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• BLUEPRINT release August 2014, Bisulfite-Seq for inflammatory macrophage

  Bisulfite-Seq data for 3 inflammatory macrophage sample(s). 38 run(s), 3 experiment(s), 3 alignment(s). Part of BLUEPRINT release August 2014. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20140811/homo_sapiens/README_bisulphite_analysis_CNAG_20140811

  Dataset EGAD00001000914

• BLUEPRINT release January 2015, Bisulfite-Seq for inflammatory macrophage

  Bisulfite-Seq data for 3 inflammatory macrophage sample(s). 38 run(s), 3 experiment(s), 3 alignment(s). Part of BLUEPRINT release January 2015. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20140811/homo_sapiens/README_bisulphite_analysis_CNAG_20140811

  Dataset EGAD00001001139

• BLUEPRINT release August 2015, DNase-Hypersensitivity for CD8-positive, alpha-beta T cell, on genome GRCh38

  DNase-Hypersensitivity data for 1 CD8-positive, alpha-beta T cell sample(s). 1 run(s), 1 experiment(s), 1 alignment(s) on human genome GRCh38. Part of BLUEPRINT release August 2015. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20150820/homo_sapiens/README_dnaseseq_analysis_20150820

  Dataset EGAD00001001475

• Colorectal cancer WES/WGS analysis in Dr. Liu’s group in Sun Yat-sen University Cancer Center

  The samples include paired tumor and normal tissues from 205 patients (201 for normal and primary tumor tissues; 4 for normal, primary tumor and liver metastatic tissues). High-coverage WES sequencing or whole genome sequencing of DNA samples were performed on the Illumina HiSeq 2000 system

  Dataset EGAD00001003452

• The contribution of POT1 variants to sporadic melanoma development (2018-06-06)

  A case-control series of melanoma cases from Leeds, UK have been sequenced in the Fluidigm platform to identify genetic variants associated with sporadic melanoma development. Samples in which potentially contributing variants have been detected are being sequenced in an orthogonal platform for variant confirmation. . This dataset contains all the data available for this study on 2018-06-06.

  Dataset EGAD00001004151

• X Ten analysis of spiked placental tissue samples

  Metagenomics data of 80 placental tissue samples analyzed by X Ten for their possible microbial content. These 80 samples from pre-labor C-section deliveries, representing Cohort 1, were spiked with 1100 CFU Salmonella bongori. These same samples were also analyzed by 16S amplicon sequencing (search for ERP109246 in ENA).

  Dataset EGAD00001004198

• BLUEPRINT release August 2014, Bisulfite-Seq for Plasma cell

  Bisulfite-Seq data for 1 Plasma cell sample(s). 11 run(s), 1 experiment(s), 1 alignment(s). Part of BLUEPRINT release August 2014. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20140811/homo_sapiens/README_bisulphite_analysis_CNAG_20140811

  Dataset EGAD00001000927

• BLUEPRINT release January 2015, Bisulfite-Seq for plasma cell

  Bisulfite-Seq data for 1 plasma cell sample(s). 11 run(s), 1 experiment(s), 1 alignment(s). Part of BLUEPRINT release January 2015. Analysis documentation available at http://ftp.ebi.ac.uk/pub/databases/blueprint/releases/20140811/homo_sapiens/README_bisulphite_analysis_CNAG_20140811

  Dataset EGAD00001001160

• Metagenome for FINRISK2002

  The dataset contains data for n=7211 FINRISK 2002 participants who underwent fecal sampling. Demultiplexed shallow shotgun metagenomic sequences were quality filtered and adapter trimmed using Atropos (Didion et al., 2017), and human filtered using Bowtie2 (Langmead and Salzberg, 2012). The files are in FASTQ format.

  Dataset EGAD00001007035

• Diverse Cellular Composition in Alveolar Rhabdomyosarcoma Revealed by Single Cell RNA Sequencing

  Using single cell RNAseq data to characterize tumor composition and cellular states for Alveolar Rhabdomyosarcoma. We find that that ARMS tumors harbor phenotypically and transcriptionally distinct malignant subpopulations within an immune-influenced microenvironment.

