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• WGS data from LCNEC patient derived tumor organoids (PDTOs) and matched parental tumors - SA

  The dataset includes cram files from WGS of 2 LCNEC tumors and matched PDTOs. For all tumors, cram files from WGS of matched normal tissue derived organoids from the corresponding patients is included. Analysis VCF files are also included in the dataset. The sequencing was done with a NovaSeq 6000 instrument.

  Dataset EGAD00001009990

• Egypt Genome Project - high coverage whole genome sequencing

  All humans outside Africa are descendants of the same single exit, usually dated at 50-70 thousand years ago. However, the route taken out of Africa is still debated. The two main candidates are a northern route via Egypt and the Levant, or a southern route via Ethiopia and the Arabian Peninsula. We are generating genetic data to evaluate these two possibilities. In this study we propose to generate high-coverage sequencing data for 3 Egyptian samples.

  Dataset EGAD00001001380

• Patient-derived neuroblastoma model system OHC-NB1

  The dataset is comprised of seven samples, one blood sample (germline control) of the patient, one neuroblastoma metastasis from the bone marrow and five derived cell models. The models include the primary culture, the first xenogenograft passage, a monolayer culture derived from the first xenograft passage and two samples of the fourth xenograft passage, cells and supernatant. For all these samples, whole-exome sequencing data have been generated. The BAM files contain the alignments against the human genome, assembly GRCh37, and also the unaligned reads.

  Dataset EGAD00001004138

• Egypt Genome Project - low coverage whole genome sequencing

  All humans outside Africa are descendants of the same single exit, usually dated at 50-70 thousand years ago. However, the route taken out of Africa is still debated. The two main candidates are a northern route via Egypt and the Levant, or a southern route via Ethiopia and the Arabian Peninsula. We are generating genetic data to evaluate these two possibilities. In this study we propose to generate low-coverage sequencing data for 100 Egyptian samples.

  Dataset EGAD00001001372

• Non-invasive prenatal diagnosis by genome-wide haplotyping of cell-free plasma DNA

  This dataset contains a total of 10 families and 51 samples presented in 'Non-invasive prenatal diagnosis by genome-wide haplotyping of cell-free plasma DNA' study, in which 9 of them are cfDNA samples and the rest of samples are gDNA samples. All the samples are targeted sequencing data with a custom 45Mb capture library . Raw pair-end fastq files for each sample is available.

  Dataset EGAD00001004989

• Genes-Environments and Admixture in Latino Asthmatics (GALA II) Study

  A case-control pharmacogenetic study of bronchodilator drug response among racially admixed Latino children with asthma. Each participant had two spirometry measurements using the KoKo PFT System. With the first spirometry test, participant was administered with 4 puffs of HFA Albuterol. The second albuterol measurement was based on age, for participants under 16 years of age, additional 2 puffs were administered and for those over 16 years of age, additional 4 puffs were administered. The overall goal is to identify genetic factors which are predictive of drug response in children with asthma. The principal tools include a questionnaire and biological specimen collection. Participants are 8-21 years old at time of recruitment. Children with asthma have physician-diagnosed asthma, symptoms and medications. The GALAII Study is utilized in the following dbGaP substudies. To view genotypes, analysis, other molecular data, and derived variables collected in these substudies, please click on the following substudies below or in the "Substudies" box located on the right hand side of this top-level study page phs001180 GALAII Study. phs001274phs001274 GALAII GWAS

  Study phs001180

• LEF1 knockdown effects on human T cell transcriptome and chromatin accessibility profiles.

