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• Center for Common Disease Genomics [CCDG] - Cardiovascular: Cardiology Biobanking for Biomarker Discovery

  This study is a part of NHGRI's Center for Common Disease Genomics, which is a collaborative large-scale genome sequencing effort to comprehensively identify rare risk and protective variants contributing to multiple common disease phenotypes. Current estimates anticipate that the CCDG program will sequence approximately 140K whole genomes and 225K whole exomes during the life of the project. The Cardiovascular Disease working group of the CCDG considered five diseases: early-onset coronary artery disease (EOCAD), stroke, atrial fibrillation, congestive heart failure and type 2 diabetes. Atrial fibrillation will affect between 6-12 million individuals in the US by 2050. AF also is associated with increased risks of stroke, dementia, heart failure, death, and high health care costs. Many risk factors for AF have been identified, including advancing age, cardiovascular disease (CVD), and CVD risk factors. However, there is little knowledge how to prevent AF. Furthermore, therapies for AF are only partially effective, and are themselves associated with substantial morbidity. Previously, heritable forms of AF have been considered rare; yet in the last decade, it has been established that AF, and in particular early-onset forms of AF, are heritable. Genome-wide association studies (GWAS) provide a powerful tool to identify common variants underlying disease risk. The AFGen Consortium currently consists of investigators from more than 25 studies with >20,000 individuals with AF and >100,000 without AF. In the latest analyses, 14 loci have been identified for AF1. Broadly, the loci implicate genes related to cardiopulmonary development, cardiac-expressed ion channels, and cell signaling molecules.Source: https://ccdg.rutgers.edu/sites/default/files/CCDG_CVD_EOAF_FINAL_w_link.pdfThe BioHEART study is a multi-center, prospective, observational cohort study to identify new biomarkers in stable coronary artery disease (CAD) and acute myocardial infarction (MI) (ACTRN12618001322224). Participants are recruited at time of clinically indicated computed tomography (CT) coronary angiogram (CTCA). 1,950 of 5,000 planned participants have been recruited and serum/plasma/erythrocytes/monocytes stored, with follow-up ongoing. CTCA imaging studies provides volumetric quantification of total calcified and non-calcified plaque, which is assessed using established and novel scoring systems. Comprehensive molecular phenotyping is performed on blood samples using state-of-the-art genomic, transcriptomic, proteomics, metabolomic, lipidomic, and immunophenotyping. Outcome data will be used to build improved risk models for CAD.Reference: http://www.anzctr.org.au/ - ACTRN12618001322224

  Study phs002726

• Exome sequencing of UK Birth Cohorts - Born in Bradford

  Birth cohort studies involve repeated surveys of large numbers of individuals from birth and throughout their lives. They collect information useful for a wide range of life course research domains, and biological samples which can be used to derive data from an increasing collection of omic technologies. This rich source of longitudinal data, when combined with genomic data, offers the scientific community valuable insights from population genetics to rare disease associations. Avon Longitudinal Study of Parents and Children (ALSPAC)recruited 14,775 babies of predominantly White ethnicity in the Avon county of south-west England between 1991 and 1992. Born in Bradford (BiB) is similarly focused on a particular local area, the city of Bradford in the north of England, and recruited 13,858 babies between 2007 and 2011, of whom ~41% self-report as white British and ~59% as other ethnicities, predominantly Pakistani. Millennium Cohort Study (MCS) is a national cohort that recruited 18,827 children born between 2000 and 2002, intentionally over-sampling areas with high child poverty, large ethnic minority populations, and smaller UK nations (Wales, Scotland and Northern Ireland) Available here is a subset of exome-sequenced parents and children from these studies (CRAMS and post-QC VCFs) as detailed in https://doi.org/10.12688/wellcomeopenres.22697 [doi.org]. Phenotypic data is also available by submitting an application to the corresponding cohort: https://borninbradford.nhs.uk/ [borninbradford.nhs.uk]

  Dataset EGAD00001015370

• Intergenerational Impact of Genetic and Psychological Factors on Blood Pressure (InterGEN Study)

  This research study focuses on the genomic and psychological environmental effects on blood pressure among mothers and their children. The study includes 250 mothers who self-identify as AA/black, and 250 children between the ages of 3 and 5 years old at the time of enrollment. The study is longitudinal and data collection interviews are scheduled every six months for two years after enrollment, for a total of four participant interviews. Assessment is as follows: genetic (time 1 only) and psychological factors (every six months for two years).

