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• WGBS data of solid liver tumor DNA, and WGBS data of cell-free DNA derived from human blood, for CancerDetector study

  The blood samples of four liver cancer patients and four healthy people, and the solid liver tumor samples of two liver cancer patients are collected for this dataset. Blood samples were centrifuged first at 1,600 × g for 10 minutes, and then the plasma was transferred into new micro tubes and centrifuged at 16,000 × g for another 10 minutes. The plasma was collected and stored at -80⁰C. CfDNA was extracted from 5 ml plasma using the Qiagen QIAamp Circulating Nucleic Acids Kit and quantified by Qubit 3.0 Fluoromter (Thermo Fisher Scientific). Bisulfite conversion of cfDNA was performed by using EZ-DNA-Methylation-GOLD kit (Zymo Research). After that, Accel-NGS Methy-Seq DNA library kit (Swift Bioscience) was used to prepare the sequencing libraries. The DNA libraries were then sequenced with 150bp paired-end reads.

  Dataset EGAD00001004317

• Pathogenesis and Immunity in Endemic Burkitt Lymphoma

  This genomic landscape of Burkitt lymphoma represents a multimodal sequencing of tumors and control tissues and individuals to better understand the etiology, and molecular pathogenesis of Burkitt lymphoma including the roles of the associated Plasmodium falciparum malaria and EBV infections. Comprehensive sequencing set includes genomic, transcriptomic, and epigenomic datasets in concert with variable clinical phenotypes and outcome information such as anatomical presentation site, in-hospital survival rates, and EBV genome type. This deposit includes additional small RNA-seq data from endemic BL (eBL) tumors and RNA-sequencing data from sorted NK cell subsets from the peripheral blood of eBL patients. The additional small RNA-seq data are from tumor specimens from 17 eBL cases, of the previously deposited polyA RNA-seq data from 28 eBL cases (phs1282.V1). The additional RNAseq data from Fluorescence-activated cell sorting (FACS) of NK cell subsets, isolated from the peripheral blood of 7 eBL cases. The additional RNAseq data are from eBL tumor samples of 5 eBL cases, BL cell lines established from these tumor samples and also NSG mouse tumors created by implanting the established BL cell lines into NSG mice. The dataset also includes RNAseq data of the NSG mouse tumors after treatment with Rituximab (RIT) and Phosphate buffered saline (PBS). The fifth batch of data includes mRNA-seq from different passages of a single eBL cell line that have variable EBV phenotypes (low passage with lytic EBV and high passage with latent EBV). This batch also includes lytic and latent lymphoblastoid cell line (LCL) clones from a single blood donor generated through infection with the strain of EBV isolated from the aforementioned eBL cell line. For initial transcriptome analysis see: Kaymaz et al. "Comprehensive Transcriptome and Mutational Profiling of Endemic Burkitt Lymphoma Reveals EBV Type-specific Difference." Molecular Cancer Research, 2017, PMID: 28465297. For initial microRNA analysis see: Oduor et al. "Human and Epstein-Barr Virus miRNA Profiling as Predictive Biomarkers for Endemic Burkitt Lymphoma." Frontiers in Microbiology 8, 2017, PMID: 28400759. For initial NK subsets RNA expression analysis see: Forconi et al. "A new hope for CD56negCD16pos NK cells as unconventional cytotoxic mediators: an adaptation to chronic diseases." Frontiers in Cellular and Infection Microbiology, 2020, PMID: 32373555.For initial eBL cell line and mouse avatar RNA expression analysis see: Saikumar et al. "Endemic Burkitt lymphoma avatar mouse models for exploring inter-patient tumor variation and testing targeted therapies." Life Science Alliance, 2023, PMID: 36878637. For general overview of cohort study see: Buckle et al. "Factors influencing survival among Kenyan children diagnosed with endemic Burkitt lymphoma between 2003 and 2011: A historical cohort study." Int J Cancer. 15:1231, 2016, PMID: 27136063.

  Study phs001282

• snRNA-seq analysis in multinucleated myogenic FSHD cells identifies heterogeneous FSHD transcriptome signatures associated with embryonic-like program activation and oxidative stress-induced apoptosis

  The sporadic nature of DUX4 expression in FSHD muscle challenges comparative transcriptome analyses between FSHD and control samples. A variety of DUX4 and FSHD-associated transcriptional changes have been identified, but bulk RNA-seq strategies prohibit comprehensive analysis of their spatiotemporal relation, interdependence and role in the disease process. In this study, we used single-nucleus RNA-sequencing of nuclei isolated from patient- and control-derived multinucleated primary myotubes to investigate the cellular heterogeneity in FSHD. Taking advantage of the increased resolution in snRNA-sequencing of fully differentiated myotubes, two distinct populations of DUX4-affected nuclei could be defined by their transcriptional profiles. Our data provides insights into the differences between these two populations and suggests heterogeneity in two well-known FSHD-associated transcriptional aberrations: increased oxidative stress and inhibition of myogenic differentiation. Additionally, we provide evidence that DUX4-affected nuclei share transcriptome features with early embryonic cells beyond the well-described cleavage stage, progressing into the 8-cell and blastocyst stages. Altogether, our data suggests that the FSHD transcriptional profile is defined by a mixture of individual and sometimes mutually exclusive DUX4-induced responses and cellular state-dependent downstream effects.