  LEF1 (Lymphoid Enhancer-Binding Factor 1) is a key transcription factor in T cell development and function, and its dysregulation has been implicated in various immune-related disorders. This study aimed to comprehensively characterize the transcriptional and epigenetic changes induced by LEF1 knockdown in human T cells. CD3+ T cells isolated from three healthy donors were transfected with either LEF1-specific siRNA or control siRNA, followed by activation with CD3/CD28 Dynabeads and culture in IL-2-containing media. Cells were harvested at 24, 48 and 72 hours post-transfection for multi-omics analysis including bulk RNA-seq, bulk ATAC-seq, single-cell CITE-seq (For CITE-seq, 48 and 72 hours only). This dataset provides insights into LEF1-dependent gene regulatory networks and chromatin accessibility patterns in activated human T cells, contributing to our understanding of T cell biology and potential therapeutic targets. This dataset is part of a comprehensive study investigating functional roles of risk polymorphisms in autoimmune diseases, particularly focusing on the rs58107865 variant at the LEF1 locus.

  Study JGAS000818

• RNA sequencing in primary human macrophages overexpressing ETS2

  This dataset consists of RNA sequencing data from an ETS2 overexpression experiment in M0 macrophages. Controlled overexpression of ETS2 mRNA or control mRNA (an equivalent amount of mRNA encoding the reverse complement of ETS2 – thereby controlling for the quantity, length and purine/pyrimidine composition of the transfected RNA but with a transcript that would not be translated) was induced in resting, non-activated (M0) macrophages by transfecting predefined amounts of in vitro transcribed mRNA. To minimise non-specific activation due to the transfected RNA, in vitro transcription was performed using co-transcriptional capping (to minimise uncapped products), and incorporating modified, minimally immunogenic nucleotides (replacing uridine with N1-methyl-pseudouridine and cytidine with methylcytidine). After 18 hours, transfected cells were were activated with low dose LPS and harvested for RNA-sequencing 6 hours later. Sequencing libraries were prepared from 10ng RNA using the SMARTer Stranded Total RNA-Seq Kit v2 - Pico Input Mammalian (Takara) following the manufacturer’s instructions. The quality and molarity of all libraries was assessed using a BioAnalyzer 2100 and the libraries were sequenced on a NovaSeq6000. Raw data are provided as 100 bp paired-end Illumina reads from n = 8 donors.

  Dataset EGAD00001011341

• Single-cell genome-wide concurrent haplotyping and copy-number profiling through genotyping-by-sequencing

  scGBS is a single-cell sequencing-based methodology to haplotype and copy-number profile single cells. Genomic size and complexity is reduced through restriction enzyme digestion and DNA is genotyped through sequencing of the restriction fragments. scGBS data serves as the input for haplarithmisis, an algorithm we previously developed for SNP array-based single-cell haplotyping (Zamani Esteki et al., 2015). We established technical parameters and developed an analysis pipeline enabling accurate concurrent haplotyping and copy-number profiling of single cells with the use of a HapMap cell line pedigree (7 single cells). A clinical validation of the methodology with a total of 14 single blastomeres and 3 trophectoderm samples biopsies from human preimplantation embryos for 6 PGT-M families were processed with scGBS and were previously haploptyped via SNP array.

  Dataset EGAD00001007794

• Center for Education and Drug Abuse Research (CEDAR)

  Under its programmatic name, the Center for Education and Drug Abuse research (CEDAR), this Center of Excellence project was completed in 2015. The CEDAR sample consists of 775 nuclear families comprising an adult male (proband), his spouse/mate, and their biological child who is 10-12 years of age at recruitment. This child is designated as index child (IC), and is followed through age 30. Minimal exclusionary criteria were applied to maximize the sample's representativeness. Follow-up evaluations on ICs were conducted at ages 14, 16, 19, 22, 25, 27 and 30. Interim questionnaires were mailed annually beginning at age 20. CEDAR utilizes the family/high-risk paradigm. The offspring thus comprise high average risk (HAR) and low average risk (LAR) groups, constituting the majority of the CEDAR children sample: 250 HAR males, 100 HAR females, 250 LAR males and 94 LAR females. The remainder of the IC sample, 50 males and 31 females, are the offspring of fathers who have a lifetime non-SUD psychiatric dis-order. The follow-up rate from baseline to the final assessment is ~65%. The cohort of children is 76% White and 22% Black. The representation of females among ICs is lower than males, due to the later start of recruit-ment (2nd funding cycle; the study originally focused on males). The CEDAR genetic study has been augmented by the inclusion of its sample into the whole-genome genotyping effort conducted under the Genes, Environment and Development Initiative (GEDI). DNA from the blood samples of target children (index cases) and their siblings submitted to the NIDA Genetics Depository a Rutgers University was obtained and genotyped on Illumina Human660W-Quad Beadchips, with a high average genotyping rate of 99.8%. The sample comprised 158 females and 271 males (37 and 63 %), ~70:30 European- and African- American, with approximately 1:1 ratio of children of affected fathers and normal controls.

