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• NIDDK IBD Genetics Consortium Repository Exome Chip

  The Illumina Infinium HumanExome+ BeadChip contains putative functional exonic variants selected from individual exome and whole-genome sequences from diverse populations. It includes nonsynonymous variants, splice variants and stop-altering variants. It also includes tags for previous GWAS-identified loci, ancestry informative markers, markers designed for identity by descent analyses, synonymous variants, fingerprint SNPs common to major genotyping platforms, mitochondrial SNPs, chromosome Y SNPs, and HLA tag SNPs. For more information as well as a detailed description of the variant calling and QC procedures, see Li et al. (2016). Li, D., et al. (2016) A pleiotropic missense variant in SLC39A8 is associated with Crohn's disease and human gut microbiome composition. Gastroenterology, 151, 1-9. PMID: 27492617.

  Study phs001723

• Cergentis FFPE-TLC

  In this study, formalin-fixed paraffin-embedded targeted locus capture (FFPE-TLC) sequencing is used as a novel technology for targeted detection of tumor-specific genomic structural variants (SVs) in the primary tumor of 29 colorectal cancer patients with metastatic disease. The tumor region was macrodissected and sequenced for 29 patients, and the "normal" region of the same slide was macrodissected and sequenced for 8 of these patients. SVs were found in the common fragile site (CFS)-associated genes MACROD2, PRKN, FHIT and WWOX as well as SVs caused by three LINE transposable elements. Tumor-specificity of selected SVs was independently verified by droplet digital PCR of tumor tissue DNA and their applicability as plasma circulating tumor DNA biomarkers was demonstrated.

  Study EGAS50000000427

• Genomic analysis of head and neck squamous cell carcinoma upon acquired resistance to cetuximab

  Anti-epidermal growth factor receptor (EGFR) monoclonal antibodies (cetuximab) remain the only FDA-approved targeted therapy for patients with recurrent/metastatic head and neck squamous cell carcinoma (HNSCC). Unfortunately, most patients develop acquired resistance to cetuximab and there is currently no further therapeutic option for these patients (unmet clinical need), thereby highlighting the need to better understand resistance-causing mechanisms. Here, we carried out whole-exome sequencing on 2 cetuximab-sensitive and -resistant patient-derived xenograft models of HNSCC. Our data reveal several genetic alterations (mutations and copy number variations) associated with acquired resistance to anti-EGFR therapy.

  Study EGAS50000000800

• Female Infertility: Primary Ovarian Insufficiency

  Premature ovarian failure, or primary ovarian insufficiency (POI) is a phenotype of diminished or absent ovarian function occurring in 1-2% of reproductive aged women. Most cases occur spontaneously. Evaluation of the gametes in women with POI is difficult and invasive. Practitioners must often rely on indirect biomarkers of ovarian function and oocyte health, making it difficult to identify patients who may benefit from therapies allowing them to achieve pregnancy utilizing their own oocytes. This study will generate exome sequences from POI patients in an effort to elucidate the causes of unexplained POI and to better understand the normal processes of ovarian aging. A better understanding of the genetics of ovarian function may lead to new non-invasive tools for managing women's reproductive health, and direct better use of existing biomarkers in diagnosis, screening and predicting clinical outcomes.

  Study phs001174

• Evolutionary Trajectories of Small Cell Lung Cancer under Therapy

  Small cell lung cancer (SCLC) is one of the deadliest human cancers with a five-years survival rate of less than 7%. The standard of care for extensive-stage SCLC consists of systemic treatment with platinum and etoposide, recently combined with PD-L1 immune checkpoint inhibitors (ICI). SCLC patients show high sensitivity to platinum-based chemotherapy, followed by rapid recurrence, which distinguishes SCLC from most human cancers. Unfortunately, second-line treatment with other chemotherapeutics or immunotherapy is only marginally effective, and patients ultimately succumb to their disease. We performed whole exome sequencing, whole genome sequencing and transcriptome sequencing of multiple tumor regions from 65 patients with SCLC. We determined tumor phylogenies at diagnosis and throughout chemotherapy and immunotherapy by multi-region sequencing of 160 tumors from 65 patients, to thus decipher the evolutionary processes underlying the remarkable sensitivity of small cell lung cancer (SCLC) to chemotherapy.

