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• Field Studies of Human Immunity to Amebiasis in Bangladesh

  Amebiasis is a common cause of diarrhea and is associated with malnutrition in grade-school aged children in an urban slum of Dhaka, Bangladesh. Field Studies of Human Immunity to Amebiasis in Bangladesh was designed to determine the contribution of amebiasis to illness in the first 2 years of life when most deaths due to diarrhea occur, and understand the immunologic and genetic factors that protect children from amebiasis. The hypothesis underlying the study is that susceptibility to amebiasis is determined by host innate and acquired immune responses that vary between individuals in part due to: human genetic polymorphisms; environmental influences including malnutrition and concurrent geohelminth infection; and virulence differences among Entamoeba histolytica genotypes. Specific aims proposed in the design of the study were to: a) Measure the incidence of amebiasis and correlate it with human and parasite genetic polymorphisms, immune responses, and environmental factors such as geohelminth infection and malnutrition; b) Test the hypothesis that protective immunity is mediated both by innate immune responses initiated via TLR stimulation as well as by mucosal IgA against the Gal/GalNAc lectin and systemic IFN-γ; c) Test for the association of common genetic polymorphisms in host innate and acquired immune genes with incidence of amebiasis. 629 newborn babies were enrolled and followed regularly through bi-weekly surveillance for diarrheal episodes, anthropometry at 3-month interval until 60 months of age. The infants that were consented for GWAS analysis were genotyped in 3 separate batches at different times, on 3 different arrays. Quality control was performed on the 3 separate data sets and then jointly after merging. Genetic data available on 447 infants together with their phenotype data is made available in this submission.

  Study phs001476

• Hip OA Functional Genomics

  The aim of this work is to apply an integrated systems approach to understand the biological underpinnings of hip osteoarthritis that culminates in the need for total joint replacement (TJR). This study is a feasibility pilot that integrates functional genomics data from diseased and non-diseased tissues of OA patients who have undergone TJR. For each tissue, we characterised epigenetic marks (methylation), gene transcription (RNASeq) and expression (quantitative proteomics). We also generated genotype data on the HumanCoreExome array for each individual.

  Study EGAS00001002483

• Knee_OA_Functional_Genomics

  The aim of this work is to apply an integrated systems approach to understand the biological underpinnings of knee osteoarthritis that culminates in the need for total joint replacement (TJR). This study is a feasibility pilot that integrates functional genomics data from diseased and non-diseased tissues of OA patients who have undergone TJR. For each tissue, we characterised epigenetic marks (methylation), gene transcription (RNASeq) and expression (quantitative proteomics). We also generated genotype data on the HumanCoreExome array for each individual.

  Study EGAS00001001899

• Elucidating Mechanisms of the Graft versus Leukemia Effect of Hematopoietic Stem Cell Transplant for Acute Myeloid Leukemia

  Donor lymphocyte infusion (DLI) is an established mode of adoptive cellular therapy for treatment of relapsed disease after allogeneic hematopoietic stem cell transplantation (HSCT). For patients with acute myeloid leukemia (AML), the response rate to DLI is only 20%. Here we use next generation sequencing technologies to understand the transcriptomic and immunologic features associated with response or resistance to therapy.

  Study phs003630

• RNA-sequençing of 21 inflammatory hepatocellular adenomas

  The French ICGC project on liver tumors is coordinated by Pr Jessica Zucman-Rossi and funded by Inca (French Institute for Cancer). The aim of the present project is to identify the catalog of somatic and germline mutations in liver tumors.The present series corresponds to 21 RNA-seq of IHCA samples. Aligned bam files correspond to hg38 human reference.

  Study EGAS00001003685

• The brain neurovascular epigenome and its association with dementia

  Cerebral small vessel disease (SVD) is frequently comorbid with Alzheimer’s disease (AD) and vascular brain endothelial cells (BECs) are enriched for the expression of genes associated with AD genetic risk. However, the gene regulatory landscapes of neurovascular cells and their intersection with genetic risk for disease remains unexplored. Here we have generated gene regulomes for human BECs, mural cells and other brain cell types to show that AD heritability is primarily immune-related and that it shows modest enrichment in BECs. By contrast, genetic risk for SVD is enriched across cells of the neurovascular unit, including astrocytes. Enhancer-to-gene interactomes implicate amyloid processes in both AD and SVD, though the risk genes are mostly distinct for the two disorders. Motifs for putative partners of lineage transcription factors in microglia and BECs were enriched for AD and SVD variants at genes linked to disease pathways. Gene prioritization and enrichment analyses further identified potential repurposable drugs for AD. Our findings highlight novel regulatory mechanisms and therapeutic targets within the neurovascular system.

