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• Losartan Effects on Emphysema Progression (LEEP-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 evaluate the efficacy of losartan, an angiotensin receptor blocker, to reduce emphysema progression in patients with COPD and mild to moderate emphysema. Background Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease comprising chronic bronchitis and emphysema. COPD is a major cause of morbidity and mortality. Smoking cessation slows the progression of the disease, and bronchodilators can provide sustained improvement in lung function, but there are no pharmacologic agents that clearly modify emphysema progression. Angiotensin receptor blockers (ARBs) have been suggested as potential drugs to slow the progression of COPD. A few trials have shown that patients treated with ARBs had slower progression of radiographic emphysema. The LEEP study was initiated to test the hypothesis that the ARB losartan would reduce the progression of emphysema in patients with COPD with mild to moderate emphysema.ParticipantsA total of 220 participants were enrolled. 108 participants were randomized to receive losartan, and 112 participants were randomized to receive the placebo.Design LEEP was a randomized, placebo-controlled multicenter trial. Participants were randomly assigned (1:1) to receive losartan or placebo. The dose was 50 mg losartan or placebo given as one capsule daily for 2 weeks, and, if well tolerated and the systolic blood pressure was >90 mm Hg, it was increased to two capsules. Participants and site investigators were masked to treatment assignment. Participant responses to the St George's Respiratory Questionnaire, the modified Medical Research Council dyspnea scale, the COPD Assessment Test, and the Physical Function–Short Form 20a were collected. The number and severity of COPD exacerbations were recorded. COPD exacerbations were defined as two or more new or worse symptoms for ≥3 days and classified by treatment as mild (neither antibiotics nor oral steroids), moderate (an antibiotic or oral steroid), or severe (hospitalization). The primary outcome measure was the change in quantitative whole-lung emphysema score after 48 weeks measured by the percentage of lung voxels less than -950 Hounsfield units (PCT950) on full inspiratory HRCT. Conclusions Losartan does not prevent progression of emphysema in patients with COPD who have mild to moderate pulmonary emphysema.

  Study phs004313

• Spatial and temporal transcriptomics of medulloblastoma with chromothripsis identifies multiple genetic clones that resist to treatment and lead to relapse

  From all paediatric brain tumours, medulloblastomas with chromothripsis, a form of genome instability leading to massive genome rearrangements, are particularly aggressive. To dissect the complex biology underlying the aggressiveness of chromothriptic medulloblastomas, we applied spatial transcriptomics to i) chromothriptic and non-chromothriptic medulloblastomas from the same molecular subgroup (n=13) and ii) patient-derived xenografts from chromothriptic medulloblastoma, from the minimal residual disease stage to regrown tumours (n=11). Chromothriptic medulloblastomas showed higher spatial intra-tumour heterogeneity, proliferation and stemness, but lower immune infiltration and differentiation, as compared with non-chromothriptic medulloblastomas. Spatial mapping of genetic clones identified phenotypic features such as degree of differentiation, proliferation and immune infiltration enriched in specific clones. Cells from multiple genetic clones resisted treatment and gave rise to relapse in patient-derived xenografts of chromothriptic medulloblastoma. We identified a potential role of tumour microtubes in treatment resistance in chromothriptic medulloblastoma.

  Study EGAS00001007128

• A human induced pluripotent stem cell toolbox for studying sex chromosome effects-Whole exome seq

  To generate autosomaly isogenic hiPSCs with various chromosome complement, we use Klinefelter syndrome patient skin fibroblasts. These cells harbour XXY sex chromosomes, which can be lost during the reprogramming event and generate cells which are autosomaly identical to each other but differ in sex chromosome complement. We use state of the art reprogramming methods to generate panels of isogenic XXY, XX and XY iPSCs from XXY patient fibroblasts. We have performed Whole exome sequencing on Klinefelter syndrome patient's skin fibroblasts in order to check if two X chromosomes are identical and to see if we can distinguish which X chromosome is more likely to be lost during the reprogramming event in XY cell lines.