  Study EGAS50000000169

• Investigation of mutational signatures associated with DNMT3A deficiency (2019-04-03)

  Mutational signatures have been shown to be attributable to specific genetic contexts, such as mutations in DNA repair genes. DNMT3A is a DNA methyltransferase that helps maintain the DNA methylation pattern in a site-specific manner and may participate in DNA repair or the stress response. We have identified an adult individual who is a germline mosaic for a DNMT3A mutation. We have obtained clonal lymphoblastoid cells (LCLs) from the subject representing both WT and mutant lines grown in the same individual for >50 years. These clones represent a unique opportunity to examine the mutational impact of the DNMT3A mutation in a well-controlled setting. Our goal is to perform WGS on whole blood, representing the pool, as well as several WT and several mutant clones, in order to investigate the contribution of DNMT3A to mutation rates and signatures. . This dataset contains all the data available for this study on 2019-04-03.

  Dataset EGAD00001004889

• Resuscitation Outcomes Consortium (ROC) Cardiac Epidemiologic Registry (Cardiac Epistry) Version 3 (ROC-Cardiac Epistry 3-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. Available Data The ROC Cardiac Epistry version 3 include all cardiac arrest cases entered into the ROC database from April 1, 2011 to June 30, 2015. This is separate from versions 1 and 2 because of the major changes in how and which data were collected. Version 3 represents the following major changes to the structure and data collection: separate ED Arrival and Hospital Admits forms, mandatory ED and Hospital elements and a revamped CPR Process form. For ROC traumatic injury Epistry data please see: ROC-Trauma Epistry Objectives To build a prospective population-based registry of participants with out-of-hospital cardiac arrest responded to by Emergency Medical Services (EMS). Specific aims included: to establish whether the results of Resuscitation Outcomes Consortium (ROC) trials can be generalized to the larger population of participants that experience cardiac arrest; to more fully establish the burden of cardiac arrest; and to examine the relationships between variation in EMS structure and process, regional and periodic factors, and participant outcomes. Background Cardiac arrest is a common, serious, debilitating and costly public health problem. Although there has been a steady decline in morbidity and mortality from most cardiovascular diseases, high mortality rates for out-of-hospital cardiac arrests continue to pose a challenge for healthcare providers and a significant public health burden. The Resuscitation Outcomes Consortium (ROC) was established in 2004 to conduct clinical research in the areas of cardiopulmonary arrest and life-threatening traumatic injury with the overall goal of improving resuscitation outcomes. Participant and care characteristics can predict favorable outcomes in cardiac arrests, but there is still a wide variation in outcomes that is not well understood. EMS factors such as service level, number of responding providers, use of procedures or drugs in the field, training, quality assurance/feedback, and response time intervals also vary significantly by region. Variations in geographic, socioeconomic and periodic factors may also be associated with differences in outcomes. Prior to ROC Cardiac Epistry, there were no North American population-based registries for out-of-hospital cardiac arrests. Therefore there was a need for standardized data collection of out-of-hospital cardiac arrests in diverse geographic locations in order to identify the independent effects of prognostic or treatment factors accounting for variations in survival. Participants There were 120,306 participants. Design ROC Epistry collected standardized data regarding episode-specific factors, participant demographics, clinical information, pre-hospital interventions and disposition, hospital information, and participant outcome for all out-of-hospital cardiac arrests in the ROC regions. Each ROC site had to ensure capture of all eligible cases within the EMS service areas. Out-of-hospital data were extracted from existing databases whenever possible and augmented with targeted review of EMS reports. Hospital data were abstracted directly from the hospital file in most cases. Alternative methods included linkage to death registries and obituaries if the death occurred within 30 days. Sites submitted data using a web-based interface or batch uploads. Participants were not contacted directly.

  Study phs003726

• The Genetic Evolution of Acral Melanoma

  Acral melanoma is a rare melanoma subtype arising on the sole, palm, or nail apparatus. We performed whole-exome sequencing (WES) for a cohort of 35 acral melanoma patients. For each patient, we sequenced multiple tumor areas representing different tumor stages, including the in situ and invasive portions of the primary tumor and available regional or distant metastases. Normal areas were included for all except one patient. We identified distinct evolutional trajectory compared to melanomas arising on the sun-exposed skin. Whole-genome sequencing and targeted sequencing were additionally performed for a subset of the samples. Particularly, in acral melanomas, complex genomic aberrations, characterized by clustered copy number transitions and focal amplifications, and telomerase reverse transcriptase (TERT) activating alterations occur very early during evolution, while MAP-kinase pathway mutations, such as BRAF V600E and NRAS hotspot mutations, can occur late and often result in striking intra-tumor heterogeneity.

