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• Population Genetics Analysis Program: Immunity to Vaccines/Infections - Smallpox Vaccination (NIAID/NIH)

  The study examines the role of candidate human immune response gene polymorphisms (and their receptors, expression and function) and variations in immune response, among 1,000 active duty members of the military who were recently vaccinated with ACAM2000 or Dryvax Smallpox vaccine. In addition to the phenotype and genotype data available through dbGaP, extensive clinical data are available through NIAID's ImmPort data portal; information to map the the data available in dbGaP to the data available in ImmPort is provided in the dataset pht005302.v1.p1 of the current study, dbGaP phs001057.v1.p1.

  Study phs001057

• Circulating RNAs in Acute Heart Failure (CRUCIAL)

  The purpose of this American Heart Association-funded and NIH-funded study is to examine circulating RNAs in the acute congestive heart failure (CHF) setting, and how they change with decongestive therapy, and their function in vitro and in vivo. The investigators are testing the hypothesis that ex-RNA levels change significantly during decongestion therapy and can be used as a marker of those individuals who respond to CHF therapy (in terms of cardiac structure or outcome). Additionally, the translational research design allows the investigators to assay the effects of these RNAs on tissue phenotypes in vitro.

  Study phs003403

• Transcriptome profiling of human plucked frontal and occipital hair follicles

  Androgenetic alopecia (AGA) is characterized by a progressive and androgen-dependent loss of hair from the frontal and vertex regions of the scalp. Although large-scale genetic analyses have identified >300 genetic risk factors, the underlying causal genes and pathways, and their involvement in core pathophysiological mechanisms, remain unclear. In the present study, systematic profiling of differential mRNA and microRNA expression was performed in human hair follicle samples from frontal and occipital scalp regions. Taken together, the present data improve understanding of the genomic regions, genes, and pathways that are implicated in AGA pathobiology.

  Study EGAS00001002832

• HudsonAlpha Institute for Biotechnology Clinical Sequencing Exploratory Research (CSER): Genomic Diagnosis in Children with Developmental Delay

  The overarching goal of this project is to explore the ability for whole exome and genome sequencing technologies to identify the genetic causes of unexplained developmental delay, intellectual disability (DD/ID), and related congenital anomalies in children. Such information may be useful as an endpoint to the otherwise fruitless "diagnostic odyssey" that many DD/ID affected families undergo and in some cases, identification of these genetic variants may point to better therapeutic or educational options by precisely defining the root cause(s) of the child's condition. We seek to identify causal, diagnostically relevant, genetic variants in children with developmental delay and/or intellectual disability (DD/ID). In addition, because our analytical approach includes sequencing probands and their parents (parent-offspring trios and duos; parents are sequenced when available), secondary findings will be returned to adults (parents) at their request. The aims of this research project include: 1) Use exome and whole genome sequencing to identify genetic variation that results in DD/ID. 2) Return primary genetic results (DD/ID causative) as well as secondary findings to probands and their parents, respectively. 3) Understand how the return of genomic test results affects the health and well-being of study participants. The children participating in this study are patients at, or referrals to, North Alabama Children's Specialist (NACS) in Huntsville, Alabama. All blood samples from probands and their parents will be collected at NACS (project 1). Sequencing will be completed at the HudsonAlpha Institute for Biotechnology, with validation (via Sanger sequencing) conducted at Emory University for all returned variants (project 2). The University of Louisville will oversee questionnaires, surveys and interviews aimed at understanding study participants' perception of, and response to, genetic test results, in addition to assessment of secondary findings preferences (project 3).A subset of variants, largely those determined to be diagnostic or variants of uncertain significance for study participants at the time of disclosure, have been submitted to ClinVar. These variants are listed as part of the "CSER-HudsonAlpha" study within the database.

  Study phs001089

• Meningioma Exome

  Meningioma Exome

  Dataset EGAD00001000099

• Family Investigation of Nephropathy and Diabetes (FIND) Study

  The Family Investigation of Nephropathy and Diabetes (FIND) is a multicenter study designed to identify genetic determinants of diabetic kidney disease. Study subjects were recruited from eleven centers and in many ethnic groups throughout the United States. A genome-wide association study (GWAS) was conducted with the Affymetrix 6.0 chip. Subjects (index cases) with diabetes and kidney disease were initially recruited, and their parents and siblings were invited to participate. Genetic material from these participants was used to genotype markers throughout the genome. For association-based testing, a case-control design was implemented with study subjects selected primarily from the index cases of the families. Unrelated controls were selected from families where a case was not already selected. Several study sites also contributed non-FIND subjects, both cases and controls (consent forms for the release of FIND and non-FIND subjects/samples are included in this dbGaP release). Cases were selected if they met study criteria for diabetic nephropathy or met inclusion criteria based on elevated serum creatinine levels and abnormal urine protein excretion. Similarly, controls were long-term diabetics with otherwise normal kidney function. See inclusion/exclusion criteria section for a detailed description for the FIND study as a whole and this GWAS. The goal of the FIND study is to identify genes that influence susceptibility to diabetic kidney disease, leading to a better understanding of how kidney disease develops. In the long run, this may lead to improved treatment and prevention of diabetic kidney disease.