  Study phs001649

• SNP array analysis of spondylocostal dysostosis patient iPSCs and gene edited isogenic controls

  This study, "SNP Array Analysis of Gene Edited SDV Patient iPSCs" is part of a larger study where we applied our recently established experimental in vitro model system of the human segmentation clock, for the analysis of human segmentation defects of the vertebrae (SDV) including spondylocostal dysostosis (SCD). To this end we generated patient-derived iPSC lines, identified putative disease-causing mutations and corrected these mutations using CRISPR/Cas9-based genome editing technology. We identified in the patient-sample originally obtained from the NIGMS Human Genetic Cell Repository at the Coriell Institute for Medical Research (#: GM13539) heterozygous compound mutations in MESP2. These mutations were corrected accordingly and the resulting clones were genotyped by SNP array analysis.

  Study phs001975

• RNAseq samples of patients with anti-PD-1 resistant HNSCC from a non-randomized, open-label phase 1b clinical trial

  Immune checkpoint blockade (ICB) is an effective treatment for a subset of patients with head and neck squamous cell carcinoma (HNSCC); however, the majority remain refractory. In a nonrandomized, open-label Phase 1b clinical trial, participants with recurrent and/or metastatic (R/M) HNSCC who had progressed on ICB were treated with low-dose 5-azacytidine (5-aza) daily for either 5 or 10 days, in combination with durvalumab and tremelimumab. The primary objective was to determine the biologically effective dose of 5-aza. In this study, RNA sequencing (RNA-seq) was performed on baseline and on-treatment samples from eight participants, and transcriptomic changes were analyzed to assess the impact of low-dose 5-aza treatment.

  Study EGAS50000000728

• WES samples of patients with anti-PD-1 resistant HNSCC from a non-randomized, open-label phase 1b clinical trial

  Immune checkpoint blockade (ICB) is an effective treatment for a subset of patients with head and neck squamous cell carcinoma (HNSCC); however, the majority remain refractory. In a nonrandomized, open-label Phase 1b clinical trial, participants with recurrent and/or metastatic (R/M) HNSCC who had progressed on ICB were treated with low-dose 5-azacytidine (5-aza) daily for either 5 or 10 days, in combination with durvalumab and tremelimumab. The primary objective was to determine the biologically effective dose of 5-aza. In this study, whole exome sequencing (WES) was performed on baseline samples from 12 participants, and genomic alterations were analyzed to access the genetic background of these participants.

  Study EGAS50000000729

• WGS_of_healhy_mesothelial_cells_and_primary_mesothelima_cell_lines

  Mesothelioma is a rare and aggressive cancer associated with previous exposure to asbestos. Currently there are no effective treatments for mesothelioma and majority of patients will die within a year after diagnosis. Although a large number of preclinical and clinical trials assessed the efficacy of various therapuetic modes, none of the tested molecules entered the clinic. Thus, to better understand what drives mesothelioma carcinogenesis and to identify novel targets for therapy, here we aim at performing WGS of heathy mesothelial cells and a panel of mesothelioma cells lines. Primary mesothelial cell lines were established in prof. Marciniak lab from human pleural specimens, while primary mesothelioma cell lines were obtained from MesobanK. Both models constitute low passage cell lines and therefore should closely represent genetics of the original tissue.