  Study phs003451

• DNA methylation in rhabdomyosarcoma PDX and PDX-derived primary cells

  Conditions to maintain primary tumor cells in culture are largely unknown for most tumor entities including rhabdomyosarcoma. In this collaborative study with Dr. Beat Schäfer's laboratory, we performed DNA methylation profiles of rhabdomyosarcoma patient-derived xenograft (PDX) and their matching PDX-derived primary cells (PPC), where the PPCs were developed and maintained under optimized culture conditions. We further compared DNA methylation profiles between these PDXs and PPCs. Exome sequencing and copy number analysis between these rhabdomyosarcoma PDXs and PPXs were also carried out. These analyses may help us to evaluate a feasibility of in vitro profiling of primary rhabdomyosarcoma cells from a genomic perspective.

  Study phs002051

• Studies of Left Ventricular Dysfunction (SOLVD-BioLINCC)

  Data Access NOTE:Please refer to the "Authorized Access" section below for information about how access to the data from this accession. Access differs from many other dbGaP accessions. ObjectivesThis study was initiated in 1986, primarily to evaluate the effects of enalapril, an ACE inhibitor, on long-term mortality and major morbidity in a group of participants with left ventricular dysfunction. Two large separate trials were run concurrently as part of SOLVD: 1) a prevention trial of participants with low ejection fraction but no overt symptoms of CHF and, 2) a treatment trial of participants with low ejection fraction and symptoms of CHF. In addition, participants at selected sites were entered into substudies to evaluate the effect of enalapril on a number of intermediate outcomes such as right and left ventricular function and hemodynamics, LV mass and wall stress, hormones, arrhythmias, exercise capacity, and quality of life in subsets of participants. Lastly, a registry of 6,336 participants with congestive heart failure of LV dysfunction was designed to describe the clinical course of an unselected group of participants. Background Congestive Heart Failure (CHF) is a major and increasingly recognized public health problem. The recognition that participants with CHF often have elevated peripheral vascular resistance has led to the introduction of vasodilator therapy, which has emerged as an important component of its treatment. Of the vasodilators, the angiotensin-converting enzyme (ACE) inhibitors appeared to be the most promising. In 1985, little was known about the impact of any long-term drug treatment on survival. SOLVD Registry: The SOLVD Registry is a hospital-based observational study, conducted at selected SOLVD hospitals, of participants with at least moderate left-ventricular dysfunction (EF ≤ 45%) and/or radiologically confirmed heart failure. It consists of a main study (n=6,273) and a substudy (n=898). Although there is overlap between the Registry and the SOLVD trials, the Registry sample is not a subset of SOLVD nor is it the pool of participants eligible for both trials. Participants A total of 2,569 participants were enrolled into the treatment study and 4,228 participants were enrolled in the prevention study. The dataset available through the NHLBI contains the prevention and treatment study data as well as the registry data. Conclusions In the prevention trial, a significant reduction in the incidence of heart failure and the rate of related hospitalizations was observed for participants in the enalapril arm. A statistically significant reduction in mortality was not observed in the enalapril treatment arm; however, there was a trend toward fewer total deaths and deaths due to cardiovascular causes among the enalapril participants (SOLVD Investigators, et al., 1992, PMID: 1463530).

  Study phs003668

• White blood cell and cell-free DNA analyses for detection of residual disease in gastric cancer

  Liquid biopsies are providing new opportunities for detection of residual disease in cell-free DNA (cfDNA) after surgery but may be confounded through identification of alterations arising from clonal hematopoiesis. Here, we identify circulating tumor-derived DNA alterations (ctDNA) through ultrasensitive targeted sequencing analyses of matched cfDNA and white blood cells from the same patient. We apply this approach to analyze samples from patients in the CRITICS trial, a phase III randomized controlled study of perioperative chemotherapy in patients with operable gastric cancer. After filtering alterations derived from matched white-blood cells, the presence of ctDNA predicts recurrence when analyzed within nine weeks after preoperative treatment and after surgery in patients eligible for multimodal treatment. These analyses provide a facile method for distinguishing ctDNA from other cfDNA alterations and highlight the utility of ctDNA as a predictive biomarker of patient outcome to perioperative cancer therapy and surgical resection in patients with gastric cancer.

