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accession-icon GSE81653
Development of complete personalized treatment plans for early stage colorectal cancer patients
  • organism-icon Homo sapiens
  • sample-icon 251 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

593 FFPE colorectal cancer samples were used to generate three prediction models: Recurrence prediction, 5FU efficacy prediction, and FOLFOX efficacy prediction

Publication Title

Building personalized treatment plans for early-stage colorectal cancer patients.

Sample Metadata Fields

Specimen part

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accession-icon GSE17777
HMVEC cells treated with vascular endothelial growth factor, anthrax edema toxin, and an Epac activator
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Human microvascular endothelial cells (HMVEC) treated with vascular endothelial growth factor (VEGF), Antrhax Edema Toxin (ET), or the Epac activator, 8-pCPT-2'-O-Me-cAMP (8CPT)

Publication Title

Anthrax edema toxin inhibits endothelial cell chemotaxis via Epac and Rap1.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE22180
In vitro carcinogenicity testing with Balb/c 3T3 Cells treated with various chemical carcinogens
  • organism-icon Mus musculus
  • sample-icon 60 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Background: Information on the carcinogenic potential of chemicals is only availably for High Production Volume products. There is however, a pressing need for alternative methods allowing for the chronic toxicity of substances, including carcinogenicity, to be detected earlier and more reliably. Here we applied advanced genomics to a cellular transformation assay to identify gene signatures useful for the prediction of risk for carcinogenicity. Methods: Genome wide gene expression analysis and qRT-PCR were applied to untransformed and transformed Balb/c 3T3 cells that exposed to 2, 4-diaminotoluene (DAT), benzo(a)pyrene (BaP), 2-Acetylaminoflourene (AAF) and 3-methycholanthrene (MCA) for 24h and 120h, at different concentrations, respectively. Furthermore, various bioinformatics tools were used to identify gene signatures predicting for the carcinogenic risk. Results: Bioinformatics analysis revealed distinct datasets for the individual chemicals tested while the number of significantly regulated genes increased with ascending treatment concentration of the cell cultures. Filtering of the data revealed a common gene signature that comprised of 13 genes whose regulation in cancer tissue has already been established. Strikingly, this gene signature was already identified prior to cell transformation therefore confirming the predictive power of this gene signature in identifying carcinogenic risks of chemicals. Comparison of fold changes determined by microarray analysis and qRT-PCR were in good agreement. Conclusion: Our data describes selective and commonly regulated carcinogenic pathways observed in an easy to use in vitro carcinogenicity assay. Here we defined a set of genes which can serve as a simply assay to predict the risk for carcinogenicity by use of an alternative in vitro testing strategy.

Publication Title

Toxicogenomics applied to in vitro carcinogenicity testing with Balb/c 3T3 cells revealed a gene signature predictive of chemical carcinogens.

Sample Metadata Fields

Cell line, Treatment, Time

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accession-icon GSE34586
Comparison of the transcripts in control and Blimp-1-deficient keratinocytes
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

We performed microarray analysis to examine the differential gene expression profiles between Prdm1 (Blimp-1)-deleted and control keratinocytes. Keratinocytes isolated from Prdm1-floxed K5-CreER positive (CKO) mice were cultured in the presence of 4OHT to induce deletion of the Prdm1 allele in vitro. Prdm1-floxed K5-CreER positive (CKO) keratinocytes treated with the ethanol solvent control (EtOH) or Prdm1-floxed K5-CreER negative (control) keratinocytes treated with 4OHT or EtOH served as controls. Microarray analyses revealed that there were 93 genes up-regulated and 109 genes down-regulated by more than 2-fold in the CKO + 4OHT group in comparison with the CKO + EtOH, Ctrl + 4OHT or Ctrl + EtOH groups. Several corneocytes-related genes, including Rptn, Lce1f, Krt1 and Lce1d, are significantly down-regulated and several cytokines/chemokines, including Cxcl1, Cxcl2, Cxcl5 and Il24, are significantly up-regulated upon the deletion of Prdm1 in vitro.

Publication Title

Inducible deletion of the Blimp-1 gene in adult epidermis causes granulocyte-dominated chronic skin inflammation in mice.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE38678
Cancer-Associated Fibroblasts Support Lung Cancer Stemness through Paracrine IGF-II/IGF1R/Nanog Signaling
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The CLS1/CAF co-culture maintained the cancer stemness. This cancer stemness was lost when the CAF feeder cells were removed during passaging.

Publication Title

Cancer-associated fibroblasts regulate the plasticity of lung cancer stemness via paracrine signalling.

Sample Metadata Fields

Cell line

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accession-icon GSE10300
head and neck squamous cell carcinoma samples
  • organism-icon Homo sapiens
  • sample-icon 40 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Patient selection and specimen collection. Thirty-six freshly frozen tumor samples were prospectively collected from patients undergoing surgery or biopsy for HNSCC at the University of North Carolina (UNC) at Chapel Hill (21 patients) and Vanderbilt University (15 patients). All tissues were snap-frozen in liquid nitrogen within 30 minutes of surgical resection or biopsy, and kept at -80oC until further processing. All patients consented to participation in this study under protocols approved by IRB at the two institutions.

