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• 2017_ AML WGS analysis result

  This data is belong to 2017 AML genome data which is aligned to human reference(human_g1k_v37.fasta). There are 10 paired tumor/normal samples from SNUH. All samples has passed QC and recalibration steps while aligning to reference.

  Dataset EGAD00001003599

• 2017_ AML prospective data analysis result

  This data is belong to 2017 AML prospective data which is aligned to human reference(human_g1k_v37.fasta). There are 10 paired tumor/normal samples from SNUH. All samples has passed QC and recalibration steps while aligning to reference.

  Dataset EGAD00001003598

• 2014 AML WES analysis result

  This data is belong to 2014 AML patients' exome data which is aligned to human reference(human_g1k_v37.fasta). There are 51 paired tumor/normal samples from SNUH. All samples has passed QC and recalibration steps while aligning to reference.

  Dataset EGAD00001003932

• TCR sequencing of head and neck cancers

  This data contains the TCR-beta sequences of 10 head and neck squamous carcinomas and 19 nasopharyngeal carcinomas. The library preparation method is a customised targeted amplification of the VDJ regions and is sequenced on the Illumina Miseq.

  Dataset EGAD00001007917

• Genetic Discovery and Application in a Clinical Setting: Continuing a Partnership (eMERGE Phase II)

  The electronic Medical Records and Genomics (eMERGE) Network is a consortium of ten participating sites funded by the NHGRI to investigate the use of electronic medical record systems for genomic research. The goal of eMERGE is to conduct genome-wide association studies in approximately 19,000 individuals using EMR-derived phenotypes and DNA from linked Biorepositories. The eMERGE Network brings together researchers with a wide range of expertise in genomics, statistics, ethics, informatics, and clinical medicine from leading medical research institutions across the country. Each center participating in the consortium is uniquely situated to provide critical resources to this highly collaborative and productive network. Each site combines a biobank or study cohort with extensive genomic data and access to clinical data derived from electronic medical records. Sites are geographically dispersed and have diverse patient populations, including two sites focusing specifically on pediatrics. The eMERGE Network is comprised of 9 sites and one coordinating center. Each site maintains its own biorepository where DNA specimens are linked to phenotypic data contained within EMRs. Children's Hospital of Pennsylvania, PI: Hakon Hakonarson, MD, PhD Cincinnati Children's Medical Center with Boston Children's Hospital, PI: John Harley, MD, PhD - CCHMC and Ingrid Holm, MD, MPH - BCH Geisinger Health System, PI: David Carey, PhD and Marc Williams, MD Group Health Cooperative with University of Washington, PI: Eric Larson, MD, MPH - GHC and Gail Jarvik, MD, PhD - UW Marshfield Clinic with Essentia Institute of Rural Health, PI: Catherine McCarty, PhD, MPH - Essentia and Murray Brilliant, PhD - Marshfield Mayo Clinic, PI: Christopher Chute, MD, DrPH and Iftikhar Kullo, MD Icahn School of Medicine at Mount Sinai, PI: Erwin Bottinger, MD Northwestern University, PI: Rex Chisholm, PhD and Maureen Smith, MS Vanderbilt University, PI: Dan Roden, MD eMERGE Coordinating Center - Vanderbilt University, PI: Paul Harris, PhD Using electronic phenotyping methods, the consortium used DNA samples from all participating sites to explore the genetic determinants of red cell indices, white blood count (WBC) differential, diabetic retinopathy, height, serum lipid levels, specifically total cholesterol, HDL (high density lipoprotein), LDL (low density lipoprotein), and triglycerides, and autoimmune hypothyroidism as well as using the phenome-wide association study (PheWAS) paradigm to replicate and discover relationships between targeted genotypes with multiple phenotypes.

