9182 results for "cancer rna-seq"

in 46.10 milliseconds.

• Reference epigenome ADMSC03_smRNA-Seq data generated from KEP study

  A ADMSC03_smRNA-Seq single end data for adipose-derived mesenchymal stroaml cells

  Dataset EGAD00001003869

• 4C-Seq datasets of EndoC-bh1

  2 Circular chromosome conformation capture (4C-Seq) datasets of the human beta cell line EndoC-bh1.

  Dataset EGAD00001005210

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

  Islet-derived-MSC01 mRNA-Seq paired end data

  Dataset EGAD00001007160

• Reference epigenome Islet-derived-MSC02 mRNA-Seq data generated from KEP study

  Islet-derived-MSC02 mRNA-Seq paired end data

  Dataset EGAD00001007161

• Reference epigenome Islet-derived-MSC03 mRNA-Seq data generated from KEP study

  Islet-derived-MSC03 mRNA-Seq paired end data

  Dataset EGAD00001007162

• Reference epigenome Islet-derived-MSC04 mRNA-Seq data generated from KEP study

  Islet-derived-MSC04 mRNA-Seq paired end data

  Dataset EGAD00001007163

• Reference epigenome Islet-derived-iPSC01 mRNA-Seq data generated from KEP study

  Islet-derived-iPSC01 mRNA-Seq paired end data

  Dataset EGAD00001007164

• Reference epigenome Islet-derived-iPSC02 mRNA-Seq data generated from KEP study

  Islet-derived-iPSC02 mRNA-Seq paired end data

  Dataset EGAD00001007165

• Reference epigenome Pancreas-Islet02 h3k36me3 ChIP-Seq data generated from KEP study

  Pancreas-Islet02 h3k36me3 ChIP-Seq paired end data

  Dataset EGAD00001007195

• Reference epigenome IPS-Fibroblast02 h3k27ac ChIP-Seq data generated from KEP study

  IPS-Fibroblast02 h3k27ac ChIP-Seq paired end data

  Dataset EGAD00001007270

• Reference epigenome IPS-Fibroblast02 input ChIP-Seq data generated from KEP study

  IPS-Fibroblast02 input ChIP-Seq paired end data

  Dataset EGAD00001007276

• Reference epigenome IPS-ENeuron02 h3k27ac ChIP-Seq data generated from KEP study

  IPS-ENeuron02 h3k27ac ChIP-Seq paired end data

  Dataset EGAD00001007298

• Characterization of genetic intratumor heterogeneity in colorectal cancer and matching patient-derived spheroid cultures.

  Patient-derived in vitro cultures of colorectal cancer (CRC) may help guide treatment strategies prior to patient treatment. However, most previous studies have been performed on a single biopsy per tumor. The purpose of this study was to analyze multiple spatially distinct biopsies from CRCs and see how well intratumor heterogeneity (ITH) was recapitulated in matching patient-derived spheroids. Three to five biopsies were collected from six CRC tumors. Each biopsy was split in two; one half was used for spheroid culturing, the other half was used for direct DNA and RNA purification. For two of the patients, lymph node metastases were analyzed. Somatic mutations were called from whole exome sequencing data. Each tumor contained multiple mutations shared across all biopsies and spheroids, including major CRC drivers such as APC, KRAS, and TP53. At the same time, all tumors exhibited ITH on both mutation and copy number level. The concordance between biopsies and spheroids ranged between 40-70% for coding mutations. For three of the patients the biopsy and spheroid from matching areas clustered together, meaning that the spheroid resembled the area of origin more than the other areas. However, all biopsies and spheroids contained private mutations. Thereby, multiple cultures from spatially distinct sites of the tumor increase the insight into the genetic profile of the entire tumor. RNA sequencing based molecular subtyping was stable and seemed independent of genetic ITH. In conclusion, all examined CRC tumors contained genetic ITH on mutation and copy number level. Spheroid cultures partly reflected this ITH, meaning that multiple cultures from distinct sites of the tumor improved the representation of the different genetic subclones in the primary tumor. This should be taken in to account when establishing patient-derived models for drug screening.