  Study EGAS00001007635

• Study of Women's Health Across the Nation (SWAN) Repository

  The Study of Womens Health Across the Nation (SWAN) is an active multi-site, multi-disciplinary, longitudinal study of women's health. Initially funded in 1994 by the National Institute on Aging (NIA), the National Institute of Nursing Research (NINR), and the Office of Research on Women's Health (ORWH), the overall goal of SWAN is to describe the natural history of the menopausal transition and the post menopause including biological, behavioral, and psychosocial characteristics. SWAN focuses on the impact of menopause on age-related chronic diseases, such as diabetes, cardiovascular disease, depression, bone loss and osteoporosis, as well as physical and cognitive functioning. SWAN has seven clinical study sites located in six states, two in California, and one each in Chicago, Boston, Detroit area, northern New Jersey and Pittsburgh. The SWAN cohort was recruited from these areas and consists of 3,302 African American, Caucasian, Chinese American, Hispanic and Japanese American women. SWAN participants were enrolled in 1996-1997 and have been seen annually or bi-annually for clinic visits, which include interviews, measurements, and the collection of blood and urine samples. SWAN participants have now been seen for the baseline and 15 follow-up visits.

  Study phs001470

• Pancreatitis after Treatment for Acute Lymphoblastic Leukemia (SJIRB XPD04-123 and XPD05-078)

  A complication of acute lymphoblastic leukemia (ALL) treatment is acute pancreatitis, which is one of the common causes of asparaginase intolerance. To determine clinical and genetic risk factors for pancreatitis, we studied a cohort of children and young adults with ALL enrolled on COG trials (9904/9905/9906, AALL0232) and on St. Jude trial Total XV. We performed a genome-wide association study using germline DNA collected from blood in patients at remission in this cohort of 5185 patients and in an independent case-control group of 213 patients on AALL0331. The frequency of pancreatitis in the cohort was 2.3% (117 of 5185). No common variants reached genome-wide significance, but a rare nonsense variant rs199695765 in CPA2, encoding carboxypeptidase A2, was highly associated with pancreatitis (odds ratio = 587, 95% confidence interval 66.8-5166, P = 9.0 x 10-9). A gene-level analysis showed an excess of additional CPA2 variants in patients who did versus those who did not develop pancreatitis (P = 0.018). Sixteen CPA2 SNPs were associated (P < 0.05) with pancreatitis, and 13 of 24 patients who carried at least one of these variants developed pancreatitis. Biological functions that were overrepresented by common variants modestly associated with pancreatitis included purine metabolism and cytoskeleton regulation.

  Study phs001350

• Genetic Epidemiology of Lung Cancer Consortium GWAS of Familial Lung Cancer

  Familial lung cancer cases were collected by the Genetic Epidemiology of Lung Cancer Consortium (GELCC) recruitment sites: University of Cincinnati, Karmanos Cancer Institute at Wayne State University, Louisiana State University Health Sciences Center-New Orleans, Mayo Clinic, and Medical College of Ohio. Familial cases for this study came from three sources: 1) one case each from families (at least 3 affected lung cancer cases in the family) included in the linkage analysis; 2) one case from linkage-eligible families (at least 3 affected lung cancer cases in the family) but where there were insufficient biospecimens available to make them informative for linkage analysis; and 3) one case from families not eligible for the linkage study with a family history of at least one first or second degree relative affected with lung cancer. Unrelated controls were selected from 1) among the spouses of family members, thus matching on socio-economic status (SES) and ethnicity (typically) of the cases or 2) from case-control studies of lung cancer conducted in the same location in which the linkage families were collected and matched on age, sex, and race. All cases and controls self-reported as European American. Biospecimens used for normal DNA extraction included blood, saliva or mouthwash. Some samples underwent whole genome amplication.