  Study EGAS50000000930

• TGS - Comprehensive Molecular Characterization of Colorectal Cancer Metastases (2015-07-02)[MOSAIC]

  Systematic next generation sequencing efforts are beginning to define the genomic landscape across a range of primary tumours, but we know very little of the mutational evolution that contributes to disease progression. We therefore propose to obtain a comprehensive description of genomic, transcriptomic and epigenomic changes in a cohort of matched primary and metastatic colorectal cancers, and additionally to explore the extent to which those mutations identified as recurrent in the metastatic setting are able to subvert normal biological processes using both genetically engineered mouse models and established cancer cell lines. This study will enable us to define to what extent primary tumour profiling can capture the biological processes operative in matched metastases as well as the significance of intratumoural heterogeneity. This dataset contains all the data available for this study on 2015-07-02.

  Dataset EGAD00001001426

• Colorectal cancer organoids expressing BRAF (fusion) genes

  Fusion genes may be oncogenic drivers and potential targets for personalized therapies in a variety of cancer types. The BRAF gene is frequently involved in oncogenic fusions, with fusion frequencies of 0.2-3% throughout different cancers. BRAF can be fused to a wide variety of genes, however, BRAF fusions rarely occur in the exact same gene configuration, making assessment of the fusion relevance and decision for drug treatment challenging. Here, we devised a colorectal cancer organoid-based platform to functionally characterize diverse BRAF fusions, containing various partner genes (AGAP3, DLG1 and TRIM24). We compared these BRAF fusions with respect to cellular behaviour, downstream signaling activation and response to targeted therapies. We found that 5’ partner choice of BRAF affects cellular localization and intracellular signaling capacities of the fusion genes. The DLG1-BRAF fusion gene showed distinct localization to the plasma membrane and exhibited increased levels of MAPK pathway activation under unperturbed conditions. Furthermore, the different BRAF fusions showed varying sensitivities to the targeted inhibition of ERK and BRAF, with the DLG1-BRAF fusion being the most sensitive. Additionally, RNA-sequencing identified distinct subsets of genes affected by the DLG1-BRAF fusion gene. Importantly, all fusion genes conveyed resistance to the clinically relevant EGFR/HER2/HER4-inhibitor afatinib, suggesting that BRAF fusions should be screened alongside other MAPK pathway alterations to identify mCRC patients amenable to cetuximab treatment. In summary, we developed a platform to efficiently assess molecular and cellular effects of fusion genes, and revealed that differential drug responses and distinct gene expression profiles can be induced by different BRAF fusions .

  Study EGAS00001003558

• Structure and evolution of double minutes in diagnosis and relapse brain tumors

  Double minute chromosomes are extrachromosomal circular DNA fragments frequently found in brain tumors. To understand their evolution, we characterized the double minutes in paired diagnosis and relapse tumors from a pediatric high-grade glioma and four adult glioblastoma patients. We determined the full structures of the major double minutes using a novel approach combining multiple types of supporting genomic evidence. Among the double minutes identified in the pediatric tumor, only one carrying EGFR was maintained at high abundance in both samples, whereas two others were resent in only trace amounts at diagnosis but abundant at relapse, and the rest were found either in the relapse sample only or in the diagnosis sample only. For the EGFR-carrying double minutes, we found a secondary somatic deletion in all copies at relapse, after erlotinib treatment, but this was rare at diagnosis, suggesting potential resistance to the EGFR inhibitor. This mutation caused an in-frame RNA transcript to skip exon 16, a novel transcript absent in EST database and in about 700 brain tumors that we reviewed. We observed similar patterns involving longitudinal copy number shift of double minutes in another four pairs (diagnosis / relapse) of adult glioblastoma. Overall, in three of five paired tumor samples, we found that although the same oncogenes were amplified at diagnosis and relapse, they were amplified on different double minutes. Our results suggest that double minutes readily evolve, increasing tumor heterogeneity rapidly. Understanding patterns of double minute evolution can shed light on future therapeutic solutions to brain tumors carrying such variants.

