9295 results for "cancer rna-seq"

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• Reference epigenome Fat-adipocyte04 h3k27ac ChIP-Seq data generated from KEP study

  Fat-adipocyte04 h3k27ac ChIP-Seq paired end data

  Dataset EGAD00001007478

• Reference epigenome Fat-adipocyte04 h3k27me3 ChIP-Seq data generated from KEP study

  Fat-adipocyte04 h3k27me3 ChIP-Seq paired end data

  Dataset EGAD00001007479

• Reference epigenome Fat-adipocyte04 h3k36me3 ChIP-Seq data generated from KEP study

  Fat-adipocyte04 h3k36me3 ChIP-Seq paired end data

  Dataset EGAD00001007480

• Reference epigenome Fat-adipocyte04 h3k4me1 ChIP-Seq data generated from KEP study

  Fat-adipocyte04 h3k4me1 ChIP-Seq paired end data

  Dataset EGAD00001007481

• Reference epigenome Fat-adipocyte04 h3k4me3 ChIP-Seq data generated from KEP study

  Fat-adipocyte04 h3k4me3 ChIP-Seq paired end data

  Dataset EGAD00001007482

• Reference epigenome Fat-adipocyte04 h3k9me3 ChIP-Seq data generated from KEP study

  Fat-adipocyte04 h3k9me3 ChIP-Seq paired end data

  Dataset EGAD00001007483

• Reference epigenome Fat-adipocyte04 input ChIP-Seq data generated from KEP study

  Fat-adipocyte04 input ChIP-Seq paired end data

  Dataset EGAD00001007484

• Reference epigenome Fat-adipocyte05 h3k27ac ChIP-Seq data generated from KEP study

  Fat-adipocyte05 h3k27ac ChIP-Seq paired end data

  Dataset EGAD00001007485

• Reference epigenome Fat-adipocyte05 h3k27me3 ChIP-Seq data generated from KEP study

  Fat-adipocyte05 h3k27me3 ChIP-Seq paired end data

  Dataset EGAD00001007486

• Reference epigenome Fat-adipocyte05 h3k36me3 ChIP-Seq data generated from KEP study

  Fat-adipocyte05 h3k36me3 ChIP-Seq paired end data

  Dataset EGAD00001007487

• Reference epigenome Fat-adipocyte05 h3k4me1 ChIP-Seq data generated from KEP study

  Fat-adipocyte05 h3k4me1 ChIP-Seq paired end data

  Dataset EGAD00001007488

• Reference epigenome Fat-adipocyte05 h3k4me3 ChIP-Seq data generated from KEP study

  Fat-adipocyte05 h3k4me3 ChIP-Seq paired end data

  Dataset EGAD00001007489

• Reference epigenome Fat-adipocyte05 h3k9me3 ChIP-Seq data generated from KEP study

  Fat-adipocyte05 h3k9me3 ChIP-Seq paired end data

  Dataset EGAD00001007490

• Reference epigenome Fat-adipocyte05 input ChIP-Seq data generated from KEP study

  Fat-adipocyte05 input ChIP-Seq paired end data

  Dataset EGAD00001007491

• ATAC-Seq of human stimulated and cultured CD4+ Treg cells

  This dataset includes whole genome sequence data for ATAC-seq (42 samples) of human stimulated and cultured CD4+ Treg cells.

  Dataset EGAD00001004829

• Whole genome sequencing of adult glioblastoma nuclei

  Nuclei were extracted from three primary adult glioblastoma samples and processed for scATAC-seq, and residual nuclei left over from these same samples were used to extract DNA and processed and sequenced for WGS. This WGS data was then used to cross-validate assessment of large-scale copy number alterations with scATAC-seq using the Copy-scAT tool.

  Study EGAS00001005256

• ChIP-seq data of Hodgkin lymphoma cell line L-428

  ChIP-seq data (H3K4Me3, H3K27Ac histone modifications) of Hodgkin lymphoma cell line L-428. Samples were processed as previously described (Sud et al., 2018). The files are in bam format, aligned to build 37.

  Study EGAS00001003033

• BLUEPRINT ATAC-seq data for cells in the haematopoietic lineages, from adult and cord blood samples

  BLLUEPRINT ATAC-seq data for cells in the haematopoietic lineages, from adult and cord blood samples.