  Study phs000333

• CRISPR screening in human trophoblast stem cells reveals both shared and distinct aspects of human and mouse placental development

  The placenta serves as the interface between the mother and fetus, facilitating the exchange of gases and nutrients between their separate blood circulation systems. Trophoblasts in the placenta play a central role in this process. Our current understanding of mammalian trophoblast development relies largely on mouse models. However, given the diversification of mammalian placentas, findings from the mouse placenta cannot be readily extrapolated to other mammalian species, including humans. To fill this knowledge gap, we performed CRISPR knockout (KO) screening in human trophoblast stem cells (hTSCs). We targeted genes essential for mouse placental development and identified more than 100 genes as critical regulators in both human hTSCs and mouse placentas. Among them, we further characterized in detail two transcription factors, DLX3 and GCM1, and revealed their essential roles in hTSC differentiation. Moreover, a gene function-based comparison between human and mouse trophoblast subtypes suggests that their relationship may differ significantly from previous assumptions based on tissue localization or cellular function. Notably, our data reveal that hTSCs may not be analogous to mouse TSCs or the extraembryonic ectoderm (ExE) in which in vivo TSCs reside. Instead, hTSCs may be analogous to progenitor cells in the mouse ectoplacental cone and chorion. This finding is consistent with the absence of ExE-like structures during human placental development. Our data not only deepen our understanding of human trophoblast development but also facilitate cross-species comparison of mammalian placentas.

  Study JGAS000659

• The long term effects of chemotherapy on normal blood - Nanoseq dataset

  In developed countries, ~10% of individuals are exposed to systemic chemotherapy for cancer and other diseases. Many chemotherapeutic agents act by increasing DNA damage in cancer cells, hence triggering cell death. However, there is limited understanding of the extent and consequences of collateral DNA damage to normal tissues. To investigate the impact of chemotherapy on mutation burdens and cell population structure of a normal tissue we sequenced blood cell genomes from 23 individuals, aged 3-80 years, treated with a range of chemotherapy regimens. Substantial additional mutation loads with characteristic mutational signatures were imposed by some chemotherapeutic agents, but there were differences in burden between different classes of agent, different agents of the same class and different blood cell types. Chemotherapy also induced premature changes in the cell population structure of normal blood, similar to those of normal ageing. The results constitute an initial survey of the long-term biological consequences of cytotoxic agents to which a substantial fraction of the population is exposed during the course of their disease management, raising mechanistic questions and highlighting opportunities for mitigation of adverse effects.

  Dataset EGAD00001015340

• Regulatory T cell transcriptomic reprogramming characterizes adverse events by checkpoint inhibitors in solid tumors

  Immune checkpoint inhibitors (ICI), which target immune regulatory pathways to unleash antitumor responses, have revolutionized cancer immunotherapy. Despite the remarkable success of ICI immunotherapy, a significant proportion of patients whose tumors respond to these treatments develop immune-related adverse events (irAEs) resembling autoimmune diseases. Although the clinical spectrum of irAEs is well characterized, their successful management remains empiric. This is in part because the pathogenic mechanisms involved in the break-down of peripheral tolerance and induction of irAEs remain elusive. Herein, we focused on regulatory T cells (Tregs) in individuals with irAEs because these cells are vital for maintenance of peripheral tolerance, appear expanded in the peripheral blood of individuals with cancer and abundantly express checkpoint molecules, hence representing direct targets of ICI immunotherapy. Our data demonstrate an intense transcriptomic reprogramming of CD4+CD25+CD127– Tregs in the blood of individuals with advanced metastatic melanoma who develop irAEs following ICI immunotherapy, with a characteristic inflammatory, apoptotic and metabolic signature. This inflammatory signature was shared by Tregs from individuals with different types of cancer developing irAEs and individuals with autoimmune diseases. Our findings propose an inflammatory Treg reprogramming as a feature of immunotherapy-induced irAEs, that may facilitate translational approaches aiming to induce robust antitumor immunity without disturbing peripheral tolerance.

  Study EGAS00001004694

• GeneScreen, a Population Based, Targeted Genomic Screening Study

  The GeneScreen research study was based at the University of North Carolina (UNC) at Chapel Hill. It brought together researchers from different disciplines, including genetics, clinical medicine, bioethics, sociology, anthropology, psychology, and public health, to study the best ways to offer targeted genetic screening to the general adult population. DNA samples were collected from people who joined GeneScreen to look at a targeted panel of 17 genes. It tested for genetic differences (called mutations) that can cause one of 11 rare, but preventable or treatable conditions, including certain types of cancer and heart disease. Each condition has specific medical advice people can follow with their doctors to prevent or treat a serious health problem. The GeneScreen study was approved by the UNC Institutional Review Board and by the Kaiser Permanente Center for Health Research Institutional Review Board. GeneScreen is funded by the National Human Genome Research Institute of the National Institutes of Health.

  Study phs001817