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• Genome-wide search for higher order epistasis as modifiers of treatment effects on bone mineral density in childhood cancer survivors

  Survivors of pediatric acute lymphoblastic leukemia (ALL) exposed to curative treatments that adversely affect BMD (age- and sex-adjusted BMD Z-scores, measured via QCT). Specifically, after SNP QC and annotation, we considered 75523 autosomal SNPs mapped to putative promoter or enhancer regions to restrict our search to 3-way SNP interactions that potentially reflect gene regulation events that influence BMD. We replicated 3-SNP interactions as modifiers of treatment effects in a cohort of adult survivors of non-ALL pediatric cancers (N=1428).

  Study EGAS00001002645

• TARGET Trial Study Cohort

  In a randomized controlled clinical trial, investigators will compare the effects on [18F]-fluorodeoxyglucose positron emission tomography-computed tomography (FDG PET/CT) from two treatment regimens in rheumatoid arthritis (RA) patients deemed methotrexate inadequate responders (MTX-IRs). Two common RA treatments will be compared: triple therapy (sulfasalazine, methotrexate, and hydroxychloroquine) versus tumor necrosis factor (TNF) inhibitor (etanercept or adalimumab, plus background methotrexate for all subjects and hydroxychloroquine for subjects who were taking this at screening). Consenting subjects will be screened for eligibility and randomized to a treatment arm. Subjects will be randomized to a treatment arm with either synthetic disease-modifying antirheumatic drugs (DMARDs) [triple therapy: sulfasalazine, methotrexate, and hydroxychloroquine] or biologic DMARDs [etanercept or adalimumab, plus background methotrexate for all subjects and hydroxychloroquine for subjects who were taking this at screening]. Once randomized, a baseline visit will be conducted with each subject. Baseline data collection includes questionnaires, disease activity score, and the first FDG-PET/CT imaging. After the baseline at week 0, subjects will visit with their rheumatologist at weeks 6, 12, 18, and 24 for safety labs and further collection of disease activity scores and questionnaires. The second FDG-PET/CT will be performed at week 24. Blood specimens will be collected at weeks 0, 6, 18, and 24 for bioassays. Subject participation will end after the week 24 visit. Patients and care providers will be unblinded. The FDG-PET/CT image readers will be blinded to treatment arm as well as timepoint of image acquisition.

  Study phs003720

• Single-cell targeted DNA-sequencing and protein sequencing

  We performed single-cell targeted DNA sequencing (MissionBio) on 13 high hyperdiploid B-ALL patients at diagnosis to study the genetic heterogeneity. For a number of patients single-cell surface protein antibody sequencing was added (DAB-seq) to better characterize the different cell types. Furthermore, additional samples during treatment were collected and analysed for some patients. In this way we want to study the clonal heterogeneity of these B-ALL samples, based both on mutations and CNVs, and identify resistant clones that could be targeted after relapse.

  Study EGAS50000000580

• Single-cell RNA and ATAC sequencing data analysis of human postmenopausal fallopian tube and ovary

  In this study, we used a combination of technologies, including Drop-seq, 10X single-cell RNA-seq (scRNA-seq), and single-cell assay on transposase accessible chromatin (scATAC-seq) to generate  a high-quality cell atlas that consists of four tissue sites from the reproductive tract of postmenopausal women. This atlas, by far the most comprehensive map of the postmenopausal female reproductive system to date, will pave the way to a better understanding of the pathophysiology of many diseases affecting older women.

  Study EGAS00001006780

• Center for Cancer Genomics (CCG) Cancers of Unknown Primary Project (CUPP)

  The Cancers of Unknown Primary Project (CUPP) aims to characterize difficult tumor types with the goal of determining future best treatment practices. NCI will utilize whole exome sequencing, copy-number variation, DNA methylation in conjunction with transcriptome sequencing to provide a comprehensive genomic landscape of Cancers of Unknown Primary (CUP). The samples will be processed and submitted for genomic characterization using pipelines and procedures established within the Center for Cancer Genomics (CCG).

  Study phs001801

• Single cell transcriptomics of human adrenal gland reveal chromosomal alterations in adrenocortical cells

  Adrenocortical cells get replenished throughout our lifetime and as such they are a cellular population of high interest in relation to adrenocortical tumours. Single cell transcriptomics of human adrenal gland were performed to identify rare subpopulations of cells, dynamics of cellular turnover and clone expansions in the adrenal cortex. The adrenal gland of this particular individual is characterized by the presence of mutant clone charecterized by aneuploidy in chromosomes 8, 9, 13 and 22, occupying the zona glomerulosa and zona fasciculata. Differential expression analysis of the mutant cells revealed upregulation of MC2R (adrenocorticotropic hormone receptor), CYP21A2, HSD3B2 genes (enzymes involved in cortisol production). Overall, this donor sample is an example of clonal tissue expansions carrying chromosomal rearrangements that likely impact organ morphology and function but are seemingly benign.

  Study EGAS00001007488

• Type 2 Diabetes Genetic Exploration by Next-generation sequencing in multi-Ethnic Samples (T2D-GENES)

  The T2D-GENES/GoT2D 13K exome sequencing study includes ~13,000 samples, half T2D cases and half T2D controls, from five ancestries (~5K Europeans, ~2K each of African-American, East-Asian, South-Asian, and Hispanic). Samples underwent deep exome sequencing, with SNVs and INDEls called according to GATK best practices; variant sites were then filtered according to the GATK best practices, and then samples and variants underwent further filtering based on aggregate genotype quality as described in Fuchsberger et al. (e.g. low call rate, excess heterozygosity for samples, low call rate or coverage for variants). Please note that one of the samples in the T2D-GENES vcf does not have phenotype data.