  Study EGAS00001005559

• 2014 sequenced Korean WES-Lung Cancer sample 36 pair

  This data is belong to WES-Lung Cancer patients' genome data which is aligned to human reference(human_g1k_v37.fasta). There are 36 paired tumor/normal samples from Samsung Hospital. All samples has passed QC and recalibration steps while aligning to reference.

  Dataset EGAD00001004027

• 2015 AML-ETO WGS additional analysis result

  This data is belong to additional 2015 AML-ETO patients' genome data which is aligned to human reference(human_g1k_v37.fasta). There are 2 paired tumor/normal samples from SNUH. All samples has passed QC and recalibration steps while aligning to reference.

  Dataset EGAD00001004012

• 2014 Lung squamous cell carcinoma WES analysis result

  This data is belong to 2014 Lung squamous patients' exome data which is aligned to human reference(human_g1k_v37.fasta). There are 104 paired tumor/normal samples from SMC. All samples has passed QC and re-calibration steps while aligning to reference.

  Dataset EGAD00001003960

• 2014 sequenced WGS-Lung Cancer sample 30 pair

  This data is belong to WGS-Lung Cancer patients' genome data which is aligned to human reference(human_g1k_v37.fasta). There are 30 paired tumor/normal samples from Samsung Hospital. All samples has passed QC and recalibration steps while aligning to reference.

  Dataset EGAD00001003978

• Dataset for B-ALL scRNA-seq

  10x Genomics 5' library scRNA-seq data for 85 B-ALL patients with different subtypes

  Dataset EGAD00001011327

• Genomics of Kidney Transplantation

  We have an established consortium consisting of 5 clinical centers which do a total of >800 kidney transplants/year. We have developed a quality-controlled multicenter database with high quality data, and obtained DNA samples and clinical data on 962 recipients and 442 donors. Using our developed infrastructure, we propose to study whether genetic variants are, in part, responsible for the differing outcomes of transplant recipients treated with contemporary immunosuppressive protocols. Our central hypotheses are that the genetic variation is associated with a) kidney transplant outcome, and b) immunosuppressive drug disposition and toxicity. Our long-term goals are to determine whether it is possible to individualize immunosuppressive therapy, based on genetics. At the same time, our studies may elicit new information on pathways important in the immune response or in immunosuppressive drug efficacy, disposition, and toxicity.Our application consists of 3 cores (Genetics Core, Clinical Core, and Administrative Core). We will do a genome wide association study (GWAS). Significant single nucleotide polymorphisms (SNPs) will be identified using the GWAS.Project 1 has 2 specific aims.Aim 1: To identify recipient SNPs that are associated with kidney allograft outcomes, including acute rejection, chronic graft dysfunction, and graft failure. Aim 2: To identify living donor SNPs that are associated with kidney allograft outcomes. Project 2 has 4 specific aims. Aim 1: To identify SNPs that are associated with tacrolimus blood levels.Aim 2: To identify SNPs that are associated with early tacrolimus-related nephrotoxicity and immune suppressant-related new onset diabetes.Aim 3: To identify SNPs that are associated with mycophenolate-related toxicity. Aim 4: To establish the relationships between candidate recipient SNPs, enzyme activity and mRNA expression of the pharmacologic targets of mycophenolate and calcineurin inhibitors. The projects use the genotyping data, which were provided by the Genetics Core, and clinical information, which were collected and entered into the multicenter database by the Clinical Core. Further, biostatistical support (Clinical Core) and administrative oversight and support (Administrative Core) will facilitate data collection, data entry, and data analyses for both projects. The Administrative Core will also facilitate interaction between Sites, Cores, and Projects.Technical note: Regarding to the study design, all transplant recipients should be unrelated. Given the nature of transplantation, some donors may be related to recipients. The donor-recipient relationships are reported in the demographic file under the "related" column. As we did not collect full pedigree information for the related donor-recipient pairs, we have included a IBD file (calculated using PLINK) with the genotype data.