  Study EGAS50000001160

• Center for Common Disease Genomics [CCDG] - Neuropsychiatric: Epilepsy: Epi25 Consortium

  Epilepsy genetics research is at an exciting stage where it is now feasible, with the power of a large cohort, to understand the more complex genetic components of epilepsy. The driving principle behind the Epi25 Consortium is collaboration and synergy - it is only possible to achieve this type of research by working together. The Epi25 Consortium was formed by the unification of various consortia, including Epi4K, EPIGEN, EuroEPINOMICS, the Epilepsy Phenome/Genome Project, EpiPGX, SANAD, and EpiCURE, and individual epilepsy investigators. The consortium's sample collection is the best resource in the world for this disease, both in terms of numbers of patients and quality of phenotypic information. As part of the NHGRI Centers for Common Disease Genomics (2016-2020), we aggregated a global sample collection from the various repositories for whole genome genotyping and whole exome sequencing (WES) at the Broad Institute (Cambridge, MA), initiating the largest and most ethnically diverse genetic study of epilepsy to date. The primary epilepsy phenotypes for Epi25 are based on strict standards agreed upon by the epilepsy community. The epilepsy cases contributed by Epi25 sites can be broadly defined as genetic generalized epilepsy (GGE), non-acquired focal epilepsy (NAFE), epileptic encephalopathies (EE), and lesional focal epilepsies. More information about eligibility criteria and phenotyping forms for Epi25, as well as the contributing centers, can be found here: epi-25.org The genomic data will be analyzed iteratively to identify genes and variants that explain these types of epilepsy. Summary clinical data compiled in the Epi25 clinical database will allow retrospective phenotypic analyses of groups of subjects with common genomic variant(s).

  Study phs001489

• Using_genetics_to_identify_cell_types_and_mechanisms_underlying_susceptibility_to_primary_sclerosing_cholangitis

  Primary sclerosing cholangitis (PSC) is a T-cell mediated, chronic inflammatory condition of the biliary tree that is strongly associated with inflammatory bowel disease. Genome-wide association studies have identified 22 non-HLA genetic risk variants associated PSC. Identifying the genes impacted by these variants has proven difficult as the majority lie in non-coding regions of the genome. Knowledge of the genes and biological pathways these non-coding variants are perturbing is vital to understanding the disease biology. One means of assessing the impact of non-coding variants within disease associated loci upon genes is via colocalisation with eQTL. Many eQTL are cell-type specific, requiring the analysis of disease relevant cell types to detect colocalisation. We have collected PSC-relevant T-cell-subtypes from the peripheral blood of PSC patients via fluorescence activated cell sorting in preparation for RNA sequencing and mapping of eQTL. Samples were collected at the Norfolk and Norwich University Hopital, for which local ethical approval has been granted. Lysed cell samples will be transferred to WTSI and DNA/RNA will be extracted from lysed cell samples by T143 before genotyping (DNA) and custom library preparation and sequencing (RNA). 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 EGAS00001002643

• Using_genetics_to_identify_cell_types_and_mechanisms_underlying_susceptibility_to_primary_sclerosing_cholangitis

  Primary sclerosing cholangitis (PSC) is a T-cell mediated, chronic inflammatory condition of the biliary tree that is strongly associated with inflammatory bowel disease. Genome-wide association studies have identified 22 non-HLA genetic risk variants associated PSC. Identifying the genes impacted by these variants has proven difficult as the majority lie in non-coding regions of the genome. Knowledge of the genes and biological pathways these non-coding variants are perturbing is vital to understanding the disease biology. One means of assessing the impact of non-coding variants within disease associated loci upon genes is via colocalisation with eQTL. Many eQTL are cell-type specific, requiring the analysis of disease relevant cell types to detect colocalisation. We have collected PSC-relevant T-cell-subtypes from the peripheral blood of PSC patients via fluorescence activated cell sorting in preparation for RNA sequencing and mapping of eQTL. Samples were collected at the Norfolk and Norwich University Hopital, for which local ethical approval has been granted. Lysed cell samples will be transferred to WTSI and DNA/RNA will be extracted from lysed cell samples by T143 before genotyping (DNA) and custom library preparation and sequencing (RNA). 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 EGAS00001002642

• NHLBI TOPMed: Severe Asthma Research Program (SARP)

  The overall goal of the Severe Asthma Research Program (SARP) is to identify and characterize subjects with severe asthma to understand pathophysiologic mechanisms in severe asthma. Subjects with mild and moderate asthma were recruited for comparison but the program was enriched for subjects with severe asthma from multiple centers. Subjects were comprehensively phenotyped for asthma related traits including lung function, atopy, questionnaires on medical and family history, exhaled nitric oxide and health care utilization including exacerbations and symptoms. Asthma is a heterogenous disease. Cluster analysis in SARP has shown multiple subphenotypes and endotypes.

  Study phs001446