  Study EGAS50000001564

• A_study_of_the_molecular_pathogenesis_of_Splenic_Marginal_Zone_and_Diffuse_Large_B_Cell_Lymphoma

  We will perform exome sequencing on selected cases of splenic marginal zone lymphoma (SMZL) and diffuse large B-cell lymphoma (DLBCL) in order to characterise their genetic makeup and identify biomarkers for prognosis and prediction of treatment response.

  Study EGAS00001000335

• TCELL_PILOT_ATAC_SEQ

  This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/

  Study EGAS00001000758

• Lymphocyte_RNA_profiling

  This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/

  Study EGAS00001000564

• Whole exome sequencing of papillary thyroid carcinoma in the Chinese population

  Papillary thyroid carcinoma (PTC) is the most common type of thyroid cancer. Here we submitted the sequencing results for PTC using 91 tumor-normal pairs through exome sequencing in the Chinese Han population.

  Study EGAS00001001268

• Preclinical_evolution_of_haematological_malignancies_

  This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/

  Study EGAS00001002128

• CELM

  This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/

  Study EGAS00001002261

• Whole-exome analysis of corticotropin-independent Cushing's syndrome

  We performed WES for 8 cases with corticotropin-independent Cushing’s syndrome, in whom paired tumor and normal DNA was obtained from fresh frozen adenomas and either normal adrenal tissues or peripheral blood, respectively.

  Study EGAS00001000661

• Genetics_and_Networks_of_Congenital_Heart_Defects

  Exome sequencing of families with Congenital Heart Defects of diverse sub-phenotypes. Comprises both parent-offspring trios for sporadic cases and multiplex families. Collaboration with David Brook, University of Nottingham. Funded by the British Heart Foundation.

  Study EGAS00001000762

• Characterization_of_iPSC_derived_macrophages___cardiovascular_pilot

  This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/

  Study EGAS00001000876

• Genetic and expression landscape of Waldenstrom macroglobulinemia

  Exome analyses for the identification of somatic mutation in Waldenstrom macroglobulinemia by comparison of tumor and CD3+(germ line control) population in 16 patients. transcription profiling of a series of Waldenstrom macroglobulinemia samples

  Study EGAS00001003603

• LifeLines-NEXT pilot study

  The pilot study from the LifeLines-NEXT (NEXT) cohort consisting of 30 mother-infant pairs with longitudinal sampling from pregnancy till 3 months after birth. Shotgun data is available for virome and microbiome annotation.

  Study EGAS00001005969

• Transcriptomic Data for Manuscript with title: Comprehensive genomic profiling in esophageal adenocarcinoma unmasks potential precision therapies

  Transcriptomic Data for Manuscript with title: Comprehensive genomic profiling in esophageal adenocarcinoma unmasks potential precision therapies

  Dataset EGAD00001015476

• WXS dataset of Oncogenic and immunological targets for matched therapy of pediatric blood cancer patients: Dutch iTHER study experience

  WXS dataset of Oncogenic and immunological targets for matched therapy of pediatric blood cancer patients: Dutch iTHER study experience

  Dataset EGAD00001015638

• Lung Tissue Research Consortium (LTRC-BioLINCC)