  Study EGAS00001004114

• Identification of 22 Novel Loci Associated with Susceptibility to Testicular Germ Cell Tumors

  Testicular germ cell tumors (TGCT) are the most common cancers in young men of European ancestry aged 20 to 39 years. The Testicular Cancer Consortium (TECAC) has brought together the largest genome-wise association study (GWAS) study of TGCT to date. We conducted a GWAS of 5,602 cases and 5,006 controls aggregated from 12 locations in the US and Europe. Logistic regression models adjusted for study center and genomic ancestry. Genotypes were imputed against the Human Haplotype Reference Consortium. Meta-analysis was performed to combine GWAS results with summary statistics from five previously published TGCT studies, UK Biobank, deCODE Genetics, and an independent set of cases and controls, for a total of 10,156 cases and 179,683 controls. 22 novel and 45 previously reported loci associated with TGCT surpassed genome-wide significance (p < 5e-08).

  Study phs001349

• whole-genome sequencing of gastric cancer

  Gastric cancer is one of the most common cancers. Genome-wide analysis of genomic signatures might reveal novel mechanisms for gastric cancer tumorigenesis. Here, we analyzed structural variations and mutational signatures via whole-genome sequencing of 168 gastric cancer samples. Our data demonstrates diverse models of complex structural variations operative in GC, which lead to high-level amplification of oncogenes.

  Study EGAS00001003512

• A Phenotypic and Genomics Approach in a Multi-Ethnic Cohort to Subtype Systemic Lupus Erythematosus

  Systemic lupus erythematosus (SLE) is a complex autoimmune disease that affects multiple organ systems and varies in severity across different populations. To examine the clinical heterogeneity of SLE, we sought to identify different lupus subtypes within our multi-ethnic cohort using a clustering approach. Additionally, with genome-wide methylation and genotype data generated for our cohort, we applied integrative methods to investigate genetic and epigenetic risk factors. This integrative and computational approach revealed molecular differences associated with phenotypic clusters.

  Study phs001850

• Single Suture Craniosynostosis: Gene and Pathway Discovery

  Craniosynostosis is the premature fusion of one or more of the calvarial sutures. In this work, we used genomics and network modeling to reveal genetic and developmental pathways which, when disrupted, result in premature calvarial fusion. Calvarial bone explants were obtained from children undergoing surgery for single suture craniosynostosis. Primary osteoblast cell lines were established from calvarial explants and used as an RNA source.  The data available includes subject sex, affected suture, RNA sequence variants and counts.

  Study phs002684

• Circulating Tumor DNA Analysis in ERBB2-Amplified Colorectal Cancer: Biomarker Analysis of the MyPathway Trial

  Combination of two HER2-directed antibodies, pertuzumab and trastuzumab (P+T), has antitumor activity in HER2-positive colorectal cancer (CRC). Although liquid biopsies are increasingly being used in clinical oncology, the association between tumor and circulating tumor DNA (ctDNA) ERBB2 status and ctDNA monitoring for early response and resistance are unknown. Eighty-five patients with ERBB2-amplified and/or overexpressed CRC were treated with P+T in the MyPathway trial; 42 had ctDNA testing at Cycle 1 Day 1 (C1D1), and 38 had longitudinal plasma tested for ctDNA. We analyzed the ctDNA vs tissue ERBB2 concordance, genomic co-alterations, and ctDNA dynamics and association with response. Forty-one (98%) of 42 patients had genomic alterations detected in ctDNA at C1D1, and 29 (69%) had ERBB2 amplification in ctDNA. There was a strong correlation between ERBB2 copy number on next-generation sequencing in tissue and C1D1 ERBB2 ctDNA copy number. Thirty-seven percent achieved a molecular response by C3D1 on P+T, which was associated with prolonged progression-free survival and overall survival (OS). CDKN2A and KRAS mutations were associated with shorter OS, and a trend was seen with PIK3CA mutations. Several emerging co-alterations were identified in ctDNA at progression, including in the MAPK and PI3K pathways and other tyrosine receptor kinases. ctDNA can detect ERBB2 amplification in many, but not all, patients with ERBB2 amplification detected in tumor samples. ctDNA molecular response was associated with better survival, and ctDNA co-alterations may offer insights into mechanisms of intrinsic and acquired resistance.