  Study EGAS00001003212

• Joint Addiction, Aging, and Mental Health (JAAMH) Data Access Committee General Research Use Datasets

  This collection contains all the Joint Addiction, Aging, and Mental Health (JAAMH) Data Access Committee General Research Use Datasets authorized individual-level genomic datasets currently in dbGaP that are approved for General Research Use (GRU) and have no further limitations beyond those outlined in the model Data Use Certification Agreement. The public posting of Genomic Summary Results is allowed. Access to this study collection will include additional authorized individual-level GRU datasets that become available. Renewal of this study collection is required annually. To request access to this study collection, select phs003202 in the dbGaP Authorized Access System.

  Study phs003202

• Joint Addiction, Aging, and Mental Health Data Access Committee General Research Use Datasets (GSR Restricted) Collection

  This collection contains the Joint Addiction, Aging, and Mental Health Data Access Committee's authorized individual-level genomic datasets currently in dbGaP that are approved for General Research Use (GRU) and have no further limitations beyond those outlined in the model Data Use Certification Agreement. The public posting of Genomic Summary Results are not allowed. Access to this study collection will include additional authorized individual-level GRU datasets that become available. Renewal of this study collection is required annually. To request access to this study collection, select phs003421 in the dbGaP Authorized Access System.

  Study phs003421

• An isoform quantitative trait locus in SBNO2 links genetic susceptibility to Crohn’s disease with defective antimicrobial activity

  Despite major advances in linking single genetic variants to single causal genes, the significance of genetic variation on transcript-level regulation of expression, transcript-specific functions, and relevance to human disease has been poorly investigated. Strawberry notch homolog 2 (SBNO2) is a candidate gene in a susceptibility locus with different variants associated with Crohn’s disease and bone mineral density. The SBNO2 locus is also differentially methylated in Crohn’s disease but the functional mechanisms are unknown. Here we show that the isoforms of SBNO2 are differentially regulated by lipopolysaccharide and IL-10. We identify Crohn’s disease associated isoform quantitative trait loci that negatively regulate the expression of the noncanonical isoform 2 corresponding with the methylation signals at the isoform 2 promoter in IBD and CD. The two isoforms of SBNO2 drive differential gene networks with isoform 2 dominantly impacting antimicrobial activity in macrophages. Our data highlight the role of isoform quantitative trait loci to understand disease susceptibility and resolve underlying mechanisms of disease.

  Study EGAS50000000183

• NINDS-Genome-Wide Genotyping in Parkinson's Disease: First Stage Analysis and Public Release of Data

  Epidemiological studies have estimated a cumulative prevalence of PD of greater than 1 per thousand. When prevalence is limited to senior populations, this proportion increases nearly 10-fold. The estimated genetic risk ratio for PD is approximately 1.7 (70% increased risk for PD if a sibling has PD) for all ages, and increases over 7-fold for those under age 66 years. The role for genes contributing to the risk of PD is therefore significant. This study utilized the well characterized collection of North American Caucasians with Parkinson's disease, and neurologically normal controls from the sample population which are banked in the National Institute of Neurological Disorders and Stroke (NINDS Repository) collection for a first stage whole genome analysis. Genome-wide, single nucleotide polymorphism (SNP) genotyping of these publicly available samples was originally done in 267 Parkinson's disease patients and 270 controls, and this has been extended to include genome wide genotyping in 939 Parkinson's disease cases and 802 controls. The NINDS repository was established in 10-2001 towards the goal of developing standardized, broadly useful diagnostic and other clinical data and a collection of DNA and cell line samples to further advances in gene discovery of neurological disorders. All samples, phenotypic, and genotypic data are available to the research community including to academics and industry scientists. In addition, well characterized neurologically normal control subjects are a part of the collection. This collection formed the basis of this first stage study by Fung et al., and the expanded study by Simon-Sanchez et al. The genotyping data was generated and provided by the laboratory of Dr. Andrew Singleton NIA, and Dr. John Hardy NIA (NIH Intramural, funding from NIA and NINDS). Important links to apply for individual-level data Data Use Certification Requirements (DUC) Apply here for controlled access to individual level data Participant Protection Policy FAQ