  Dataset EGAD00001002246

• RNA-seq data for study 'Smoking-dependent expression alterations in nasal epithelium reveal immune impairment linked to germline variation and lung cancer risk.'

  RNA-seq data from nasal and bronchial tissues in 649 subjects, many with lung cancer. Lung cancer is the leading cause of cancer-related death in the world. In contrast to many other cancers, a direct connection to lifestyle risk in the form of cigarette smoke has long been established. More than 50% of all smoking-related lung cancers occur in former smokers, often many years after smoking cessation. Despite extensive research, the molecular processes for persistent lung cancer risk are unclear. CT screening of current and former smokers has been shown to reduce lung cancer mortality by up to 26%. To examine whether clinical risk stratification can be improved upon by the addition of genetic data, and to explore the mechanisms of the persisting risk in former smokers, we have analyzed transcriptomic data from accessible airway tissues of 487 subjects. We developed a model to assess smoking associated gene expression changes and their reversibility after smoking is stopped, in both healthy subjects and clinic patients. We find persistent smoking associated immune alterations to be a hallmark of the clinic patients. Integrating previous GWAS data using a transcriptional network approach, we demonstrate that the same immune and interferon related pathways are strongly enriched for genes linked to known genetic risk factors, demonstrating a causal relationship between immune alteration and lung cancer risk. Finally, we used accessible airway transcriptomic data to derive a non-invasive lung cancer risk classifier. Our results provide initial evidence for germline-mediated personalised smoke injury response and risk in the general population, with potential implications for managing long-term lung cancer incidence and mortality.

  Dataset EGAD50000000333

• Research in Adaptive Interests, Skills, and Environment

  The Research on Adaptive Interest, Skills, and Environments (RAISE) project is a coordinated set of pilot studies funded and otherwise supported by the Center for the Study of Adolescent Risk and Resilience (C-StARR) at Duke University. The initial data collection effort (Adolescent T1; 2015; NAHDAP 100737) was conducted by telephone and focused on self-regulation and related skills during early adolescence and their role in early instances of health risk behavior. The survey was comprised of brief measures of constructs in six areas of interest to C-StARR investigators: (1) background and home environment; (2) self-regulation and personality; (3) physical and mental health; (4) problem behaviors; (5) academics and school; and (6) technology use. The representative sample of 2104 adolescents was drawn from the population of fifth through eighth graders enrolled in North Carolina public schools during the 2014-2015 school year.In 2016, a subsample of 395 participants from the Adolescent T1 survey (selected on the basis of having resided within 100 miles of study personnel hubs in Durham, North Carolina and Sylva, North Carolina) participated in an additional home visit study that involved the collection of biological data and measures of cognitive ability and executive functioning. The molecular data made available to dbGaP were obtained from saliva samples that were collected (a) in person from 377 of 395 home visit study participants and (b) by mail from 60 participants who had participated in the Adolescent T1 survey but had not participated in the home visit study. The resulting data file was imputed to a 1000G phase 3 panel and is comprised of N = 437 individuals and 7,193,135 markers after filtering. Data were filtered with MAF ≥ 0.01, HWE p-value > 10-6, and genotype rate > 95%.

  Study phs003982

• Low mutation burden and frequent loss of CDKN2A/B and SMARCA2, but not PRC2, define pre-malignant neurofibromatosis type 1-associated atypical neurofibromas

  Neurofibromatosis type 1 (NF1) is a tumor-predisposition disorder caused by germline mutations in NF1. NF1 patients have an 8-16% lifetime risk of developing a malignant peripheral nerve sheath tumor (MPNST), a highly aggressive soft-tissue sarcoma, often arising from pre-existing benign plexiform neurofibromas (PN) and atypical neurofibromas (ANF). ANF are distinct from both PN and MPNST, representing an intermediate step in malignant transformation. In the first comprehensive genomic analysis of ANF, we performed tumor/normal exome sequencing (ES) of 16 ANFs. In addition, we conducted ES of three MPNSTs, copy-number meta-analysis of 26 ANF and 28 MPNST, and whole transcriptome RNA-seq analysis of five ANF and five MPNST. We identified low mutation burden (median 1, range 0-5) in the exomes of ANF (only NF1 somatic mutations were recurrent), and frequent deletions of CDKN2A/CDKN2B (69%) and SMARCA2(42%) loci. We determined that polycomb repressor complex 2 (PRC2) genes EED or SUZ12 were frequently mutated, deleted or downregulated in MPNST but not in ANF. Our gene expression study revealed upregulated NRAS, MDM2, CCND1/CCND2/CCND3 and CDK4/CDK6 in both ANF and MPNST, and overexpression of EZH2 in MPNST only. We conclude that the PN-ANF transition is primarily driven by the deletion of CDKN2A/CDKN2B in addition to already present inactivated NF1. Further progression from ANF to MPNST likely involves broad chromosomal rearrangements and frequent inactivation of the PRC2 genes, loss of the DNA repair genes, and copy-number increase of signal transduction, cell cycle and pluripotency self-renewal genes.

  Study phs001993