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• Genome_Diversity_in_Africa_Project___GemCode_libraries_

  High depth whole genome sequencing from GemCode (10x Genomics) DNA libraries containing long range linkage information for one Baganda trio and one Baganda child (parent already sequenced at high depth). 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 EGAS00001001828

• Mapping_genetic_variants_underlying_gene_regulation_in_inflammed_intestinal_cell_types_to_identify_novel_IBD_drug_targets

  Biopsies from the terminal ileum and rectum of individuals with Crohn's disease are digested on ice to single cells and processed for single-cell RNA-sequencing (10X Genomics and Illumina) 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 EGAS00001003770

• Drug-induced epigenomic plasticity reprograms circadian rhythm regulation to drive prostate cancer towards androgen-independence (RNA-seq)

  Understanding how prostate cancer cells adapt to AR-targeted interventions is critical for identifying novel drug targets to improve the clinical management of treatment-resistant disease. Our study revealed an enzalutamide-induced epigenetic plasticity towards pro-survival signaling, and uncovered circadian regulator ARNTL as an acquired vulnerability after AR inhibition, presenting a novel clinical lead for therapeutic development.

  Study EGAS00001006016

• Drug-induced epigenomic plasticity reprograms circadian rhythm regulation to drive prostate cancer towards androgen-independence (ChIP-seq)

  Understanding how prostate cancer cells adapt to AR-targeted interventions is critical for identifying novel drug targets to improve the clinical management of treatment-resistant disease. Our study revealed an enzalutamide-induced epigenetic plasticity towards pro-survival signaling, and uncovered circadian regulator ARNTL as an acquired vulnerability after AR inhibition, presenting a novel clinical lead for therapeutic development.

  Study EGAS00001006017

• November 2020 data update (fastq) for reference epigenomes generated at Centre for Epigenome Mapping Technologies, Genome Sciences Center, B.C. Cancer Agency as part of the International Human Epigenome Consortium.

  November 2020 data update (fastq) for reference epigenomes generated at Centre for Epigenome Mapping Technologies (Canadian Epigenetics, Environment and Health Research Consortium), Genome Sciences Center, B.C. Cancer Agency, Vancouver, Canada as part of the International Human Epigenome Consortium.

  Dataset EGAD00001007529

• HV31 - Read identifier list for local CCS, CLR, ONT and MGI reads

  This file contains read identifiers for local CCS, CLR, ONT and MGI reads for each of the eight selected genomic regions (HLA, KIR, IGH, IGK, IGL, TRA, TRD, andTRG). We extracted these reads by aligning whole-genome sequencing data to a draft whole-genome de novo assembly, and selecting reads that map to contigs representing each region. These reads were involved in the polishing and validation of the HV31 assembly. Please refer to the relevant manuscript (https://doi.org/10.1101/2021.02.03.429586) for additional details. Read identifiers are stored in JSON format. Along with the full FASTQ files, this file enables convenient re-analysis of the HV31 sequencing data in the eight selected regions.

  Dataset EGAD00001007761

• Chromatin accessibility (ATAC-seq) and transcriptome (RNA-seq) data from immune cells for healthy young and healthy old subjects

  Dataset consisting of: (1) N=234 genome-wide chromatin accessibility (ATAC-seq) profiles for distinct N=21 healthy old and N=28 healthy young subjects. ATAC-seq biological samples provided for the following tissues: PBMC (N=24), CD14+ monocytes (N=18), CD8+ memory T cells (N=7), CD8+ naive T cells (N=7), CD4+ memory T cells (N=7), CD4+ naive T cells (N=7), and naive B cells (N=7). (2) N=39 genome-wide transcription (RNA-seq) data for distinct N=15 healthy old and N=24 healthy young subjects' PBMCs.

  Dataset EGAD00001003602

• NHLBI TOPMed - NHGRI CCDG: The Johns Hopkins University School of Medicine Atrial Fibrillation Genetics Study

  Atrial fibrillation (AF), the most common sustained cardiac arrhythmia, is the primary cause of many hospital admissions, and is associated with significant secondary morbidity by increasing the risk of stroke, heart failure, and all-cause mortality. The incidence of AF is on the rise, and it is projected that by the year 2050 more than 10 million patients will be affected by AF in the United States alone. Anti-arrhythmic medications have limited success in maintaining sinus rhythm, are associated with side effects, and appear ineffective at reducing mortality compared to a strategy of rate control and anticoagulation. Given the significant morbidity associated with this common arrhythmia, surgical and catheter ablation techniques have been developed to treat AF. However, despite the incorporation of various strategies for ablation, long-term recurrence rates of AF remain higher than 25 percent after ablation. Current techniques for catheter ablation of AF include pulmonary vein isolation and complex fractionated atrial electrogram (CFAE) ablation. However, the contribution of each strategy to long-term procedural success and the relative importance of each strategy for different patients remain unknown. Recent advances in cardiac imaging have allowed detailed analysis of left atrial myocardial anatomy. Parallel advances in molecular genetics have identified several candidate genes involved in familial and non-familial AF. However, the pathophysiology of AF generation and maintenance, and the potential contribution of such genetic or anatomic substrates for patient selection, and for target identification during catheter ablation have not yet been examined. Advances in molecular genetics and imaging, coupled with techniques for endocardial and epicardial mapping in the electrophysiology laboratory present an opportunity to significantly improve our understanding of (1) The relation of paroxysmal versus persistent AF with (a) structural left atrial changes (left/right atrial scar, wall thinning, pulmonary vein anomalies, and coronary sinus dilation) and with (b) candidate genetic variants. (2) The relation of candidate genetic variants with (a) structural left atrial changes and with (b) electrophysiologic properties (atrial effective refractory period (AERP) inhomogeneity, voltage abnormalities, trigger burden and location, C FAE extent and location), (3) The relation of structural left atrial changes with (a) CFAE location as targets for catheter ablation and with (b) reversible conduction block/myocardial injury after pulmonary vein isolation, and (4) Individualized endocardial targets for AF ablation based on candidate genes and anatomic substrates. The proposed study will improve our understanding of the underlying pathophysiology of AF, and may improve current techniques for treatment of this important arrhythmia.

  Study phs001598

• Caregiving as a Natural Stressor in Studies of the Role of Genes That Affect Serotonin Function in Regulating Risk Factors for Coronary Heart Disease (CAREGIVER)

  The burden of caregiving for an ill relative has been shown to interact with existing comorbidities to increase risk of several health outcomes including metabolic syndrome and blood pressure reactivity. The CAREGIVER study was developed to compare cardiometabolic risk factors in caregivers and controls. These risk factors include physiologic measures, psychologic measures, neighborhood characteristics, and genetic and genomic factors. DNA and plasma were collected and used for examination of cardiometabolic and stress biomarkers, genotyping and methylation analysis.

  Study phs001747

• Development of targeted DNA sequencing panel for brain tumors

  A prompt and reliable molecular diagnosis for brain tumors has become crucial in precision medicine. While Comprehensive Genomic Profiling (CGP) has become feasible, there remains room for enhancement in brain tumor diagnosis due to the partial lack of essential genes and limitations in broad copy number analysis. In addition, the long turnaround time of commercially available CGPs poses an additional obstacle to the timely implementation of results in clinics. To address these challenges, we developed a CGP encompassing 113 genes, genome-wide copy number changes, and MGMT promoter methylation.

  Study EGAS50000000699