  Study phs000089

• Collaborative Cohort of Cohorts for COVID-19 Research (C4R): Coronary Artery Risk Development in Young Adults Study (CARDIA)

  Cohort Description The Coronary Artery Risk Development in Young Adults (CARDIA) study is a study examining the development and determinants of clinical and subclinical cardiovascular disease and their risk factors. It began in 1985-6 with a group of 5115 black and white men and women aged 18-30 years. The participants were selected so that there would be approximately the same number of people in subgroups of race, gender, education (high school or less and more than high school), and age (18-24 and 25-30 years) in each of 4 centers: Birmingham, AL; Chicago, IL; Minneapolis, MN; and Oakland, CA. These same participants were asked to participate in follow-up examinations during 1987-1988 (Year 2), 1990-1991 (Year 5), 1992-1993 (Year 7), 1995-1996 (Year 10), 2000-2001 (Year 15), 2005-2006 (Year 20), 2010-2011 (Year 25), 2015-2016 (Year 30), and 2021-2022 (Year 35). Data Being Submitted Wave 1 questionnaire data includes 397 variables for up to 2434 CARDIA participants in C4RWave 2 questionnaire data includes 448 variables for up to 1901 CARDIA participants in C4RDried Blood Spot/Serosurvey data includes 7 variables for up to 1332 CARDIA participants in C4RDerived data includes 43 variables for up to 2723 CARDIA participants in C4RPhenotype data includes 113 variables for up to 2723 CARDIA participants in C4R

  Study phs003045

• MSI_Cancer_Models___WGS

  The study will use whole genome sequencing to aid in define determinants of WRN dependency in MSI Cancer models.

  Study EGAS00001004178

• Renal_habitat_WXS

  This project aims at correlating genetic diversity (as well as transcriptomic, metabolic and immune diversity) observed in multiple targeted tumour biopsies and circulating tumour DNA with heterogeneity on multiparametric MRI. To this end, 20 patients with RCC (15 patients with localised/locally advanced disease and 5 with mRCC) will undergo multiparametric MRI including metabolic assessment by 13C-MRSI as well as measurements of tumour perfusion, oxygenation and water diffusion. Based on unique combinations of these imaging parameters, tumour habitats will be defined through cluster mapping. Intra-operative biopsy and immediate freezing of tumour cores from different imaging habitats will be performed. Multiregional ex-vivo tumour biopsies will be spatially registered to the MR data by using 3D printed tumour moulds generated from high-resolution volumetric sequences. These moulds allow slicing tumour specimens in identical planes to the MR acquisition and increase the accuracy of tissue sampling. The biopsies will then undergo molecular profiling such as metabolomic and RNA sequencing (including mRNA immune profiling), as well as DNA sequencing to assess driver and clonal mutations in different tumour habitats and guide design of appropriate cfDNA probes. The targeted cfDNA capture panel will be employed to determine the ability of cfDNA to capture the full genetic diversity observed in the primary tumour and to relate cfDNA to various imaging habitats in both renal and pancreatic cancer. Data integration will be undertaken between imaging habitats and molecular profiles for each region.

  Study EGAS00001003703

• NHLBI TOPMed: Genetic Epidemiology Network of Salt Sensitivity (GenSalt)

  The GenSalt study aims to identify genes which interact with dietary sodium and potassium intake to influence blood pressure in Han Chinese participants from rural north China. Whole genome sequencing will be conducted among 1,860 participants of the Genetic Epidemiology Network of Salt Sensitivity (GenSalt) Study. We will work in collaboration with participating TOPMed studies to identify novel common, low-frequency and rare variants associated with an array of cardiometabolic phenotypes. In addition, we will explore the relation of low-frequency and rare variants with salt-sensitivity among GenSalt study participants.