Publication Title

A feed-forward loop involving protein kinase Calpha and microRNAs regulates tumor cell cycle.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE10299
Tumor Growth and Prognosis of Squamous Cell Carcinoma of the Head and Neck is Linked to Protein Kinase C Alpha
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Protein Kinase C alpha (PKC) is a critical mediator of cell signaling and cancer growth. We show that PKC inhibitors decrease proliferation in squamous cell carcinoma of the head and neck (SCCHN) cells and abrogate growth of SCCHN tumors in mouse xenografts. Analysis of gene expression arrays reveals that PKC regulates cell cycle genes required for DNA synthesis. In particular, PKC increases cyclin E protein expression, cyclinE/cdk2 complex formation, and transcription of cyclin E and E2F target genes. Consistent with this mechanism, expression of cyclin E rescues the block in DNA synthesis caused by PKC inhibition. In SCCHN tissue, PKC and cyclin E expression increase progressively from normal and dysplastic to malignant human head and neck tissue. Furthermore, PKC expression correlates with poor prognosis in SCCHN. These results demonstrate that PKC regulates growth by stimulating DNA synthesis through cyclin E and E2F and identify PKC as a therapeutic target that is highly expressed in aggressive SCCHN.

Publication Title

A feed-forward loop involving protein kinase Calpha and microRNAs regulates tumor cell cycle.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP051518
The transcriptome of Kawasaki Disease arteritis
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Background: Kawasaki Disease (KD) is a childhood illness of suspected infectious etiology that causes medium-sized muscular arteritis, most critically affecting the coronary arteries. No single diagnostic test exists, hampering early diagnosis and treatment. Approximately 25% of untreated patients develop coronary artery disease, and children who are treated with intravenous gammaglobulin but do not respond are also at high risk. Subacute/chronic arteritis and luminal myofibroblastic proliferation are the pathologic processes occurring in KD CA after the second week of illness, when neutrophilic necrotizing arteritis has subsided. The specific dysregulated immune pathways contributing to subacute/chronic arteritis have been unknown, hampering the development of effective immunomodulatory therapies for patients not responding to intravenous gammaglobulin therapy. Methods and Results: Deep RNA sequencing was performed on KD (n=8) and childhood control (n=7) coronary artery tissues, revealing 1074 differentially expressed mRNAs. Molecular pathways involving T helper cell, cytotoxic T lymphocyte, dendritic cells, and antigen presentation were the most significantly dysregulated. There was significant upregulation of immunoglobulin and type I interferon-stimulated genes. 80 upregulated extracellular genes encoding secreted proteins are candidate biomarkers of KD arteritis. Conclusions: The immune transcriptional profile in KD coronary artery tissues is primarily T helper and cytotoxic lymphocyte-mediated, and has features of an antiviral immune response such as type I interferon-stimulated gene expression. This first report of the KD coronary artery transcriptome identifies specific dysregulated immune response pathways that can inform the development of new therapies for and biomarkers of KD arteritis, and provide direction for future etiologic studies. Overall design: Primary analysis: 8 KD coronary arteries versus 7 childhood control coronary arteries. Subanalysis 1: 4 untreated KD coronary arteries versus 7 childhood control coronary arteries and subanalysis 2: 4 treated KD coronary arteries versus 7 childhood control coronary arteries

Publication Title

The transcriptional profile of coronary arteritis in Kawasaki disease.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP154995
REST and Neural Gene Network Dysregulation in iPS Cell Models of Alzheimer's Disease (RNA-seq data set)
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Alzheimer's disease (AD) is preceded by a long prodromal period of decades during which pathology accumulates in the brain prior to the onset of dementia. The molecular basis of these changes as well as how and when they start are unclear. Here we have analyzed neural progenitor (NP) cells and neurons generated from induced pluripotent stem cells (iPSCs) from individuals with sporadic AD (AD) and age-matched controls. Transcriptome analysis does not distinguish between iPSCs from individuals with SAD and age-matched controls, but shows major differences in iPSC-derived NP cells and neurons in gene networks related to neuronal differentiation, neurogenesis and synaptic transmission. SAD NP cells exhibit accelerated neuronal differentiation, leading to the generation of neurons with increased synapse formation and electrical excitability. Network analysis of the transcriptome implicates the transcriptional repressor REST/NRSF and two components of the polycomb repressive complex 2, SUZ12 and EZH2. Accelerated differentiation of SAD NP cells was reversed by exogenous REST expression and mimicked in normal NP cells by REST knockdown. The phenotype of accelerated neural differentiation was recapitulated in NP cells and cerebral organoids derived from gene-edited iPSC lines that express apolipoprotein E4 (APOE4), the major genetic risk factor for AD. Network analysis of the APOE4-related transcriptome again showed reduced function of REST, EZH2 and SUZ12 to be the major predicted regulatory changes. Reduced function of the REST repressor was due to reduced nuclear translocation and chromatin binding, and was associated with disruption of the nuclear membrane and lamina in SAD and APOE4 NP cells. Thus, impaired function of specific transcription factors and changes in nuclear architecture may be among the earliest events in the pathogenesis of AD. Overall design: Explore the effects of isogenic editing of APOE E4 to E3 in cerebral organoids. Comparison of APOE E4 vs E3 isogenic organoids with 3 biological replicates per group.

Publication Title

REST and Neural Gene Network Dysregulation in iPSC Models of Alzheimer's Disease.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE41409
Sense and antisense exon profiling across human, mouse, and rat
  • organism-icon Mus musculus, Homo sapiens, Rattus norvegicus
  • sample-icon 79 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Transcription profiling of sense and antisense transcripts of 10 tissues each from human, mouse, and rat.

Publication Title

Conserved expression of natural antisense transcripts in mammals.

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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