  Data Access NOTE: Please refer to the "Authorized Access" section below for information about how access to the data from this accession differs from many other dbGaP accessions. Biospecimens: Access to Biospecimens is through the NHLBI Biologic Specimen and Data Repository Information Coordinating Center (BioLINCC). Biospecimens from LTRC include DNA, Plasma, Serum, Tissue - FFPE Cassettes, Tissue – RNALater Frozen, and Tissue - Snap Frozen. Please note that use of biospecimens in genetic research is subject to a tiered consent. Objectives: The LTRC was a biobank resource established by the NHLBI to collect and distribute lung tissue, blood samples, clinical data, and radiographic studies from participants with chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), other related idiopathic interstitial pneumonias (IIP) and interstitial pneumonias associated with connective tissue diseases who undergo medically-indicated lung resection. All tissue and blood specimens and clinical data were banked centrally and stored for distribution to external investigators who have approved study proposals to investigate the pathogenesis or management of lung diseases. The ultimate goal of this program was to enable research that illuminates the pathobiology of lung diseases and leads to novel interventional treatments for these conditions. Background: Chronic lung diseases are a main cause of death and disability in the United States. COPD affects over 14 million individuals in the United States and represents the third leading cause of mortality. Cigarette smoking is a major risk factor. However, only one of six individuals who smoke develops COPD. This could imply either an individual susceptibility or an additional immunologic or infectious injury to lung cells. Current treatments offer symptomatic relief, but do not prevent disease progression. Better understanding of disease pathogenesis, including the potential roles of lung parenchymal cell apoptosis, immunologic injury, and inflammation may lead to therapies that improve survival and quality of life. Interstitial pneumonias, including IPF and those associated with connective tissue disease, are less common than COPD, but for many of these diseases there are poor outcomes. For example, IPF has a 50% survival rate 2-3 years following diagnosis, and currently no treatment exists which prolongs survival. The prevalence of IPF is approximately 28 cases per 100,000. The underlying histology of IPF is usual interstitial pneumonia (UIP), which can also occur in connective tissue diseases. The incidences of other interstitial pneumonias such as non-specific interstitial pneumonia (NSIP) or acute interstitial pneumonia (AIP) are less frequent but also occur as an expression of interstitial lung disease in the connective tissue diseases. Moreover, there is significant crossover of these three interstitial pneumonias so that cases of IPF/UIP may also reveal fibrotic NSIP and be complicated by episodes of AIP. This implies common injuries but dissimilar histological responses. All of these processes are characterized by epithelial injury, uncontrolled fibroproliferation and the deposition of collagen, irrespective of the histology. It is clear that a better understanding of the genesis of the interstitial pneumonias is required before effective interventions can be developed. Participants: A total of 4,486 participants were enrolled, and lung tissue was obtained from 3,333 of these participants.Design: Written informed consent of each participant was required before any LTRC procedure was performed. Phenotypic data were then obtained that included recording of relevant medical information, a limited exposure history, radiological evaluation, and pulmonary physiological and lung function testing. Questionnaires were administered to determine the extent of symptoms, associated medical illnesses, smoking, environmental and occupational exposures, and quality of life. Laboratory testing included pulmonary function testing, a six-minute walk test, and chest x-ray CT. Blood specimens were collected both for defining the clinical phenotype of donors and to obtain serum, plasma, and DNA for later investigative purposes. At the time of surgery, lung tissues were collected and processed for long-term storage. The LTRC collected only the 'non-tumorous' portions of lung tissue from surgical procedures performed for primary or metastatic lung tumors and received those specimens only after the local pathologist had procured all tissue required for clinical care. Samples of appropriate size were cut and placed in formalin, RNAlater, glutaraldehyde, or liquid nitrogen within 30 minutes of excision (approximately 5% of cases exceeded this target time). Blood and tissue specimens were subsequently shipped to a central Tissue Repository for further processing and long-term storage. A Radiology Center provided quality control and quality assessment of CT data. A Data Coordinating Center managed study operations and maintained a repository of study data. Conclusions: LTRC established a biospecimen collection that is unique in its size, diseases included, standardization of methods, and extent of phenotypic data, serving as a valuable resource to facilitate research on the pathobiology of lung diseases.