  Study phs001217

• NHLBI's Collection of Datasets for General Research Use (Public Posting of Genomic Summary Results: Not Allowed)

  This collection contains all of NHLBI's authorized individual-level genomic datasets currently in dbGaP that are approved for General Research Use (GRU) and have no further limitations beyond those outlined in the model Data Use Certification Agreement. The public posting of Genomic Summary Results are not allowed. Access to this study collection will include additional authorized individual-level GRU datasets that become available. Renewal of this study collection is required annually. To request access to this study collection, select phs003132 in the dbGaP Authorized Access System.

  Study phs003131

• NHLBI's Collection of Datasets for Health / Medical / Biomedical Research Use (Public Posting of Genomic Summary Results: Allowed)

  This collection contains all of NHLBI's authorized individual-level genomic datasets currently in dbGaP that are approved for Health/Medical/Biomedical (HMB) Research Use and have no further limitations beyond those outlined in the model Data Use Certification Agreement. The public posting of Genomic Summary Results are allowed. Access to this study collection will include additional authorized individual-level HMB datasets that become available. Renewal of this study collection is required annually. To request access to this study collection, select phs003134 in the dbGaP Authorized Access System.

  Study phs003134

• NHLBI's Collection of Datasets for Health / Medical / Biomedical Research Use (Public Posting of Genomic Summary Results: Not Allowed)

  This collection contains all of NHLBI's authorized individual-level genomic datasets currently in dbGaP that are approved for Health/Medical/Biomedical (HMB) and have no further limitations beyond those outlined in the model Data Use Certification Agreement. The public posting of Genomic Summary Results are not allowed. Access to this study collection will include additional authorized individual-level HMB datasets that become available. Renewal of this study collection is required annually. To request access to this study collection, select phs003133 in the dbGaP Authorized Access System.

  Study phs003133

• HudsonAlpha Long Read Sequencing Data of Individuals with Rare Suspected Genetic Conditions

  The data included in this project were generated from several IRB projects focused on the identification of the underlying genetic cause of undiagnosed rare conditions in infants, children and adults enrolled across the southeastern United States. Long read genome sequencing was performed on DNA samples collected as part of an IRB-approved study and findings from this testing was returned to enrolled study participants and the clinical team providing care. Proband participants in these studies were enrolled in both inpatient (neonatal intensive care units) and outpatient settings. When possible, biological relatives (including both biological parents) were also enrolled to help clarify inheritance of variants identified. Sequencing and analysis for SouthSeq is conducted at the HudsonAlpha Institute for Biotechnology in Huntsville, Alabama (https://www.hudsonalpha.org/). Results of testing are disclosed to participants by genetic counselors or trained non-genetics providers who also facilitate sharing of results with the participants' medical care teams when appropriate. Further, participant families may choose to opt-into return of secondary findings identified in the proband, which focus on pathogenic and likely pathogenic variation identified within the current ACMG gene list.

  Study phs003537

• A human induced pluripotent stem cell toolbox for studying sex chromosome effects -transcriptional landscape

  We use state of the art reprogramming methods to generate panels of isogenic XXY, XX and XY iPSCs from XXY patient fibroblasts. We use CRISPR/Cas9 system to evict Y chromosome from XY cells and generate XO iPSCs. The generation and characterisation of panels of isogenic XXY, XX, XY and XO iPSCs will provide a foundational toolkit to study sex differences in vitro. As iPSCs can be differentiated into any somatic cell type, we can apply the model to any human disease. We have generated bulk RNA-Seq from 12 autosomally isogenic hiPSCs to investigate transcriptional landscape and any differences in those cells in pluripotent state.

