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accession-icon GSE84887
Molecular Characterization of Down Syndrome Embryonic Stem Cells Reveals a Role for RUNX1 in Neural Differentiation
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Down syndrome (DS) is the leading genetic cause of mental retardation and is caused by a third copy of human chromosome 21. The different pathologies of DS involve many tissues with a distinct array of neural phenotypes. Here we characterize new embryonic stem cell lines with DS (DS-ESCs), and focus on the neural aspects of the diease. Our results show that neural progenitor cells (NPCs) differentiated from five independent DS-ESC lines display increased apoptosis and down-regulation of forehead developmental genes. Analysis of differentially expressed genes suggested RUNX1 as a key transcription regulator in DS-NPCs. Using genome editing we were able to disrupt all three copies of RUNX1 in DS-ESCs, leading to down-regulation of several RUNX1 target developmental genes accompanied by reduced apoptosis and neuron migration. Our work sheds new light on the role of RUNX1 and the importance of dosage balance in the development of neural phenotypes in DS.

Publication Title

Molecular Characterization of Down Syndrome Embryonic Stem Cells Reveals a Role for RUNX1 in Neural Differentiation.

Sample Metadata Fields

Sex, Specimen part

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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 GSE83686
Chromosomal Instability and Molecular Defects in Induced Pluripotent Stem Cells with Nijmegen Breakage Syndrome
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Nijmegen breakage syndrome (NBS) results from the absence of the NBS1 protein, responsible for detection of DNA double-strand breaks (DSBs). NBS is characterized by microcephaly, growth retardation, immunodeficiency, and cancer predisposition. Here we show successful reprogramming of NBS fibroblasts into induced pluripotent stem cells (NBS-iPSCs). Our data suggest a strong selection for karyotypically normal fibroblasts to go through the reprogramming process. NBS-iPSCs then acquire numerous chromosomal aberrations and show a delayed response to DSB induction. Furthermore, NBS-iPSCs display slower growth, mitotic inhibition, a reduced apoptotic response to stress and abnormal cell cycle-related gene expression. Importantly, NBS neural progenitor cells (NBS-NPCs) show down-regulation of neural developmental genes, which seems to be mediated by P53. Our results demonstrate the importance of NBS1 in early human development, shed new light on the molecular mechanisms underlying this severe syndrome and further expand our knowledge of the genomic stress cells experience during the reprogramming process.

Publication Title

Chromosomal Instability and Molecular Defects in Induced Pluripotent Stem Cells from Nijmegen Breakage Syndrome Patients.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE94746
Differential gene expression in the adipose tissue of crossbred beef cows with divergent gain after feed restriction and ad libitum feeding studies.
  • organism-icon Bos taurus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Bovine Gene 1.1 ST Array (bovgene11st)

Description

Beef cow adipose tissue transcriptome

Publication Title

Differential transcript abundance in adipose tissue of mature beef cows during feed restriction and realimentation.

Sample Metadata Fields

Specimen part

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accession-icon GSE64913
Altered epithelial gene expression in peripheral airways of severe asthma
  • organism-icon Homo sapiens
  • sample-icon 70 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Management of severe asthma remains a challenge despite treatment with glucocorticosteroid therapy. The majority of studies investigating disease mechanisms in treatment-resistant severe asthma have previously focused on the large central airways, with very few utilizing transcriptomic approaches. The small peripheral airways, which comprise the majority of the airway surface area, remain an unexplored area in severe asthma and were targeted for global epithelial gene expression profiling in this study.

Publication Title

Altered Epithelial Gene Expression in Peripheral Airways of Severe Asthma.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Subject

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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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accession-icon GSE73159
Differential gene expression in the duodenum, jejunum, and ileum among crossbred beef steers with divergent gain and feed intake phenotypes.
  • organism-icon Bos taurus
  • sample-icon 47 Downloadable Samples
  • Technology Badge Icon Bovine Gene 1.1 ST Array (bovgene11st)

Description

Steer small intestine transcriptome

Publication Title

Differential gene expression in the duodenum, jejunum and ileum among crossbred beef steers with divergent gain and feed intake phenotypes.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE70760
Gene expression patterns in house dust mite stimulated CD4 T cells and IgG:IgE ratios
  • organism-icon Homo sapiens
  • sample-icon 89 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

PBMC from house dust mite (HDM) sensitized atopics were cultured in the presence or absence of HDM extract for 24 hours.

Publication Title

Distinguishing benign from pathologic TH2 immunity in atopic children.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE16032
Gene expression data from severe asthmatic children: PBMC profiles during acute exacerbation versus convalescence
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Severe asthma exacerbations in children requiring hospitalisation are typically associated with viral infection, and occur almost exclusively amongst atopics, but the significance of these comorbidities is unknown. We hypothesised that underlying interactions between immunoinflammatory pathways related to responses to aeroallergen and virus are involved, and that evidence of these interactions is detectable in circulating cells during exacerbations.

Publication Title

Interactions between innate antiviral and atopic immunoinflammatory pathways precipitate and sustain asthma exacerbations in children.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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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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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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