  Study phs003913

• NHGRI GREGoR Consortium: Genomics Research to Elucidate the Genetics of Rare Disease

  The NHGRI GREGoR (Genomics Research to Elucidate the Genetics of Rare Disease) Consortium was established in June 2021 with the goal of developing novel tools and approaches to advance the discovery of the genetic basis of rare conditions. Numerous types of molecular data are generated in GREGoR and available on the AnVIL cloud platform via dbGaP application, including short- and long-read genome and exome sequencing, transcriptomics, metabolomics, methylomics, and proteomics. De-identified clinical and demographic data is obtained, with a focus on standardized ontologies.Visit the GREGoR Consortium data webpage for summary information about the GREGoR Dataset, including numbers of participants and data types, methods documentation, and Release Notes. The Consortium comprises five Research Centers (RCs - see below), a Data Coordinating Center (DCC), and various partner members and external collaborators.Baylor College of Medicine Research Center (BCM-GREGoR) The Baylor College of Medicine GREGoR program, which is part of the GREGoR consortium, enrolls individuals, families, and cohorts with suspected rare disease across a range of syndromic and non-syndromic phenotypes. Subjects are enrolled from national and international collaborating physician referrals. Subjects provide written informed consent for future re-contact. Data generated and shared include family structure, detailed phenotypes, exome or short-read genome data, and in some cases long-read genome or RNA-sequencing, and these are shared upon completion of standard quality control checks and annotation. Broad Institute (Broad) The Broad Center for Mendelian Genomics, part of the GREGoR consortium uses next-generation sequencing (exome, genome, transcriptome, and long read sequencing), computational approaches, and functional studies to discover the variants and genes that underlie Mendelian conditions with a particularly focus on neuromuscular, neurodevelopmental, and syndromic phenotypes. Samples come from collaborators and direct enrollment through the Rare Genomes Project and we are committed to rapid data sharing without an embargo period. University of California, Irvine (UCI-GREGoR) To accelerate the pace of Mendelian disease gene discovery and clinical implementation, we propose a Mendelian Genomics Research Center, part of the GREGoR Consortium, leveraging the broad pediatric and adult clinical and research expertise at Children's National Hospital and University of California, Irvine. Our goal is to develop best practices to increase the diagnostic yield of rare diseases, engage the community to reduce health disparities for complex diagnoses, while creating a dataset accessible to all. Our Center will unite world class experts combining basic and translational research with innovative approaches to phenotyping, variant identification and functional investigation of both coding and non-coding sequence changes with the goals of discovering novel Mendelian gene variations and identifying variants not detected on current sequencing pipelines, disambiguating uncertain variants into disease-causing versus benign categorizations, and sharing information by working collaboratively with the GREGoR community.GREGoR Stanford Site (GSS) The goal of the GREGoR Stanford Site (GSS) is to provide a platform for functional genomics research and validation to improve diagnosis in Mendelian disease. Participants included individuals with undiagnosed suspected Mendelian disease who had non-diagnostic exome sequencing and their immediate family members. Participants and their family members provided written, informed consent and biological samples from which DNA, RNA, plasma, fibroblasts, PBMCs and other cell types were generated and stored. Samples from research participants and their immediate family members may have undergone short and long-read genome sequencing, transcriptome sequencing, metabolomics and/or lipidomics profiling, methyl-capture-sequencing and ATAC-sequencing. De-identified clinical data extracted from participant medical records are linked to the samples. University of Washington Center for Rare Disease Research (UW-CRDR) The goals of the University of Washington Center for Rare Disease Research are to: (1) maximize novel gene discovery for Mendelian conditions by recruitment, short- and long-read whole genome sequencing, transcriptome sequencing and analysis of families with rare conditions for which the gene is either unknown or the gene is known but no pathogenic variant can be identified via clinical testing; (2) develop new strategies for gene discovery for Mendelian conditions caused by variants that are difficult to detect using conventional testing strategies, variants of unknown function effect (e.g., regulatory, structural variants) or have unusual modes of inheritance; and (3) implement high-throughput screening and targeted follow-up functional studies to prioritize and validate candidate non-coding variants. De-identified data and phenotypic information are shared via MyGene2, ClinVar, and AnVIL.

  Study phs003047