  Study phs000629

• Genomic Sequencing of Cervical Cancers

  Cervical cancer is responsible for 10-15% of cancer related deaths in women worldwide. The etiological role of infection with high-risk human papilloma viruses (HPV) in carcinomas of the cervix is well established. In general, the development of cervical carcinomas follows a progression from persistent HPV infection through precancerous lesions to invasive cancer. Previous studies have implicated somatic mutations in PIK3CA, PTEN, TP53, STK11 and KRAS as well as chromosome-arm level copy number alterations in the pathogenesis of cervical carcinomas. Here, we report whole exome sequencing analysis of 118 cervical carcinoma-normal paired samples from patients in Norway and Mexico, as well as transcriptome sequencing of 80 cases and whole genome sequencing of 13 tumor-normal pairs. Novel somatic mutations include recurrent E322K substitutions in the MAPK1 gene encoding the ERK2 kinase and inactivating mutations in the HLA-B gene. In addition, recurrent somatic mutations in FBXW7, EP300, and NFE2L2 are novel in the context of primary cervical carcinomas. Analysis of HPV integration sites revealed recurrent integration into the RAD51B locus as well as co-occurrence of HPV genome integration and copy number gains within several genomic loci. These findings shed new light on the pathogenesis of cervical carcinomas and suggest potential novel therapeutic targets.

  Study phs000600

• Single Cell and Tissue Level Functional Genomics Analysis of Astrocyte-Related Mechanisms in Taupathy

  This data is the first part of a larger single cell and tissue level functional genomics analysis of dementias with tau pathology.  Cellular resolution will clarify the role of glial genes and pathways in neurodegenerative disease. This includes understanding the role of microglia and astrocytes in neurodegenerative disorders characterized by Tau protein pathology. To achieve a refined view of microglial neuroinflammatory signaling in tau-associated neurodegeneration, we performed a functional genomic analysis that integrated time-course gene expression data from mouse models expressing human mutant MAPT (the tau gene) with single nuclear sequencing data obtained from patients with frontotemporal dementia with Tau protein pathology (Pick’s disease). This included microglia-specific gene expression data obtained from single nuclear sequencing of postmortem frozen precentral gyrus samples collected from 16 total individuals, including 8 subjects with clinical diagnosis of behavior variant frontotemporal dementia and neuropathological diagnosis of Pick’s disease (Tau protein pathology) and controls (n=8). Our findings present detailed molecular profiles of disease-associated microglial transitions over the course of tau-associated neurodegeneration. Furthermore, we demonstrate overlap between microglia profiles obtained from precentral gyrus of patients with Pick’s disease with those up-regulated during the neurodegenerative stage in mice expressing human MAPT mutations.

  Study phs002197

• NIDDK IBD Genetics Consortium Repository Immunochip

  The Immunochip is a custom Illumina Infinium chip comprising 196,524 SNPs and small indels selected primarily based on GWAS analysis of 12 autoimmune and inflammatory diseases. The chip has two purposes: fine mapping of 289 established associations corresponding to 187 distinct loci, and deep replication of suggestive, but not yet proven, associations. Fine-mapping regions were defined as 0.2cM centered on GWAS hit SNPs, and all SNPs and short indels in these regions from the 1000 Genomes Project low coverage pilot CEU samples, as well as variants discovered in resequencing experiments conducted by groups collaborating in the chip design were selected for inclusion. Replication of autoimmune and inflammatory GWAS (including Crohn's disease and ulcerative colitis) contributed the bulk of the remaining SNP lists. Approximately 25,000 SNPs were included as replication of unrelated diseases as part of the WTCCC2 project, which serve as useful null SNPs for these analyses. In total, approximately 240,000 SNPs were selected for inclusion, with an assay design success rate of ~80%. Reprinted from Jostins et al. (2012), with permission from Springer Nature (see https://www.nature.com/reprints/permission-requests.html). Jostins, L., et al. (2012) Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease. Nature, 491, 119-24. PMID: 23128233.

  Study phs001721

• A Large Data Resource of Genomic Copy Number Variation across Neurodevelopmental Disorders

  This study presents the first genome-wide copy number variation (CNV) analysis across autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), schizophrenia (SCZ), and obsessive-compulsive disorder (OCD). A total of 2,691 subjects diagnosed with a neurodevelopmental disorder (NDD), and a total of 1,769 unaffected family members from Ontario, Canada were assayed using the Affymetrix CytoScan HD array. We identified rare CNVs, (< 0.1% frequency in 10,851 population control samples), and found clinically relevant CNVs in 10.5% of total subjects. Among all NDD subjects, we identified 17 (0.63%) with aneuploidies and 115 (4.3%) with known genomic disorder variants. We searched further for genes impacted by different CNVs in multiple disorders. Examples of NDD-associated genes linked across more than one disorder (listed in order of occurrence) are NRXN1, SEH1L, LDLRAD4, GNAL, GNG13, MKRN1, DCTN2, KNDC1, PCMTD2, KIF5A, SYNM, and long non-coding RNAs: AK127244, NRON, and PTCHD1-AS. We demonstrated that identical CNVs or genes could potentially contribute to the etiology of multiple NDDs. The CNVs identified will serve as a useful resource for both research and diagnostic laboratories for prioritization of variants and clinical interpretations.CNV data from this study are available through dbVar at https://www.ncbi.nlm.nih.gov/dbvar/studies/nstd173/.

  Study phs001881