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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 GSE22103
Clinical Microfluidics for Neutrophil Genomics and Proteomics
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Neutrophils play critical roles in modulating the immune response. However, neutrophils have a short circulating half life, are readily stimulated in vitro, and have low levels of cellular mRNA when compared to other blood leukocyte populations. All of these factors have made it difficult to evaluate neutrophils from clinical populations for molecular and functional studies.

Publication Title

Clinical microfluidics for neutrophil genomics and proteomics.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP101938
Abnormal RNA splicing and genomic instability after induction of DNMT3A mutations by CRISPR/Cas9 gene editing [RNA-Seq]
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Purpose: DNA methyltransferase 3A (DNMT3A) mediates de novo DNA methylation. Mutations in DNMT3A are associated with hematological malignancies, most frequently acute myeloid leukemia. DNMT3A mutations are hypothesized to establish a pre-leukemic state, rendering cells vulnerable to secondary oncogenic mutations and malignant transformation. However, the mechanisms by which DNMT3A mutations contribute to leukemogenesis are not well-defined. Methods: mRNA profiles of wild-type (WT) and DNMT3A mutated k562 cell lines were generated by deep sequencing, using Illumina HiSeq2500. Sequence reads were trimmed to remove possible adapter sequences and nucleotides with poor quality at the ends. Remaining sequence reads were then aligned to the human reference genome (hg19) using Tophat2. Gene read counts were measured using FeatureCounts and FPKM values were calculated with cufflinks. edgeR was used to identify differentially expressed genes between conditions, and topGO was used for annotation (Alexa, Rahnenfuhrer, and Lengauer, 2006). Sample comparison for differential gene expression was as follows: WTblk and WT1 versus MT2, MT3, MT4, and MT5. Gene enrichment set analysis (GSEA) was conducted with KEGG, Biocarta, and Reactome pathway datasets (Subramanian et al., 2005). Results: DNMT3A-mutated cells displayed impaired differentiation capacity. RNA-seq was used to compare transcriptomes of DNMT3A-mutated and WT cells; DNMT3A ablation resulted in downregulation of genes involved in spliceosome function, causing dysfunction of RNA splicing. Unexpectedly, we observed DNMT3A-mutated cells to exhibit marked genomic instability and an impaired DNA damage response compared to WT. Conclusions: CRISPR/Cas9-mediated DNMT3A-mutated K562 cells may be used to model effects of DNMT3A mutations in human cells. Our findings implicate aberrant splicing and induction of genomic instability as potential mechanisms by which DNMT3A mutations might predispose to malignancy. Overall design: mRNA profiles of wild type (WT) and DNMT3A mutated K562 cell lines were generated by deep sequencing using Illumina HiSeq2500

Publication Title

Abnormal RNA splicing and genomic instability after induction of DNMT3A mutations by CRISPR/Cas9 gene editing.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE36809
A genomic storm in critically injured humans
  • organism-icon Homo sapiens
  • sample-icon 856 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Human survival from injury requires an appropriate inflammatory and immune response. We describe the circulating leukocyte transcriptome after severe trauma and show that the severe stress produce a global

Publication Title

A genomic storm in critically injured humans.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE37069
Gene response to major burn injuries
  • organism-icon Homo sapiens
  • sample-icon 587 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Blood was sampled from severe burns patients over time as well as healthy subjects. Genome-wide expression analyses were conducted using the Affymetrix U133 plus 2.0 GeneChip.

Publication Title

Genomic responses in mouse models poorly mimic human inflammatory diseases.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE19743
A large-scale clinical study of gene expression response to severe burn injury
  • organism-icon Homo sapiens
  • sample-icon 177 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To understand the age-dependent response to burn injury, blood samples from pediatric and adult patients were collected at different times after severe burn injury.

Publication Title

Analysis of factorial time-course microarrays with application to a clinical study of burn injury.