  Study EGAS50000000931

• High-throughput telomere length measurement at nucleotide resolution using the PacBio high fidelity sequencing platform

  Telomeres are specialized nucleoprotein structures at the ends of linear chromosomes that are essential for the stability as well as the complete replication of the human genome. The progressive shortening of steady-state telomere length in normal human somatic cells is a promising biomarker for age-associated diseases. However, there remain substantial challenges in quantifying telomere length in clinics and research laboratories due to the lack of accurate and high-throughput telomere length measurement method. Here, we describe a novel workflow to capture and analyze telomeres accurately at the single-nucleotide resolution. By using newly designed telobaits that are complementary to the single-stranded G-rich 3’ telomeric overhangs, we can specifically and efficiently capture full-length telomeres and subject them to single-molecule real-time (SMRT) sequencing. We show that the telomere length can be measured at nucleotide resolution using the PacBio high fidelity (HiFi) sequencing platform, which provides the necessary accuracy and throughput to uncover the steady-state telomere length distribution in human culture cell lines as well as clinical patient samples. This new method is a valuable tool not only in population-wide epidemiology studies but also for the longitudinal assessment of telomere attrition in individuals. Our results also reveal the extreme heterogeneity of telomeric variant sequences (TVSs) that is dispersed throughout the telomere repeat region. Importantly, the unique distribution pattern and sequence of TVSs in individuals may be used as a fingerprint for sample identification. In addition, the presence of TVSs disrupts the continuity of the canonical (5’-TTAGGG-3’)n telomere repeats, which could affect the binding of shelterin complexes at the chromosomal ends. Therefore, TVSs may act as a form of genetic polymorphisms that impairs telomere protection. Together with the absolute telomere length in each individual, TVSs may have profound implications in human aging and diseases.

  Study EGAS00001006103

• High-throughput telomere length measurement at nucleotide resolution using the PacBio high fidelity sequencing platform, P49-P104 and run1 replicates

  Telomeres are specialized nucleoprotein structures at the ends of linear chromosomes that are essential for the stability as well as the complete replication of the human genome. The progressive shortening of steady-state telomere length in normal human somatic cells is a promising biomarker for age-associated diseases. However, there remain substantial challenges in quantifying telomere length in clinics and research laboratories due to the lack of accurate and high-throughput telomere length measurement method. Here, we describe a novel workflow to capture and analyze telomeres accurately at the single-nucleotide resolution. By using newly designed telobaits that are complementary to the single-stranded G-rich 3’ telomeric overhangs, we can specifically and efficiently capture full-length telomeres and subject them to single-molecule real-time (SMRT) sequencing. We show that the telomere length can be measured at nucleotide resolution using the PacBio high fidelity (HiFi) sequencing platform, which provides the necessary accuracy and throughput to uncover the steady-state telomere length distribution in human culture cell lines as well as clinical patient samples. This new method is a valuable tool not only in population-wide epidemiology studies but also for the longitudinal assessment of telomere attrition in individuals. Our results also reveal the extreme heterogeneity of telomeric variant sequences (TVSs) that is dispersed throughout the telomere repeat region. Importantly, the unique distribution pattern and sequence of TVSs in individuals may be used as a fingerprint for sample identification. In addition, the presence of TVSs disrupts the continuity of the canonical (5’-TTAGGG-3’)n telomere repeats, which could affect the binding of shelterin complexes at the chromosomal ends. Therefore, TVSs may act as a form of genetic polymorphisms that impairs telomere protection. Together with the absolute telomere length in each individual, TVSs may have profound implications in human aging and diseases.

