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• Sporadic multiple meningioma Genomics

  Wes for 15 multiple meningioma samples from 6 individual

  Dataset EGAD00001008710

• PDX WES

  2 patient-derived xenograph tumours, and associated normal blood samples. Duplicated samples for each gave 8 pairs of fastq files

  Dataset EGAD00001009657

• Variant Calls

  Variant Calls for all 97 consenting participants in the study.

  Dataset EGAD00001009971

• Validation of a genome-wide polygenic score for body mass index in South Asians

  Genotyping data of BMI model markers generated using Global Screening Array (Illumina Inc.)

  Dataset EGAD00001015700

• Reference epigenome DB31_N_Alpha_WGBS data generated from KEP study

  A DB31_N_Alpha_WGBS paired end data for alpha cells(PSA-NCAM(-), pancreas)

  Dataset EGAD00001003472

• Reference epigenome ADMSC01_ChIP-Seq(H3K27me3) data generated from KEP study

  A ADMSC01_ChIP-Seq(H3K27me3) paired end data for adipose-derived mesenchymal stroaml cells

  Dataset EGAD00001003854

• Reference epigenome ADMSC02_ChIP-Seq(H3K27me3) data generated from KEP study

  A ADMSC02_ChIP-Seq(H3K27me3) paired end data for adipose-derived mesenchymal stroaml cells

  Dataset EGAD00001003855

• Reference epigenome ADMSC03_ChIP-Seq(H3K27me3) data generated from KEP study

  A ADMSC03_ChIP-Seq(H3K27me3) paired end data for adipose-derived mesenchymal stroaml cells

  Dataset EGAD00001003856

• Reference epigenome ADMSC04_ChIP-Seq(H3K27me3) data generated from KEP study

  A ADMSC04_ChIP-Seq(H3K27me3) paired end data for adipose-derived mesenchymal stroaml cells

  Dataset EGAD00001003857

• Reference epigenome SMC01_smRNA-Seq data generated from KEP study

  A SMC01_smRNA-Seq single end data for skeletal muscle cells

  Dataset EGAD00001003858

• Reference epigenome SMC02_smRNA-Seq data generated from KEP study

  A SMC02_smRNA-Seq single end data for skeletal muscle cells

  Dataset EGAD00001003859

• Reference epigenome SMC03_smRNA-Seq data generated from KEP study

  A SMC03_smRNA-Seq single end data for skeletal muscle cells

  Dataset EGAD00001003860

• Reference epigenome SMC04_smRNA-Seq data generated from KEP study

  A SMC04_smRNA-Seq single end data for skeletal muscle cells

  Dataset EGAD00001003861

• Reference epigenome SMC05_smRNA-Seq data generated from KEP study

  A SMC05_smRNA-Seq single end data for skeletal muscle cells

  Dataset EGAD00001003862

• Reference epigenome SMC06_smRNA-Seq data generated from KEP study

  A SMC06_smRNA-Seq single end data for skeletal muscle cells

  Dataset EGAD00001003863

• Reference epigenome SMC07_smRNA-Seq data generated from KEP study

  A SMC07_smRNA-Seq single end data for skeletal muscle cells

  Dataset EGAD00001003864

• Reference epigenome SMC08_smRNA-Seq data generated from KEP study

  A SMC08_smRNA-Seq single end data for skeletal muscle cells

  Dataset EGAD00001003865

• Reference epigenome SMC09_smRNA-Seq data generated from KEP study

  A SMC09_smRNA-Seq single end data for skeletal muscle cells

  Dataset EGAD00001003866

• Reference epigenome ADMSC01_WGBS data generated from KEP study

  A ADMSC01_WGBS paired end data for adipose-derived mesenchymal stroaml cells

  Dataset EGAD00001003878

• Reference epigenome ADMSC02_WGBS data generated from KEP study

  A ADMSC02_WGBS paired end data for adipose-derived mesenchymal stroaml cells

  Dataset EGAD00001003879

• Reference epigenome ADMSC03_WGBS data generated from KEP study

  A ADMSC03_WGBS paired end data for adipose-derived mesenchymal stroaml cells

  Dataset EGAD00001003880

• Reference epigenome ADMSC04_WGBS data generated from KEP study

  A ADMSC04_WGBS paired end data for adipose-derived mesenchymal stroaml cells

  Dataset EGAD00001003881

• Prader-Willi Syndrome and Early-onset Morbid Obesity Natural History Protocol

  This observational study will involve the comprehensive assessment of the medical, behavioral and nutritional history and the clinical features of individuals with Prader-Willi syndrome and individuals with features of PWS-like/EMO. A blood sample will be obtained from the participants in order to create a DNA and RNA repository. In those PWS participants with a known deletion a blood sample will be collected for DNA in order to perform array comparative genome hybridization (aCGH) microarray or Methylation-Specific Multiplex Ligation-dependent Probe Amplification (MS-MLPA) studies to characterize the extent of the deletion. DNA samples will be sent to the Consortium Center at Baylor College of Medicine for the performance of the aCGH studies and to either Dr. Driscoll or Dr. Butler lab for MS-MLPA analysis. No drugs or treatments will be administered through this protocol. Our goal is to enroll as many participants as possible over a 8 year period. Currently we have enrolled 297 total subjects of which 265 have PWS and 32 EMO. Our original goal was to have enrolled over the first 5 years a clinical database of 200 individuals with PWS and 100 with EMO. We have exceeded expectations in PWS enrollment, but have fallen short in the enrollment of individuals with EMO. Therefore, we would like to reset our goals. We now propose to have an enrollment goal of 400 total subjects of which 350 will have PWS and 50 will have EMO. Eligible participants will be initially enrolled in the natural history study from the 4 clinic sites currently involved with PWS (University of Florida, Kansas University Medical Center, Vanderbilt University and University of California at Irvine). Participants assessed will serve to provide a background of information and a willing cohort for future interventional studies. All participants will have had standard genetic testing at a commercial laboratory prior to entry into the study. The PWS participants will be classified into one of the 3 main molecular classes (deletion, UPD and ID). The EMO participants will have had laboratory testing ruling out PWS and chromosomal aneuploidy (e.g., trisomy 21, Klinefelter syndrome, etc.). Going forward we feel it is important that all newly recruited EMO subjects have an aCGH as part of their evaluation so we can identify those with discrete deletions, duplications or copy number variants (CNV) and compare them to those without aCGH abnormalities. The participants will be assessed annually (0-3 years of age) or biennially (> 3 years) in the Clinical Research Center (or equivalent facility) using standardized protocol including photographs for documentation purposes to compare the evolution of the clinical phenotype.