  Study EGAS00001002684

• Whole Genome Sequencing of a Triple Negative Breast Cancer Patient: Matched Primary Tumor, Normal, Metastasis and Xenograft samples

  Breast Cancer Subject Participant ID 700064 (Source Sample names: 6888 and 206). We used massively parallel DNA sequencing technologies to screen entire genomes, in an unbiased manner, for genetic changes associated with tumor growth and metastasis. We describe the complete genome sequence analysis of four DNA samples from a 44-year old African-American patient with basal-like breast cancer: peripheral blood, the primary tumor, a brain metastasis that developed within a year of initial therapy, and a first-passage xenograft derived from the primary tumor. A total of 50 validated mutations were discovered within coding, RNA, or splice site sequences. Of these, 20 mutations were abundantly present in all three tumors, including mutations in CSMD1 and JAK2. These two genes subsequently were found to be mutated in other breast tumors. The metastasis contained two de novo mutations not present in the primary tumor, and was significantly enriched for 20 shared mutations, suggesting that they may be involved in the metastatic process. The xenograft contained no unique coding, RNA, or splice site mutations and retained all primary tumor mutations, albeit at different frequencies. However, a significant increase in copy number alterations was observed in the xenograft as compared to the primary tumor. We validated 28 large deletions and six inversions, as well as seven translocations in at least one of the three tumor samples. Among them, a 26 kb deletion in MECR was solely identified, assembled, and validated in the brain metastasis and two overlapping large deletions on chromosome 5 encompassing CTNNA1, a potential tumor suppressor gene, were identified in all three tumors. The differential mutation frequencies and structural variation patterns between primary and metastatic tumors suggest that metastatic tumors may arise from minor subpopulations of cells within the primary. Namely, the metastatic and xenografting processes apparently select for cells harboring a distinct subset of the primary tumor mutation repertoire.

  Study phs000245

• ICR_RNASeq_pHGG

  RNA sequencing of paediatric high grade gliomas and diffuse intrinsic pontine gliomas. RNA was sequenced from fresh frozen surgical material or from primary cells cultured under stem cell conditions. RNA was subjected to Illumina whole transcriptome paired end sequencing. Data is provided as paired-end FASTQ files

  Dataset EGAD00001004116

• 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

• Oxford Human islet ATAC-seq dataset of 5 human islets

  ATAC-seq data for 5 non-diabetic human pancreatic islet samples

  Dataset EGAD00001003759

• 4C-seq data of a primary AML with t(3;8)

  The viewpoints used in the 4C-seq data were either the EVI1 promoter or the MYC super-enhancer

  Dataset EGAD00001006818

• Reference epigenome Pancreas-Islet02 h3k27ac ChIP-Seq data generated from KEP study

  Pancreas-Islet02 h3k27ac ChIP-Seq paired end data

  Dataset EGAD00001007193

• Reference epigenome Pancreas-Islet02 h3k27me3 ChIP-Seq data generated from KEP study

  Pancreas-Islet02 h3k27me3 ChIP-Seq paired end data

  Dataset EGAD00001007194

• Reference epigenome Pancreas-Islet02 h3k4me1 ChIP-Seq data generated from KEP study

  Pancreas-Islet02 h3k4me1 ChIP-Seq paired end data

  Dataset EGAD00001007196

• Reference epigenome Pancreas-Islet02 h3k4me3 ChIP-Seq data generated from KEP study

  Pancreas-Islet02 h3k4me3 ChIP-Seq paired end data

  Dataset EGAD00001007197

• Reference epigenome Pancreas-Islet02 h3k9me3 ChIP-Seq data generated from KEP study

  Pancreas-Islet02 h3k9me3 ChIP-Seq paired end data

  Dataset EGAD00001007198

• Reference epigenome Pancreas-Islet02 input ChIP-Seq data generated from KEP study

  Pancreas-Islet02 input ChIP-Seq paired end data

  Dataset EGAD00001007199

• Reference epigenome Pancreas-Islet03 h3k27ac ChIP-Seq data generated from KEP study

  Pancreas-Islet03 h3k27ac ChIP-Seq paired end data

  Dataset EGAD00001007200

• Reference epigenome Pancreas-Islet03 h3k27me3 ChIP-Seq data generated from KEP study

  Pancreas-Islet03 h3k27me3 ChIP-Seq paired end data

  Dataset EGAD00001007201

• Reference epigenome Pancreas-Islet03 h3k36me3 ChIP-Seq data generated from KEP study

  Pancreas-Islet03 h3k36me3 ChIP-Seq paired end data

  Dataset EGAD00001007202

• Reference epigenome Pancreas-Islet03 h3k4me1 ChIP-Seq data generated from KEP study

  Pancreas-Islet03 h3k4me1 ChIP-Seq paired end data

  Dataset EGAD00001007203

• Reference epigenome Pancreas-Islet03 h3k4me3 ChIP-Seq data generated from KEP study

  Pancreas-Islet03 h3k4me3 ChIP-Seq paired end data

  Dataset EGAD00001007204

• Reference epigenome Pancreas-Islet03 h3k9me3 ChIP-Seq data generated from KEP study

