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accession-icon GSE60674
Upregulation of Interferon-inducible and damage response pathways in chronic graft-versus-host disease
  • organism-icon Homo sapiens
  • sample-icon 34 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

To identify systemic cytokine patterns in Chronic Graft-versus-Host-Disease (CGVHD), we profiled the gene expression of circulating monocytes. Pathway analysis identified two gene sets that were significantly upregulated across a broad range of patients with inflammatory and sclerotic presentations: (1) genes induced by Type I and Type II IFN, and (2) receptor genes for innate immune responses to cellular damage. Multiple IFN-inducible genes involved in signal transduction, anti-viral function, lymphocyte homeostasis, trafficking, and antigen presentation were increased. Furthermore, upregulation of TLR/NLR/CLR receptor genes for nucleic acids, ribonucleoproteins and annexin implicated response to damaged cells as a source of activation of inflammasomes and induction of Type I IFN.

Publication Title

Upregulation of IFN-Inducible and Damage-Response Pathways in Chronic Graft-versus-Host Disease.

Sample Metadata Fields

Specimen part, Disease

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accession-icon GSE41229
Expression data from T-cells isolated from healthy mice or mice with polyposis
  • organism-icon Mus musculus
  • sample-icon 44 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

There is much controversy about the role of T-regulatory cells (Treg) in human colon cancer. High densities of tumor-infiltrating Treg can correlate with better or worse clinical outcomes depending on the sutdy. Treg have potent anti-inflammatory functions that have been shown to control cancer progression. However, Treg isolated from patient with colon cancer or in mouse models of polyposis do not have the ability to suppress inflammation and instead promote cancer. Gene expression was preformed to determine differences between Treg isolated from healthy mice and Treg isolated from polyp-ridden mice.

Publication Title

Expression of RORγt marks a pathogenic regulatory T cell subset in human colon cancer.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE27131
Peripheral blood cells expression data form 7 patients with severe pdm(H1N1) influensa and 7 gender and age matched healthy controls
  • organism-icon Homo sapiens
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Using PAXgene tubes, peripheral blood samples were collected from seven patients >18 years with documented pdm(H1N1) influenza, bilateral chest infiltrates, and in need of ventilation support. Significant co-morbidity was exclusion criterion. Expression profiles were compared with 7 age matched controls. Using a false discovery rate < 5% and an absolute fold change > 2, 370 genes were differentially expressed in case and controls.

Publication Title

Excessive innate immune response and mutant D222G/N in severe A (H1N1) pandemic influenza.

Sample Metadata Fields

Sex, Age, Specimen part, Subject

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accession-icon GSE6116
Transcriptional Biomarkers to Predict Female Mouse Lung Tumors in Rodent Cancer Bioassays - A 13 Chemical Training Set
  • organism-icon Mus musculus
  • sample-icon 70 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The primary goal of toxicology and safety testing is to identify agents that have the potential to cause adverse effects in humans. Unfortunately, many of these tests have not changed significantly in the past 30 years and most are inefficient, costly, and rely heavily on the use of animals. The rodent cancer bioassay is one of these safety tests and was originally established as a screen to identify potential carcinogens that would be further analyzed in human epidemiological studies. Today, the rodent cancer bioassay has evolved into the primary means to determine the carcinogenic potential of a chemical and generate quantitative information on dose-response behavior in chemical risk assessments. Due to the resource-intensive nature of these studies, each bioassay costs $2 to $4 million and takes over three years to complete. Over the past 30 years, only 1,468 chemicals have been tested in a rodent cancer bioassay. By comparison, approximately 9,000 chemicals are used by industry in quantities greater than 10,000 lbs and nearly 90,000 chemicals have been inventoried by the U.S. Environmental Protection Agency as part of the Toxic Substances Control Act. Given the disparity between the number of chemicals tested in a rodent cancer bioassay and the number of chemicals used by industry, a more efficient and economical system of identifying chemical carcinogens needs to be developed.

Publication Title

Application of genomic biomarkers to predict increased lung tumor incidence in 2-year rodent cancer bioassays.