  Study EGAS50000000916

• Context-specific regulatory genetic variation in MTOR dampens neutrophil-T cell crosstalk in pneumonia-associated sepsis, modulating disease

  Sepsis is a heterogeneous clinical syndrome with a high mortality, requiring personalised stratification strategies. Here, we characterise genetic variation that modulates MTOR, a critical regulator of metabolism and immune responses in sepsis. The effects are highly context specific, involving a regulatory element that affects MTOR expression in activated T cells with opposite direction of effect in neutrophils. We show that the G-allele of the lead variant, rs4845987, associated with decreased risk of T2D, reduces MTOR expression in T cells and improves survival in sepsis due to pneumonia, with effects specific to sepsis endotype. Using ex vivo models, we demonstrate that activated T cells promote immunosuppressive sepsis neutrophils through released cytokines, a process dampened by hypoxia and the mTOR inhibitor rapamycin. Our work demonstrates a novel epigenetic mechanism that fine-tunes MTOR transcription and T cell activity via the variant-containing regulatory element, which further exhibits an allelic effect upon vitamin C treatment. These findings reveal how genetic variation interacts with disease state to modulate immune cell-cell communication, providing a patient stratification strategy to inform more effective sepsis treatment.

  Study EGAS50000000894

• TRACERx 100: RRBS data from a subset of the first 100 TRACERx tumours

  TRACERx (TRAcking Cancer Evolution through therapy (Rx)) is a prospective cohort study designed to investigate intratumor heterogeneity (ITH) in relation to clinical outcome, and to determine the clonal nature of driver events and evolutionary processes in early stage non-small cell lung cancer (NSCLC). This study looks at multi-region RRBS data from the TRACERx100 cohort selected for quantity of material available and high tumour purity. RRBS data was collected for 122 tumour regions across 36 patients each with matched normal. A subset of this cohort was used in a sister study looking at tumour neo-antigen promoter methylation status in NSCLC (71 tumour regions across 28 patients for a total of 99 samples).

  Study EGAS00001003484

• Urothelial Cancer - Genomic Analysis to Improve Patient Outcomes and Research (UC-GENOME): a Bladder Cancer Advocacy Network (BCAN)-Led Collaborative Research Pilot Study - for Samples Collected at Johns Hopkins

  UC-GENOME is a real-world cohort of patients with metastatic urothelial carcinoma (UC). The study consisted of two co-equal aims: 1) to provide targeted DNA sequencing for clinical decision making at no cost to patients; and 2) to create a resource for collaborative translational science including a clinically annotated biobank. The submitted data represents the foundational analysis of 218 patients accrued at 7 academic medical centers. The analysis includes 176 patients with both targeted DNA sequencing and RNA sequencing. The genomic data was combined with clinical variables to model response to chemotherapy and immune checkpoint inhibitors (ICI).The larger dataset for this study can be found in dbGaP study phs003066.

  Study phs003094

• Analysis of recent shared ancestry in a familial cohort identifies coding and noncoding autism spectrum disorder variants

  Autism spectrum disorder (ASD) is a collection of neurodevelopmental disorders characterized by deficits in social communication and restricted, repetitive patterns of behavior or interests. ASD is highly heritable, but genetically and phenotypically heterogeneous, reducing the power to identify causative genes. We performed whole genome sequencing (WGS) in an ASD cohort of 68 individuals from 22 families enriched for recent shared ancestry. We identified an average of 3.07 million variants per genome, of which an average of 112,512 were rare. We mapped runs of homozygosity (ROHs) in affected individuals and found an average genomic homozygosity of 9.65%, consistent with expectations for multiple generations of consanguineous unions. We identified potentially pathogenic rare exonic or splice site variants in 12 known (including KMT2C, SCN1A, SPTBN1, SYNE1, ZNF292) and 12 candidate (including CHD5, GRB10, PPP1R13B) ASD genes. Furthermore, we annotated noncoding variants in ROHs with brain-specific regulatory elements and identified putative disease-causing variants within brain-specific promoters and enhancers for 5 known ASD and neurodevelopmental disease genes (ACTG1, AUTS2, CTNND2, CNTNAP4, SPTBN4). We also identified copy number variants in two known ASD and neurodevelopmental disease loci in two affected individuals. In total we identified potentially etiological variants in known ASD or neurodevelopmental disease genes for ~61% (14/23) of affected individuals. We combined WGS with homozygosity mapping and regulatory element annotations to identify candidate ASD variants. Our analyses add to the growing number of ASD genes and variants and emphasize the importance of leveraging recent shared ancestry to map disease variants in complex neurodevelopmental disorders.