  Study phs000575

• Genome-Wide Association Studies of Prematurity and Its Complications (African American)

  Preterm delivery resulting in the birth of a premature infant is a complex problem with a devastating impact on individuals, families and society. The prevalence of preterm birth has increased steadily in developed countries over the last 20 years and more than three million children die of preterm birth worldwide each year. Despite the importance of the problem and its disproportionate occurrence in poor and minority populations, the underlying causes have been difficult to identify. Spontaneous preterm labor has as its suspected triggers infection, stress, poor nutrition and inherited factors. The single best predictor for preterm delivery is a previous preterm birth. Studies of twins and of recurrences within families provide evidence that genetic factors underlie a substantive component of the risk for prematurity. One major challenge in studying genetic factors in prematurity is that the risk case is not truly established. The genetic risk could reside either in the mother and her uterus or in the infant/placenta. Identification of genetic factors in the mother and/or infant could provide insights into identifying relevant environmental covariates that may be more amenable to rapid interventions but difficult to find using standard epidemiology alone. A comprehensive genome-wide association study (GWAS) is the ideal way to identify those genes that would not be suspected based on our current understanding of the biology of parturition. We are using 2200 African American samples with term or preterm labor. A subset of these (~800) are infant samples recruited by the Neonatal Research Network as part of a study on cytokines and infection in extremely low birth weight infants (Schelonka RL, et al., 2011. PMID: 21145756). Therefore, this group consists of infants <1,000 grams with clinical outcome data for the infant allowing study of the genetic contributors for not only preterm birth but also the complications that often accompany preterm birth. The result will enable a better understanding of the biology of parturition and suggest environmental modifications that can prolong gestations to improve neonatal and adult outcomes. This study is part of the Gene Environment Association Studies initiative (GENEVA, http://www.genevastudy.org) funded by the trans-NIH Genes, Environment, and Health Initiative (GEI). The overarching goal is to identify novel genetic factors that contribute to preterm birth through large-scale genome-wide association studies of African-American cases and controls from multiple sites in the United States. Genotyping was performed at the Johns Hopkins University Center for Inherited Disease Research (CIDR). Data cleaning and harmonization were done at the GEI-funded GENEVA Coordinating Center at the University of Washington.

  Study phs000353

• Inflammatory Bowel Disease Exome Sequencing Study

  The Broad Institute and Massachusetts General Hospital (MGH) are launching a new initiative to perform large-scale exome sequencing in inflammatory bowel disease (Crohn's disease and ulcerative colitis). Given the considerable unmet therapeutic need in inflammatory bowel disease (IBD), the recent emergence of rapid and efficient genome sequencing technologies and the compelling evidence for the role of genetics in these disorders have motivated the founding of a collaborative sequencing effort geared toward the discovery of high-impact genetic variants influencing IBD risk that can serve as guides to future therapeutic development and diagnostic tools. The initiative will be directed by experienced IBD researchers from MGH and the Broad Institute but aims to develop a collaborative exome sequencing network that will partner with researchers worldwide. Two large pilot exome sequencing projects are being launched immediately as part of this initiative based on established genetic study designs that enrich for the discovery of rare, high-impact risk and protective variants. 1) Early-onset pediatric IBD: a major focus of the work will surround full-exome sequencing of the earliest-onset childhood IBD cases. It has long been recognized in many diseases that penetrant genetic risk factors are much more likely to be found in cases with unusually early onset. The Broad Institute has completed more than 50,000 exomes in the past two years; and their technical expertise in generating and processing such sequencing data, along with population genetic variation patterns from these experiments, will provide a foundation for obtaining the best outcome in the interpretation of these cases. Samples with IBD onset before 6 years of age - and in some cases going up to age 10 - collected by IBD researchers around the world are welcomed for inclusion in this study. 2) Adult-onset IBD case-control study: Genetic mapping has provided dramatic insights into IBD pathogenesis in recent years, but a substantial amount of heritability - in particular the role of strong-acting rare mutations - is yet to be elucidated. To deliver those insights, IBD cases with an unusually low burden of known genetic risk factors (particularly emphasizing those with positive family history and/or from isolated or enriched populations) will be contrasted with population controls that have an extremely high burden of known IBD risk factors, enhancing discovery of critical protective variants that may provide the best clues for therapeutic development. This project will also be initiated as an international collaboration, particularly among researchers with sample sets with Immunochip genotyping that will enable the immediate genetic identification of these enriched target populations. This project will be supported by the NHGRI Large-Scale Sequencing Program, with all generated data made publicly available to the research community through standard NIH databases.

  Study phs001076