  Study phs001667

• Assessment_of_epigenetic_variation_in_human_iPS_cells_Medip

  n order to progress human induced pluripotent stem cells (hiPSCs) towards the clinic, several outstanding questions must be addressed. It is possible to reprogram different somatic cell types into hiPSCs and from studies in the mouse, it appears that an epigenetic memory of the starting cell type is carried over to hiPSCs. However a comprehensive comparative study of the characteristics of these hiPSCs has been missing from the literature. Importantly studies which aimed to address these aspects of hiPSCs have used cells from different patients. In order to avoid this important confounding variable and to keep the genetic background constant, tissue samples were procured from the patients and reprogrammed to iPS cells. The methylation status of these iPS cells will be compared.Protocol:Primary cell cultures were generated and reprogrammed to iPS cells. DNA was extracted and immunoprecipitated using anti-methyl cytosine and anti-hydroxymethyl cytosine antibodies.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 EGAS00001000741

• Genomic Studies of Gilles de la Tourette Syndrome

  This study consists of three components. The first component includes genome-wide association study (GWAS) data on 695 TS cases and 198 ancestry matched controls from the first TS GWAS of 1285 TS cases and 4964 ancestry matched controls. The second component includes genome-wide association study (GWAS) data on 2106 TS cases from the second TS GWAS of 2716 TS cases and 3762 ancestry matched controls. The third component consists of 438 individuals representing 146 probands with DSM-IV-TR diagnosed Tourette Syndrome and their parents (146 complete parent-offspring trios). These individuals are part of the whole exome sequencing study, aiming to use whole exome sequencing of TS parent-offspring to identify de novo protein-truncating variants (PTVs) that are present in the child with TS but not in either parent. All subjects were collected by the Tourette Association of America International Consortium for Genetics (TAAICG) at seven sites in the United States and Canada. Both affected individuals and unaffected relatives were assessed for the presence of Tourette Syndrome and Chronic (Persistent) Tic Disorder (CTD) using a standardized, semi-structured interview, which has high clinical validity and reliability for the diagnoses of TS and CTD (TSAICG, Am J Hum Genet, 2007 (PMID: 17304708)); Darrow et al., Psychiatric Research, 2015 (PMID: 26054936)).

  Study phs001380

• DNA Methylation Analysis of Prostate Cancer Cell Lines and Tissues Using Next Generation Sequencing

  Aberrant DNA methylation changes are known to occur during prostate cancer progression beginning with precursor lesions. Utilizing fifty nanograms of genomic DNA in Methylplex-Next Generation Sequencing (M-NGS) we mapped the global DNA methylation patterns in prostate tissues (n=17) and cells (n=2). Peaks were located from mapped reads obtained in each sequencing run using a Hidden Markov Model (HMM)-based algorithm previously used for Chip-Seq data analysis(http://www.sph.umich.edu/csg/qin/HPeak). The total methylation events in intergenic/intronic regions between benign adjacent and cancer tissues were comparable. Promoter CGI methylation gradually increased from -12.6% in benign samples to 19.3% and 21.8% in localized and metastatic cancer tissues and approximately 20% of all CpG islands (CGIs) (68,508) were methylated in tissues. We observed distinct patterns in promoter methylation around transcription start sites, where methylation occurred directly on the CGIs, flanking regions and on CGI sparse promoters. Among the 6,691 methylated promoters in prostate tissues, 2481 differentially methylated regions (DMRs) are cancer specific and several previously studied targets were among them. A novel cancer specific DMR in WFDC2 promoter showed 77% methylation in cancer (17/22), 100% methylation in transformed prostate cell lines (6/6), none in the benign tissues (0/10) and normal PrEC cells. Integration of LNCaP DNA methylation and H3K4me3 data suggested a role for DNA methylation in alternate transcription start site utilization. While methylated promoters containing CGIs had mutually exclusive H3K4me3 modification, the histone mark was absent in CGI sparse promoters. Finally, we observed difference in methylation of LINE-1 elements between transcription factor ERG positive and negative cancers. The comprehensive methylome map presented here will further our understanding of epigenetic regulation of the prostate cancer genome. Overall Design: We mapped the global DNA methylation patterns in prostate tissues (n=17) and cells (n=2) from fifty nanograms of genomic DNA using Methylplex-Next Generation Sequencing (M-NGS). For replicate analysis in cell lines, a total of 4 runs were completed for PrEC prostate normal cell line, and 5 runs were completed for LNCaP prostate cancer cell line. For tissue samples, 2 benign prostate samples were sequenced twice on Illumina next generation sequencing platform to access overall repeatability of M-NGS.

