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accession-icon GSE89997
Expression data from 2 cohorts of human pancreatic ductal adenocarcinoma (PDAC) tumors
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

In this dataset, we included expression data obtained from 30 resected human PDAC tumors, to examine what genes are differentially expressed in different cohorts that might lead to various outcomes

Publication Title

Identification of unique neoantigen qualities in long-term survivors of pancreatic cancer.

Sample Metadata Fields

Specimen part

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accession-icon GSE77167
Differential gene expression analysis of peripheral blood leukocytes reveals overexpression of tumor progression-related genes in patients with intra-abdominal infection after surgery for colon cancer: a prospective matched cohort study
  • organism-icon Homo sapiens
  • sample-icon 59 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The aim was to investigate the effect of postoperative intra-abdominal infection on the gene expression patterns of peripheral blood leukocytes (PBL) after surgery for colorectal cancer

Publication Title

Peripheral blood leucocytes show differential expression of tumour progression-related genes in colorectal cancer patients who have a postoperative intra-abdominal infection: a prospective matched cohort study.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon GSE73464
Diagnosis of Kawasaki Disease in children using host RNA expression
  • organism-icon Homo sapiens
  • sample-icon 839 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip, Illumina HumanHT-12 V3.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Diagnosis of Kawasaki Disease Using a Minimal Whole-Blood Gene Expression Signature.

Sample Metadata Fields

Sex

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accession-icon GSE73461
Diagnosis of Kawasaki Disease in children using host RNA expression [Discovery_Dataset]
  • organism-icon Homo sapiens
  • sample-icon 459 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip, Illumina HumanHT-12 V4.0 expression beadchip

Description

Genome-wide analysis of transcriptional profiles in children <17 years of age with inflammatory diseases, bacterial or viral infections or with clinical features suggestive of infection.

Publication Title

Diagnosis of Kawasaki Disease Using a Minimal Whole-Blood Gene Expression Signature.

Sample Metadata Fields

Sex

View Samples
accession-icon GSE73463
Diagnosis of Kawasaki Disease in children using host RNA expression [Validation_HT12V4_Dataset]
  • organism-icon Homo sapiens
  • sample-icon 233 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip, Illumina HumanHT-12 V4.0 expression beadchip

Description

Genome-wide analysis of transcriptional profiles in children <17 years of age with inflammatory diseases, bacterial or viral infections or with clinical features suggestive of infection.

Publication Title

Diagnosis of Kawasaki Disease Using a Minimal Whole-Blood Gene Expression Signature.

Sample Metadata Fields

Sex

View Samples
accession-icon GSE73462
Diagnosis of Kawasaki Disease in children using host RNA expression [Validation_HT12V3_Dataset]
  • organism-icon Homo sapiens
  • sample-icon 147 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

Genome-wide analysis of transcriptional profiles in children <17 years of age with inflammatory diseases, bacterial or viral infections or with clinical features suggestive of infection.

Publication Title

Diagnosis of Kawasaki Disease Using a Minimal Whole-Blood Gene Expression Signature.

Sample Metadata Fields

Sex

View Samples
accession-icon SRP090108
RNA Sequencing Quantitative Analysis of RNA editing sites of Wild Type and ADAR1 editing deficient (ADAR1E861A) murine fetal RNA of various tissues
  • organism-icon Mus musculus
  • sample-icon 43 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The Adar1 deaminase inactive mutant mouse tissue samples were obtain from the Walkley lab as described in http://www.ncbi.nlm.nih.gov/pubmed/26275108. We performed mmPCR-seq on the samples and measured the editing levels of. Overall design: Fetal mRNA profiles of E12.5 wild type (WT) and ADAR E861A mutant mice were generated by deep sequencing using Illumina HiSeq 2000.