  Study phs001792

• Genentech Colon Cancer Screen

  Identifying and understanding changes in cancer genomes is essential for the development of targeted therapeutics. Here we analyse systematically more than 70 pairs of primary human colon tumours by applying next-generation sequencing to characterize their exomes, transcriptomes and copy-number alterations. We have identified 36,303 protein-altering somatic changes that include several new recurrent mutations in the Wnt pathway gene TCF7L2, chromatin-remodelling genes such as TET2 and TET3 and receptor tyrosine kinases including ERBB3. Our analysis for significantly mutated cancer genes identified 23 candidates, including the cell cycle checkpoint kinase ATM. Copy-number and RNA-seq data analysis identified amplifications and corresponding overexpression of IGF2 in a subset of colon tumours. Furthermore, using RNA-seq data we identified multiple fusion transcripts including recurrent gene fusions involving R-spondin family members RSPO2 and RSPO3 that together occur in 10% of colon tumours. The RSPO fusions were mutually exclusive with APC mutations, indicating that they probably have a role in the activation of Wnt signalling and tumorigenesis. Consistent with this we show that the RSPO fusion proteins were capable of potentiating Wnt signalling. The R-spondin gene fusions and several other gene mutations identified in this study provide new potential opportunities for therapeutic intervention in colon cancer.

  Study EGAS00001000288

• Dataset_for_linked_WES_and_WGS_data_from_EGAS00001004813 which belong also to EGAS00001005537 for germline controls of rare cancers

  WES/WGS sequencing data of 37 germline runs, which were uploaded to umbrella studies. The sequencing was always paired. The WGS sequencing was on HiSeq X Ten using the Illumina TruSeq DNA Nano Kit. The WES Sequencing was on HiSeq4000 with Agilent Sureselect V5+UTR.

  Dataset EGAD00001010046

• Dataset for upper_gastrointestinal_tumor-WHOLE_GENOME

  Rare cancer sequencing data of 28 runs in tumor/control pairs, which were uploaded to umbrella studies. The sequencing was always paired

  Dataset EGAD00001008901

• Sickle Cell Disease Implementation Consortium Registry (SCDIC Registry-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.Objectives: To understand the barriers to care and other factors related to reduced healthcare utilization after the transition from pediatric to adult SCD care which may contribute to increased morbidity and mortality.Background: Fifty years ago, it was rare for individuals with SCD to live beyond childhood. Advances in care delivery and treatment have more than doubled the life expectancy of individuals with sickle cell disease (SCD) since 1972. Beginning in the 1970s, measures such as newborn screening, prophylactic administration of penicillin, and immunization against bacterial infections decreased complications and morbidity, increasing the length and quality of life of children with SCD. Blood transfusions are currently the only proven way to prevent some of the major complications of SCD, especially recurrent stroke. They are also used frequently to help manage some of the acute complications of SCD. More recently, the use of hydroxyurea (HU) as a therapeutic agent to increase fetal hemoglobin has been shown to further reduce the debilitating symptoms of and improve survival in SCD. L-glutamine and crizanlizumab are additional treatments to reduce pain crises and voxelotor is approved to lower the risk of anemia and improve blood flow. In the absence of a widely accessible cure, treatment for SCD is usually aimed at avoiding crises, relieving symptoms, and preventing complications. Many of the advances in treatment have not translated into an increase in longevity or quality of life for adolescents and adults because of disparities in access to routine primary health care.Individuals with SCD experience a markedly increased mortality beginning in the second decade of life. The third and later decades of life are frequently associated with severe chronic pain progressive organ damage and frequent hospitalizations. The provision of evidence-based and expert opinion-based care in SCD is complicated by the difficulties that many patients experience in obtaining access to the health care system and in receiving long-term care from knowledgeable providers. A registry of 2,400 people with SCD was established to provide a rich resource to study the natural history of SCD and to understand barriers to care during the transition from pediatric to adult care. Participants: 2,438 participants with a confirmed diagnosis of SCD were enrolled into the registry over an 18-month period. At the time of enrollment, all participants were 15-45 years of age, English speaking, and without a bone marrow transplant.Design: The SCDIC Registry is a longitudinal observational cohort study. At enrollment, data collection included a medical record abstraction of clinical history, the most recent lab results, and a participant survey which included several patient reported outcomes from PROMIS, ASCQ-Me and NeuroQoL. Similar surveys were administered at annual follow-up. Four to five years after enrollment, a second record abstraction was completed with all clinical events that occurred since enrollment and another set of recent labs. There were many research questions proposed to be answered with the study data thus there was no primary outcome.Conclusions: As noted previously, there were no primary outcomes determined at the start of the study. Research questions included examination of co-morbidities, healthcare utilization, and patient reported outcomes. Key findings from the Registry include:Executive dysfunction, learning difficulties, and poor comprehension significantly associated with poor activities of daily living skills. Executive dysfunction also associated with HU non-adherence. Continuing HU after conception increased odds of miscarriage or stillbirth compared to women who were not using HU. Continuing HU after conception increased odds of low birth weight in infants. Compared to adolescents, young adults had significantly more severe pain, organ dysfunction, mental health disorders, sleep problems, and barriers to medical care. Young adults were significantly less likely to see a sickle cell specialist in the past 2 years. Females had higher pain frequency and severity, more pain episodes, anxiety, depression, hospitalizations, and higher fetal hemoglobin levels. Males had more respiratory, musculoskeletal, genitourinary, and cardiovascular complications, more skin ulcers, and more use of HU. Among 128 subjects that died during the study period, iron overload, pulmonary hypertension, and depression, were significant predictors of the risk of death in multivariate analyses.