  Study phs000597

• Role of Tobacco Smoke in Clear Cell Renal Cell Carcinoma

  Background. Clear cell renal cell carcinoma (ccRCC) is the most common histologically defined renal cancer. However, it is not a uniform disease and includes several genetic subtypes with different prognoses. ccRCC is also characterized by distinguished metabolic reprogramming. Tobacco smoking (TS) is an established risk factor for ccRCC with unknown effects on tumor pathobiology.Methods. We investigated the landscape of ccRCCs and paired normal kidney tissues (NKTs) using integrated transcriptomic, metabolomic and metallomic approaches in a cohort of never smokers (NS) and long-term current smokers (LTS) Caucasian males. Results. All three Omics domains consistently identified a distinct metabolic subtype of ccRCCs in LTS, characterized by activation of oxidative phosphorylation (OxPhos) coupled with reprogramming of the malate-aspartate shuttle and metabolism of aspartate, glutamate, glutamine and histidine. Cadmium, copper and inorganic arsenic accumulated in LTS tumors showing redistribution among intracellular pools, including relocation of copper into the cytochrome c oxidase complex. Gene expression signature based on the LTS metabolic subtype provided prognostic stratification of The Cancer Genome Atlas (TCGA) ccRCC tumors that was independent from genomic alterations.Conclusions. The work identified the TS related metabolic subtype of ccRCC with vulnerabilities that can be exploited for precision medicine approaches targeting metabolic pathways. The results provided rationale for the development of metabolic biomarkers with diagnostic and prognostic applications using evaluation of OxPhos status. The metallomic analysis revealed the role of disrupted metal homeostasis in ccRCC highlighting the importance of studying effects of metals from e-cigarettes and environmental exposures.

  Study phs002083

• Colorectal adenomas, carcinomas and adjacent normal NKI-AvL TGO series NGS-ProToCol

  Cancer is caused by changes in the genome of cells, resulting in aberrant transcripts and proteins. In order to understand why normal cells become cancer cells and how we can identify and destroy them, the CTMM-NGS-ProToCol project aimed to understand prostate and colorectal cancer through DNA and RNA molecular profiling, to further improve diagnosis, prognosis and treatment.The state-of-the-art within the field of genome sequencing makes it possible to identify all the modifications in our genome that encode for RNA and of the transcripts themselves. The latest development in RNA sequencing is that if one does not select for polyA RNA, but first removes rRNA from the total RNA and then performs ‘random’ RNA sequencing, 30-60% of the reads are intronic. Since about 40% of the genome consists of genes (and only 1.6% is exonic), deep RNA sequencing will cover not only the exons, but also a large portion of the introns and therefore much of the genome. The power of the combined sequencing of genome and transcriptome is the full view of copy number aberrations (CNA), exon mutations and the consequence and relevance of the mutations at the RNA level in the form of differential gene expression, alternative splicing, alternative promoter usage, novel transcripts, fusion transcripts, read-through transcripts and mutations. For the colorectal (tumor) tissue dataset, we applied molecular profiling to 30 colorectal adenomas, 30 colorectal carcinomas and 18 normal adjacent colon tissues.

  Study EGAS00001002854