  Study EGAS00001001596

• Gene Expression and Regulatory Networks in Human Leukocytes - Immunological Variation Consortium

  Profiling of gene expression with microarrays holds great potential for human health, for illuminating disease pathways or providing biomarkers to monitor disease or its resolution. Using high-throughput approaches for genotyping, immunophenotyping and gene expression analysis, the project will examine the basis for the control of gene expression in human immune cells, and how it is influenced by natural genetic variation or aging. In practice, the project will combine several cross-informative approaches: 1) Building on the established sample/data pipelines and robust protocols of the Immunological Genome (ImmGen) project, and on established cohorts of ethnically diverse healthy volunteers at hand, microarray techniques will be used to generate whole-genome expression profiles from purified naive CD4+ lymphocytes and monocytes from 600 healthy volunteers. A dense genetic map will be established for all donors. The results will elucidate how variation in the human genome affects the expression of immune genes, of key importance in understanding gene variants that bring susceptibility to immune or inflammatory disease. Computational analysis of these rich data will allow the reconstruction of regulatory connections between genes, helping to establish general modules and those specific of a given immune cell type. These data will be complemented by an orthogonal data group, generated from a restricted subset of 10 individuals, in which we will profile a larger set of 28 carefully delineated cell populations that exist in human blood. This work will also benefit from powerful interspecies comparison with similar experiments being performed in mice by ImmGen. 2) In addition, RNA from the same set of 28 defined cell populations will be probed with microarrays that explore other aspects of the transcriptome: i) microRNAs and other non-coding RNAs; ii) exon or splice junction arrays that will establish a map of differential splicing in human blood leukocyte. 3) The composition and reactivity of blood cells from the same donors will be established at the time of sample collection using high-throughput flow cytometry, correlating immune phenotypes with gene expression and genetic variation. 4) Genetic variability conditions the baseline levels of gene expression, but also the responsiveness to activating challenges. With samples from the same donors, NanoString technology for transcript counting will be used to analyze the transcriptional response of defined gene sets, representing response signatures of T or dendritic cells, for a fine-grained dissection of responses to different triggers (different bacterial ligands for dendritic cells, different cytokine environment for T cells). In keeping with the resource aspect of this project, all data and interpretations will be made publicly available rapidly upon curation, allowing public querying and browsing of the data, by using and evolving the existing web architectures of the ImmGen project, of the Broad Institute, and of international repositories. RELEVANCE: Exploration with DNA chips of the genome's expression microarrays holds great potential for human health, to better understand disease and to serve as diagnostic tools. Using a combination of high-throughput genomic techniques and computational biology, we will perform a broad exploration of gene expression in human blood cells across groups of African-American, Asian and European ancestry, asking how these profiles are affected by genetic variation or by age. These results will provide an invaluable reference benchmark for the interpretation of genetic and immunological studies. Additionally, over 90% of genetic variants associated with complex human traits map to non-coding regions, but little is understood about how they modulate gene regulation in health and disease. One possible mechanism is that genetic variants affect the activity of one or more cis-regulatory elements leading to gene expression variation in specific cell types. To identify such cases, in a second study we analyzed ATAC-seq and RNA-seq profiles from stimulated primary CD4+ T cells in up to 105 healthy donors. We found regions of accessible chromatin (ATAC-peaks) are co-accessible at kilobase and megabase resolution. 15% of genetic variants located within ATAC-peaks affected the accessibility of the corresponding peak (ATAC-QTLs). ATAC-QTLs have the largest effects on co-accessible peaks, are associated with gene expression, and are enriched for autoimmune disease variants. Our results provide insights into how natural genetic variants modulate cis-regulatory elements, in isolation or in concert, to influence gene expression. In another study we analyzed RNA-seq profiles from primary CD4+ T cells of two healthy donors at six time points from 0 to 72 hours after stimulation with bead-bound antibodies against CD3 and CD28.

  Study phs000815

• miRNA seq data of 43 cases out of dataset EGAD00001000650 (+ one read_me file)

  miRNA seq data of 43 cases out of dataset EGAD00001000650 (MMML)

  Dataset EGAD00001001619

• BLUEPRINT Bisulfite-seq and Whole Genome Sequencing of mantle cell lymphoma

  BLUEPRINT Bisulfite-seq and Whole Genome Sequencing of mantle cell lymphoma

  Dataset EGAD00001001892

• ATAC-seq

  ATAC-seq data for 26 CLL samples (7 controls, 19 tumor) of the CancerEpiSys-PRECiSe project.

  Dataset EGAD00001005967

• Reference epigenome Islet-derived-MSC01 h3k27ac ChIP-Seq data generated from KEP study

  Islet-derived-MSC01 h3k27ac ChIP-Seq paired end data

  Dataset EGAD00001007402

• Reference epigenome Islet-derived-MSC01 h3k27me3 ChIP-Seq data generated from KEP study

  Islet-derived-MSC01 h3k27me3 ChIP-Seq paired end data

  Dataset EGAD00001007403

• Reference epigenome Islet-derived-MSC01 h3k36me3 ChIP-Seq data generated from KEP study

  Islet-derived-MSC01 h3k36me3 ChIP-Seq paired end data

  Dataset EGAD00001007404