Sample Metadata Fields

Sex, Age, Subject

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accession-icon SRP180359
Epithelial mesenchymal transition (EMT) in A549 NSCLC cells. TGFbeta was used to induce EMT, RNA isolated and subjected to RNAseq on Illumina HiSeq
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The capacity of cancer cells to undergo epithelial mesenchymal trans-differentiation has been implicated as a factor driving metastasis, through the acquisition of enhanced migratory/invasive cell programs and the engagement of anti-apoptotic mechanisms promoting drug and radiation resistance. Our aim was to define molecular signaling changes associated with mesenchymal trans-differentiation in two KRas mutant NSCLC models. We focused on central transcription and epigenetic regulators predicted to be important for mesenchymal cell survival. Overall design: Haley, J.A., Haughney, E., Ullman, E., Bean, J., Haley, J.D.* and Fink, M.Y. (2014) 'Altered Transcriptional Control Networks with Trans-Differentiation of Isogenic Mutant KRas NSCLC Models' Front. Oncology, doi/10.3389/fonc.2014.00344.

Publication Title

Altered Transcriptional Control Networks with Trans-Differentiation of Isogenic Mutant-KRas NSCLC Models.

Sample Metadata Fields

Treatment, Subject

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accession-icon GSE22295
Lack of chemokine signaling through CXCR5 causes mortality, ventricular dilatation and deranged matrix during pressure overload
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Inflammatory mechanisms have been suggested to play a role in the development of heart failure (HF), but a role for chemokines is largely unknown. The aim of this study was to analyze the role of the chemokine CXCL13 and its receptor CXCR5 in cardiac pathophysiology leading to HF

Publication Title

Lack of chemokine signaling through CXCR5 causes increased mortality, ventricular dilatation and deranged matrix during cardiac pressure overload.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP114515
Novel Form of JARID2 is Required to Regulate Differentiation in Keratinocytes.
  • organism-icon Homo sapiens
  • sample-icon 32 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Polycomb repressive complex-2 (PRC2) is a group of proteins that play important role during development and in cell differentiation. PRC2 is a histone-modifying complex that catalyses methylation of lysine 27 of histone H3 (H3K27me3) at differentiation genes leading to their transcriptional repression. JARID2 is a co-factor of PRC2 and is important for targeting PRC2 to chromatin as well as modulating its activity. Here, we show that in many human cells, including human epidermal keratinocytes, JARID2 predominantly exists as a novel low molecular weight form, which lacks the N-terminal PRC2-interacting domain (?N-JARID2). We show that ?N-JARID2 is a cleaved product of full-length JARID2 spanning the C-terminal conserved region consisting of jumonji domains. JARID2 knockout in keratinocytes results in up-regulation of cell cycle genes and repression of many epidermal differentiation genes. Surprisingly, repression of epidermal differentiation genes in JARID2-null keratinocytes can be relieved by expression of ?N-JARID2 suggesting that this form promotes activation of these genes and has opposing function to that of PRC2 in regulation of differentiation. We propose that a switch from expression of full-length JARID2 to ?N-JARID2 is important for the up-regulation of genes during differentiation. Overall design: RNA-seq analysis of Wildtype and JARID2-null keratinocytes (HaCaTs) on day 0 and day 3 of calcium induced differentiation.

Publication Title

A novel form of JARID2 is required for differentiation in lineage-committed cells.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP128913
Next Generation Sequencing Facilitates Quantitative Analysis of the Effect of GM-CSF on the Transcriptomes of Alveolar and Exudative Lung Macrophages from Influenza-infected C57BL/6 Mice
  • organism-icon Mus musculus
  • sample-icon 26 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The transcriptomes of FACS-sorted siglec-F+ alveolar macrophages and siglec-f- CD11b+ exudative macrophages from inducible airway GM-CSF over-expressing transgenic mice (DTGM) were compared to non-inducible littermate controls during influenza A virus infection. Overall design: Examination of effect of GM-CSF on airway macrophages during influenza A virus infection

Publication Title

GM-CSF overexpression after influenza a virus infection prevents mortality and moderates M1-like airway monocyte/macrophage polarization.

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

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accession-icon GSE16179
BT474 and BT474-J4 microarray data
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

These data provide scientific information to understand the mechanism of action of lapatinib resistance in HER2-positive patients and to test the combination of HER2-targeted agents and GSK1363089 (foretinib) in the clinic by using an acquired lapatinib-resistant cell line.

Publication Title

Novel mechanism of lapatinib resistance in HER2-positive breast tumor cells: activation of AXL.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE113717
De novo lipogenesis represents a therapeutic target in Kras mutant NSCLC
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

We examine the potential of Kras as a metabolic target in lung cancer using the KrasLSL-G12D lung cancer model. We demonstrate that mutant Kras drives a lipogenic gene expression program, and that fatty acid synthesis is important in Kras-induced tumorigenesis.

Publication Title

De novo lipogenesis represents a therapeutic target in mutant Kras non-small cell lung cancer.

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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