  Study phs000948

• The Chromatin Landscape of Pathogenic Transcriptional Cell States in Rheumatoid Arthritis

  In this study, we characterized 24 rheumatoid arthritis (RA) synovial tissue chromatin classes (i.e., cell states defined by chromatin accessibility) across 5 cell types (T, B/plasma, myeloid, stromal, and endothelial). We also investigated the transcription factors that may regulate these chromatin classes, their connections to transcriptional cell states in a proposed superstate model, and their interplay with RA pathology through associations with histological parameters and risk variants.As part of the Accelerating Medicines Partnership (AMP) network, we obtained 18 synovial tissue samples from 14 RA and 4 osteoarthritis (OA) patients for this study. Samples were collected from 7 clinical sites. We performed a 10x single cell ATAC-seq experiment on each sample.We further collected synovial tissue samples from 11 RA patients and 1 OA patient from 2 clinical sites; each sample was used for a 10x single cell multimodal ATAC and Gene Expression experiment.For additional support of the proposed superstate model, we also collected peripheral blood mononuclear cells (PBMCs) from 4 RA patients, sorted for 4 populations (CD4+CD127-CD25hi Tregs, CD4+CD127-CD25int Tregs, CD4+CD25-PD1+CXCR5- TPH, CD4+CD25-PD1+CXCR5+ TFH), tagged each population with a hashing antibody, and pooled populations for one multimodal sequencing run.The FASTQ files are available for controlled access via dbGaP. Additional data can be found on Synapse.The presence of pooled subjects inflates the automatically-generated subject count; the actual consented subject count for this data is 34.

  Study phs003417

• Direct Comparative Analysis of 10X Genomics Chromium and Smart-seq2

  Single cell RNA sequencing (scRNA-seq) is widely used for profiling transcriptomes of individual cells. The droplet-based 10X Genomics Chromium (10X) approach and the plate-based Smart-seq2 full-length method are two frequently-used scRNA-seq platforms, yet there are only a few thorough and systematic comparisons of their advantages and limitations. Here, by directly comparing the scRNA-seq data by the two platforms from the same samples of CD45- cells, we systematically evaluated their features using a wide spectrum of analysis. Smart-seq2 detected more genes in a cell, especially low abundance transcripts as well as alternatively spliced transcripts, but captured higher proportion of mitochondrial genes. The composite of Smart-seq2 data also resembled bulk RNA-seq data better. For 10X-based data, we observed higher noise for mRNA in the low expression level. Despite the poly(A) enrichment, approximately 10-30% of all detected transcripts by both platforms were from non-coding genes, with lncRNA accounting for a higher proportion in 10X. 10X-based data displayed more severe dropout problem, especially for genes with lower expression levels. However, 10X-data can better detect rare cell types given its ability to cover a large number of cells. In addition, each platform detected different sets of differentially expressed genes between cell clusters, indicating the complementary nature of these technologies. Our comprehensive benchmark analysis offers the basis for selecting the optimal scRNA-seq strategy based on the objectives of each study.

  Study EGAS00001003973

• Transcriptome of Chronic Pain and Disease

  The Functional Genomics Section (FGS) is a part of the National Institute of Dental and Craniofacial Research (NIDCR) within the National Institutes of Health (NIH). Research at the FGS focuses on understanding the mechanics involved in nociception through both clinical samples from patients with chronic pain and mouse models of pain. Pain is relayed from the periphery to the central nervous system through specialized sensory neurons known as nociceptors. The cell body of nociceptors resides in neuronal structures that branch off of the spinal cord known as dorsal root ganglia (DRG). The DRG is a heterogenous tissue containing not only sensory neurons like nociceptors, but also glial cells, capillaries, fibroblasts, and resident macrophages. The interaction between the nociceptors and these DRG cell types can have a significant role in affecting neuronal hyperexcitability and downstream pain sensitivity. To better understand the cellular factors involved in producing conditions of chronic pain, DRGs from consenting organ donors were collected from individuals experiencing pain disorders such as painful diabetic neuropathy and rheumatoid arthritis. A multi-omics approach is being used to identify molecular mechanisms that lead to pain hypersensitivity in patients with chronic pain.  