  Pancreas-Islet03 h3k9me3 ChIP-Seq paired end data

  Dataset EGAD00001007205

• Reference epigenome Pancreas-Islet03 input ChIP-Seq data generated from KEP study

  Pancreas-Islet03 input ChIP-Seq paired end data

  Dataset EGAD00001007206

• Reference epigenome Pancreas-Islet04 h3k27ac ChIP-Seq data generated from KEP study

  Pancreas-Islet04 h3k27ac ChIP-Seq paired end data

  Dataset EGAD00001007207

• Reference epigenome Pancreas-Islet04 h3k27me3 ChIP-Seq data generated from KEP study

  Pancreas-Islet04 h3k27me3 ChIP-Seq paired end data

  Dataset EGAD00001007208

• Reference epigenome Pancreas-Islet04 h3k36me3 ChIP-Seq data generated from KEP study

  Pancreas-Islet04 h3k36me3 ChIP-Seq paired end data

  Dataset EGAD00001007209

• Reference epigenome Pancreas-Islet04 h3k4me1 ChIP-Seq data generated from KEP study

  Pancreas-Islet04 h3k4me1 ChIP-Seq paired end data

  Dataset EGAD00001007210

• Reference epigenome Pancreas-Islet04 h3k4me3 ChIP-Seq data generated from KEP study

  Pancreas-Islet04 h3k4me3 ChIP-Seq paired end data

  Dataset EGAD00001007211

• Reference epigenome Pancreas-Islet04 h3k9me3 ChIP-Seq data generated from KEP study

  Pancreas-Islet04 h3k9me3 ChIP-Seq paired end data

  Dataset EGAD00001007212

• Reference epigenome Pancreas-Islet04 input ChIP-Seq data generated from KEP study

  Pancreas-Islet04 input ChIP-Seq paired end data

  Dataset EGAD00001007213

• Reference epigenome Pancreas-beta01 h3k27ac ChIP-Seq data generated from KEP study

  Pancreas-beta01 h3k27ac ChIP-Seq paired end data

  Dataset EGAD00001007214

• Reference epigenome Pancreas-beta01 h3k27me3 ChIP-Seq data generated from KEP study

  Pancreas-beta01 h3k27me3 ChIP-Seq paired end data

  Dataset EGAD00001007215

• Reference epigenome Pancreas-beta01 h3k36me3 ChIP-Seq data generated from KEP study

  Pancreas-beta01 h3k36me3 ChIP-Seq paired end data

  Dataset EGAD00001007216

• Reference epigenome Pancreas-beta01 h3k4me1 ChIP-Seq data generated from KEP study

  Pancreas-beta01 h3k4me1 ChIP-Seq paired end data

  Dataset EGAD00001007217

• Reference epigenome Pancreas-beta01 h3k4me3 ChIP-Seq data generated from KEP study

  Pancreas-beta01 h3k4me3 ChIP-Seq paired end data

  Dataset EGAD00001007218

• Reference epigenome Pancreas-beta01 h3k9me3 ChIP-Seq data generated from KEP study

  Pancreas-beta01 h3k9me3 ChIP-Seq paired end data

  Dataset EGAD00001007219

• Reference epigenome Pancreas-beta01 input ChIP-Seq data generated from KEP study

  Pancreas-beta01 input ChIP-Seq paired end data

  Dataset EGAD00001007220

• Reference epigenome Fat-Preadipocyte01 h3k27ac ChIP-Seq data generated from KEP study

  Fat-Preadipocyte01 h3k27ac ChIP-Seq paired end data

  Dataset EGAD00001007221

• Reference epigenome Fat-Preadipocyte01 h3k27me3 ChIP-Seq data generated from KEP study

  Fat-Preadipocyte01 h3k27me3 ChIP-Seq paired end data

  Dataset EGAD00001007222

• Reference epigenome Fat-Preadipocyte01 h3k36me3 ChIP-Seq data generated from KEP study

  Fat-Preadipocyte01 h3k36me3 ChIP-Seq paired end data

  Dataset EGAD00001007223

• Reference epigenome Fat-Preadipocyte01 h3k4me1 ChIP-Seq data generated from KEP study

  Fat-Preadipocyte01 h3k4me1 ChIP-Seq paired end data

  Dataset EGAD00001007224

• Reference epigenome Fat-Preadipocyte01 h3k4me3 ChIP-Seq data generated from KEP study

  Fat-Preadipocyte01 h3k4me3 ChIP-Seq paired end data

  Dataset EGAD00001007225