  Study EGAS00001006058

• SS18-SSX-mediated hijacking of BAF complexes drives synovial sarcoma

  Synovial sarcoma (SS) is defined by a recurrent t(x;18) chromosomal translocation, which produces the hallmark SS18-SSX oncogenic fusion. Incorporation of SS18-SSX into BAF complexes renders BAF complexes aberrant in two distinct manners: the addition of 78aa of SSX onto SS18, and concomitant loss of BAF47 assembly. However, the importance and functional contributions of each of these perturbations on BAF complex targeting and gene expression regulation remain unclear. Here we use an integrative set of genomic approaches in human cancer cell lines and primary tumor samples to define the mechanistic consequences of the SS18-SSX fusion oncoprotein. We find that SS18-SSX hijacks BAF complexes to broad polycomb domains to activate bivalent genes, driving a unique gene expression program distinct from other loss-of-function BAF complex malignancies. Importantly, restoration of BAF47 rescues enhancer activation but is dispensable for proliferative arrest in cell lines. These results demonstrate that gain-of-function SS18-SSX-mediated BAF complex targeting and gene activation is the driving event in SS, and present a mechanism by which distinct functions of BAF complexes can be co-opted to drive oncogenesis.

  Study EGAS00001002920

• Genetic architecture of autism spectrum disorder in India

  The dataset consists of whole exome sequencing data (fastq format) of 100 non-syndromic autism spectrum disorder patients from India. Whole exome sequencing data is generated using Agilent SureSelect v6 capture kit and Illumina HiSeq sequencing platform. Paired end fastq files are available.

  Dataset EGAD00001008621

• Combined Targeting of CDK4/6 and HER2 Signaling in Orthotopic Patient-Derived Xenografts of HER2-Positive Breast Cancer Brain Metastases

  Patients with metastatic HER2-positive (HER2+) breast cancer will frequently develop brain metastases (BCBMs). Here, we report that p16INK4A, a tumor suppressor, is deficient in the majority of HER2+ BCBMs. Furthermore, p16INK4A deficiency, as measured by protein immunohistochemistry, can be a predictive marker associated with response to combined treatment with tucatinib and abemaciclib in our orthotopic patient-derived xenografts (PDXs) models of HER2+ BCBMs. Our findings provide the rationale for a biomarker-driven clinical trial of combined treatment with CDK4/6- and HER2-targeted agents for patients with HER2+ BCBM.  

  Study phs002482

• CD74-NRG1 fusions in lung adenocarcinoma

  We discovered a novel somatic gene fusion, CD74-NRG1, by transcriptome sequencing of 25 lung adenocarcinomas of never smokers. By screening 102 lung adenocarcinomas negative for known oncogenic alterations we found four additional fusion-positive tumors, all of which were of the invasive mucinous subtype. Mechanistically, CD74-NRG1 leads to extracellular expression of the EGF-like domain of NRG1 III-beta3, thereby providing the ligand for ERBB2-ERBB3 receptor complexes. Accordingly, ERBB2 and ERBB3 expression was high in the index case and expression of phospho-ERBB3 was specifically found in tumors bearing the fusion (p<0.0001). Ectopic expression of CD74-NRG1 in lung cancer cell lines expressing ERBB2 and ERBB3 activated ERBB3 and the PI3K-AKT pathway, and led to increased colony formation in soft agar. Thus, CD74-NRG1 gene fusions are activating genomic alterations in invasive mucinous adenocarcinomas and may offer a therapeutic opportunity for a lung tumor subtype with, so far, no effective treatment.

  Study EGAS00001000653

• InterPregGen-GWAS-UZB-2

  GWAS genotype data for maternal and fetal (baby) cases of preeclampsia and controls from Uzbekistan. This dataset is a component of the InterPregGen FP7 project. DNA samples for this component were collected by InterPregGen Consortium members in Tashkent, Uzbekistan at the Institute of Immunology, Uzbek Academy of Sciences and at the Republic Specialized Scientific Practical Medical Centre of Obstetrics and Gynecology

  Dataset EGAD00010001917