSO control.

Publication Title

Taxane-Platin-Resistant Lung Cancers Co-develop Hypersensitivity to JumonjiC Demethylase Inhibitors.

Sample Metadata Fields

Sex, Age, Treatment, Race, 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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