Sample Metadata Fields

Sex, Disease

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accession-icon GSE2328
Application of genome-wide expression analysis to human health & disease
  • organism-icon Homo sapiens
  • sample-icon 88 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

expression files supporting: Application of genome-wide expression analysis to human health and disease. PNAS

Publication Title

Application of genome-wide expression analysis to human health and disease.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP186406
A temporal proteogenomic atlas of HCV-host interactions unravels cell circuits driving viral and metabolic liver disease.
  • organism-icon Homo sapiens
  • sample-icon 63 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Background and aims: Hepatitis C virus (HCV) infection is a major cause of liver disease including steatosis, fibrosis and liver cancer. Viral cure cannot fully eliminate the risk of disease progression and hepatocellular carcinoma (HCC) in advanced liver disease. The mechanisms for establishment of infection, liver disease progression and hepatocarcinogenesis are only partially understood. To address these questions, we probed the functional proteogenomic architecture of HCV infection within a hepatocyte-model. Methods: Time-resolved HCV infection of hepatocyte-like cells was analyzed by RNA sequencing, proteomics, metabolomics, and leveraged by integrative genomic analyses. Using differential expression, gene set enrichment analyses, and protein-protein interaction mapping we identified pathways relevant for liver disease pathogenesis that we validated in livers of 216 cirrhotic patients with HCV. Results: We uncovered marked changes in the protein expression of gene sets involved in innate immunity, metabolism and hepatocarcinogenesis. In infected cells, HCV enhances glucose metabolism and creates a Warburg-like shift of the lactate flux. HCV infection impaired the formation of peroxisomes -organelles required for long-chain fatty acid oxidation- causing intracellular fatty acid accumulation, which is a hallmark of non-alcoholic fatty liver disease (NAFLD). Ex vivo studies confirmed perturbed peroxisomes and revealed an association of hepatic catalase expression with clinical outcomes and phenotypes in HCV-associated cirrhosis, NAFLD and HCC cohorts. Conclusion: Our integrative analyses uncover how HCV perturbs the hepatocyte cell circuits to drive chronic liver disease and hepatocarcinogenesis. This proteogenomic atlas of HCV infection provides a model for the discovery of novel drivers for viral- and non-viral induced liver disease. Overall design: mRNA profiles of either mock or HCV-infected Huh7.5.1dif cells, performed in triplicates and collected every day between days 0 and 10 post infection. HCV infection reached plateau at day 7 post infection (pi). After day 7 pi unspecific effects cannot be excluded.

Publication Title

Combined Analysis of Metabolomes, Proteomes, and Transcriptomes of Hepatitis C Virus-Infected Cells and Liver to Identify Pathways Associated With Disease Development.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE63941
Expression data from cultured human esophageal squamous cell carcinoma cell lines and cultured human fibroblasts.
  • organism-icon Homo sapiens
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Cancer cells express different sets of receptor type tyrosine kinases. These receptor kinases may be activated through autocrine or paracrine mechanisms. Fibroblasts may modify the biologic properties of surrounding cancer cells through paracrine mechansms.

Publication Title

The role of HGF/MET and FGF/FGFR in fibroblast-derived growth stimulation and lapatinib-resistance of esophageal squamous cell carcinoma.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE4935
wheat expression level polymorphism study 39 genotypes 2 biological reps
  • organism-icon Triticum aestivum
  • sample-icon 77 Downloadable Samples
  • Technology Badge Icon Affymetrix Wheat Genome Array (wheat)

Description

The use of statistical tools established for the genetic analysis of quantitative traits can be applied to gene expression data. Quantitative trait loci (QTL) analysis can associate expression of genes or groups of genes with particular genomic regions and thereby identify regions that play a role in the regulation of gene expression. A segregating population of 41 doubled haploid (DH) lines from the hard red spring wheat cross RL4452 x AC Domain was used. This population had previously been mapped with microsatellites and includes a full QTL analysis for agronomic and seed quality traits. Expression analysis from 5 day post anthesis developing seed was conducted on 39 of the 41 DH lines using the Affymetrix wheat array. Expression analysis of developing seeds from field grown material identified 1,327 sequences represented by Affymetrix probe sets whose expression varied significantly between genotypes of the population. A sub-set of 378 transcripts were identified that each mapped to a single chromosome interval illustrating that major expression QTLs can be found in wheat. Genomic regions corresponding to multiple expression QTLs were identified that were coincident with previous identified seed quality trait QTL. These regions may be important regulatory regions governing economically important traits. Comparison of expression mapping data with physical mapping for a sub-set of sequences showed that both cis and trans acting expression QTLs were present.

Publication Title

Identifying regions of the wheat genome controlling seed development by mapping expression quantitative trait loci.

Sample Metadata Fields

No sample metadata fields

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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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Developed by the Childhood Cancer Data Lab

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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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