  Study EGAS00001006595

• Functional Mapping of AKT Signaling and Biomarkers of Response From the FAIRLANE Trial of Neoadjuvant Ipatasertib Plus Paclitaxel for Triple-Negative Breast Cancer

  Purpose: Despite extensive genomic and transcriptomic profiling, it remains unknown how signaling pathways are differentially activated and how tumors are differentially sensitized to certain perturbations. Here, we aim to characterize AKT signaling activity and its association with other genomic or immunohistochemistry-based PI3K/AKT pathway biomarkers as well as the clinical activity of ipatasertib (AKT inhibitor) in the FAIRLANE trial. Experimental Design: In FAIRLANE, 151 patients with early triple-negative breast cancer were randomized 1:1 to receive paclitaxel with ipatasertib or placebo for 12 weeks prior to surgery. Adding ipatasertib did not increase pathologic complete response rate and numerically improved overall response rate by magnetic resonance imaging (MRI). We used reverse-phase protein microarrays (RPPA) to examine the total level and/or phosphorylation states of over 100 proteins in various signaling or cell processes including PI3K/AKT and mTOR signaling. 125 baseline and 127 on-treatment samples were evaluable by RPPA, with 110 paired samples at both time points. Results: Tumors with genomic/protein alterations in PIK3CA/AKT1/PTEN were associated with higher levels of AKT phosphorylation. In addition, phosphorylated(p)AKT levels exhibited a significant association with enriched clinical benefit of ipatasertib, and identified patients who received benefit in the absence of PIK3CA/AKT1/PTEN alterations. Ipatasertib treatment led to a down-regulation of AKT/mTORC1 signaling, which was more pronounced among the tumors with PIK3CA/AKT1/PTEN alterations or among the responders to the treatment. Conclusions: We showed that the high baseline pAKT levels are associated with the alterations of PI3K/AKT pathway components and enriched benefit of ipatasertib in TNBC.

  Study EGAS00001005892

• Genome-Wide Environment Interaction Study on Neurodevelopment in Children from Mexico and Bangladesh

  Cognitive development is known to be highly heritable, but various genome wide association studies (GWAS) have failed to find common single nucleotide polymorphisms (SNPs) which can explain a large proportion of the variance in cognitive ability. We hypothesized that an interaction between genes and exposure to potentially toxic metals may account for some proportion of this missing heritability. We genotyped 749 infants in Mexico and 636 infants in Bangladesh. Criteria for inclusion into the study are given below. We then performed a Genome Wide Environmental Interaction Study (GWEIS) with neurodevelopment outcomes. There were 552,487 SNPs in common between the two cohorts.

  Study phs000996

• Diagnosis of multisystem inflammatory syndrome in children by a whole-blood transcriptional signature

  To identify a diagnostic blood transcriptomic signature that distinguishes multisystem inflammatory syndrome in children (MIS-C) from Kawasaki Disease (KD), bacterial infections and viral infections. Children presenting with MIS-C to participating hospitals in the United Kingdom and the European Union between April 2020-April 2021 were prospectively recruited. Whole blood RNA Sequencing was performed, contrasting the transcriptomes of children with MIS-C to those from children with KD, definite bacterial and viral infections. Data deposited here comprises samples from patients recruited into the DIAMONDS study.

  Study EGAS00001007409

• Epidemiologic Architecture for Genes Linked to Environment (EAGLE) MetaboChip Study

  The Epidemiologic Architecture for Genes Linked to Environment (EAGLE) study is a study site of the larger Population Architecture using Genomics and Epidemiology (PAGE) I study.  EAGLE accessed two data resources during the course of study: the National Health and Nutrition Examination Surveys (NHANES) and BioVU, the Vanderbilt University Medical Center biorepository linked to de-identified electronic health records.The EAGLE MetaboChip Study, also known as EAGLE BioVU in the literature, is a data resource of Illumina MetaboChip genotypes for ~15,000 DNA samples from African American/Black, Hispanic, and Asian patients in BioVU (PMID: 26201699). Several EAGLE BioVU and PAGE I study phenotypes were extracted using structured and unstructured data available in de-identified electronic health records linked to the DNA samples. 

  Study phs002767