Publication Title

Dynamic landscape and regulation of RNA editing in mammals.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP032812
Chromatin stretch enhancer states drive cell-specific gene regulation and harbor human disease risk variants (RNA-seq)
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Chromatin-based functional genomic analyses and genomewide association studies (GWASs) together implicate enhancers as critical elements influencing gene expression and risk for common diseases. Here, we performed systematic chromatin and transcriptome profiling in human pancreatic islets. Integrated analysis of islet data with those generated by the ENCODE project in nine cell types identified specific and significant enrichment of type 2 diabetes and related quantitative trait GWAS variants in islet enhancers. Our integrated chromatin maps reveal that most enhancers are short (median = 0.8 kb). Each cell type also contains a substantial number of more extended (=3 kb) enhancers. Interestingly, these stretch enhancers are often tissue-specific and overlap locus control regions, suggesting that they are important chromatin regulatory beacons. Indeed, we show that (i) tissue specificity of enhancers and nearby gene expression increase with enhancer length; (ii) neighborhoods containing stretch enhancers are enriched for important cell type-specific genes; and (iii) GWAS variants associated with traits relevant to a particular cell type are more enriched in stretch enhancers compared with short enhancers. Reporter constructs containing stretch enhancer sequences exhibited tissue-specific activity in cell culture experiments and in transgenic mice. These results suggest that stretch enhancers are critical chromatin elements for coordinating cell type-specific regulatory programs and that sequence variation in stretch enhancers affects risk of major common human diseases. Overall design: Integrated analysis of islet chromatin modification and transcriptome data with those generated by the ENCODE project. NISC Comparative Sequencing Program

Publication Title

Chromatin stretch enhancer states drive cell-specific gene regulation and harbor human disease risk variants.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE52904
Impact of Gene Dosage on Gene Expression, Biological Processes and Survival in Cervical Cancer: a Genome-Wide Follow-Up Study
  • organism-icon Homo sapiens
  • sample-icon 66 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st), Affymetrix Mapping 250K Nsp SNP Array (mapping250knsp)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Impact of gene dosage on gene expression, biological processes and survival in cervical cancer: a genome-wide follow-up study.

Sample Metadata Fields

Age

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accession-icon GSE52903
Gene Dosage, Mainly 3q Amplification, Deregulates a Quarter of Genes in Cervical Cancer: It Induces Glycolysis, Anaphase-dependent Proteasome Proteolysis, and Low Survival
  • organism-icon Homo sapiens
  • sample-icon 66 Downloadable Samples
  • Technology Badge Icon Affymetrix Mapping 250K Nsp SNP Array (mapping250knsp), Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The contribution of copy number (CN)-altered genes in cervical carcinogenesis is unknown owing to a lack of correlation with gene expression. We mapped CN-altered genes in 31 cervical cancers (CCs), and investigated the expression of 21,000 genes in 55 CCs using microarrays. Biological processes associated with genes deregulated by gene dosage and the relationship between gene dosage and patient survival were investigated. CN-altered genome (CN-AG) percentages varied widely among tumors from 0% to 32.2% (mean = 8.1 8.9). Tumors were classified as low (mean = 0.5 0.6, n = 11), medium (mean = 5.4 2.4, n = 10), or high (mean = 19.2 6.6, n = 10) CN. The highest %CN-AG was found in 3q, which contributed an average of 55% of all CN alterations. Genome-wide, only 5.3% of CN-altered genes were deregulated by gene dosage; by contrast, the rate in fully duplicated 3q was twice as high. Amplification of 3q explained 23.6% of deregulated genes in whole tumors (r2 = 0.236, p = 0.006; analysis of variance), including those in 3q and other chromosomes. A total of 862 genes were deregulated exclusively in high-CN tumors, but only 22.9% were CN altered. This result suggests that the remaining genes are not deregulated directly by gene dosage but by mechanisms induced in trans by CN-altered genes. Anaphase-promoting complex/cyclosome (APC/C)-dependent proteasome proteolysis, glycolysis, and apoptosis were upregulated, whereas cell adhesion and angiogenesis were downregulated exclusively in high-CN tumors. The high %CN-AG and upregulated gene expression profiles of APC/C-proteasome-dependent proteolysis and glycolysis were associated with poor patient survival, although only the first 2 correlations were statistically significant (p < 0.05, log-rank test). The data suggest that inhibitors of APC/C-dependent proteasome proteolysis and glycolysis may be useful treatments in these patients.

Publication Title

Impact of gene dosage on gene expression, biological processes and survival in cervical cancer: a genome-wide follow-up study.

Sample Metadata Fields

Age

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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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