  Study phs004203

• Genomic_landscape_of_liver_cirrhosis

  We are interested in the genomic landscape of liver cirrhosis and its potential manifestations for liver physiology and risk for hepatocellular carcinoma. Previous work in CASM has shown that there is a strong element of clonality within cirrhotic nodules and that some recurring mutations have been identified. However how this relates to the overall liver is not known and therefore by taking geographically disparate biospies, we aim to correlate our findings and make conclusions as to the characteristics of the overall genomic landscape.

  Study EGAS00001004329

• Identification_of_genes_involved_in_congenital_disorders_of_glycosylation_and_3_methylglutaconic_aciduria

  Identification of genes involved in congenital disorders of glycosylation and 3-methylglutaconic aciduria. There are more than 100 genes known for congenital disorders of glycosylation and new disorders are discovered each year. WE included patients with a so far unsolved glycosylation disease. The diagnostic group 3-methyglutaconic aciduria is a heterogenous group of disorders mostly caused by abnormal phospholipid synthesis or in association with mitochondrial dysfunction. We included patients with a so far unsolved disease and 3-methylglutaconic aciduria. 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 EGAS00001002064

• Systems biology of Colorectal Cancer

  Colorectal cancer (CRC) is one of the most common cancers in both males and females, and it is perhaps the best understood of all epithelial tumors in terms of its molecular origin. Yet, despite large amount of work that has concentrated on understanding of colon tumorigenesis, we still do not know the full complement of molecular lesions that are individually necessary – and together sufficient – to cause colorectal cancer. Neither do we understand why some specific mutations that are relatively rare in other tumors (e.g. loss of the APC tumor suppressor) are extremely common in colorectal cancer. We propose here to use the tools of systems biology to develop a quantitative and comprehensive model of colorectal tumorigenesis. The model will include identification of cell-type specific and oncogenic pathways that contribute to colon tumorigenesis, and explain in molecular detail how a genotype of an individual CRC leads to activation of downstream genes that drive uncontrolled cell growth. This model will subsequently be used to find novel therapeutic targets, to guide genetic screening to identify individuals with elevated risk for developing CRC, and to classify patients into molecular subgroups to select the treatment combination that is optimal for each patient (personalized medicine). The specific objectives of the SYSCOL project are: 1. Identify genetic markers for individual risk using genotyping and sequencing of constitutional DNA from sporadic and familial CRC cases and controls 2. Identify genes and regulatory elements that contribute to colorectal cancer cell growth 3. Use data from Aims 1-2 to develop a quantitative model for colorectal tumorigenesis 4. Apply the model for identification of high-risk individuals, for molecular classification of the disease, and for identification of novel molecular treatment targets

  Study EGAS00001000854