  Study phs002548

• Whole Exome Sequencing in Alopecia Areata Identifies Rare Mutations in KRT82

  Alopecia areata (AA) is an autoimmune disorder, in which the body's own immune cells attack hair follicels resulting in hair loss. It is a complex genetic disease with 14 associated loci previously identified in our genome-wide association study (GWAS). In the study, we performed the whole-exome sequencing (WES) on 849 AA patients with the aim to identify the novel rare variants in genes contributing to AA susceptibility. We performed gene-collapsing analyses and identified keratin 82 (KRT82 Gene ID: 3888) as the highest associated AA gene in the three rare damaging collapsing models with p<6.7E-07 in one of the models. The KRT82 gene is a hair-specific type II keratin expressed in the hair shaft cuticle during the anagen phase of the hair cycle. We reported the lower expression of KRT82 in AA hair follicles, compared to controls, and the KRT82 expression is absent from the bulb region, the site of AA immune attack. This study emphasizes the significance of using WES and gene collapsing analyses to identify rare variation in a functionally relevant risk gene using a moderate sample size.  

  Study phs002632

• EOSC4Cancer Longitudinal Synthetic Colorectal Cancer Genomic data developed at BSC

  The synthetic genomes have been created trying to mimic real cancer data of 4 patients (Named 185,186,187 and 188). Mutations are based on real CRC patients from the PCAWG dataset. For each patient, two tumor samples at different time points and one healthy sample have been simulated. The cancer intra-tumor heterogeneity and evolution in the patients is depicted by simulating reads from tumor subclones separately and then mixing them according to their clonal proportions in each sample. For rapid use and transfer only selected chromosomes have been generated for each patient. Chromosomes per patient: -185: chr4, chr5, chr7, chr17 -186: chr1, chr7, chr12, chr17 -187: chr1, chr2, chr5, chr12, chr17 -188: chr2, chr5, chr12, chr13, chr17 Worflows used to create BAM/BAI, VCF and MAF files from FASTQ (Alignment with GRCh38): - https://usegalaxy.eu/published/workflow?id=2c3d05023c02113e - https://usegalaxy.eu/published/workflow?id=1da86d74f8535f4e

  Dataset EGAD50000000276

• Whole-genome sequencing in 14 cases and whole-exome sequencing in 90 cases of Chinese ESCC

  Esophageal cancer is one of the most aggressive cancers and the sixth leading cause of cancer death worldwide1. Approximately 70% of the global esophageal cancers occur in China and over 90% histopathological forms of this disease are esophageal squamous cell carcinoma (ESCC)2-3. Currently, there are limited clinical approaches for early diagnosis and treatment for ESCC, resulting in a 10% 5-year survival rate for the patients. Meanwhile, the full repertoire of genomic events leading to the pathogenesis of ESCC remains unclear. Here we show a comprehensive genomic analysis in 158 ESCC cases, as part of the International Cancer Genome Consortium (ICGC) Research Projects (http://icgc.org/icgc/cgp/72/371/1001734). We conducted whole-genome sequencing in 14 ESCC cases and whole-exome sequencing in 90 cases.

  Dataset EGAD00001001691

• Neuroblastoma relapse trio series from the AMC

  The majority of neuroblastoma patients have tumors that initially respond to chemotherapy, but a large proportion of patients will experience therapy-resistant relapses. The molecular basis of this aggressive phenotype is unknown. Whole genome sequencing of 23 paired diagnostic and relapsed neuroblastomas showed clonal evolution from the diagnostic tumor with a median of 29 somatic mutations unique to the relapse sample. Eighteen of the 23 relapse tumors (78%) showed RAS-MAPK pathway mutations. Seven events were detected only in the relapse tumor while the others showed clonal enrichment. In neuroblastoma cell lines we also detected a high frequency of activating mutations in the RAS-MAPK pathway (11/18, 61%) and these lesions predicted for sensitivity to MEK inhibition in vitro and in vivo. Our findings provide a rationale for genetic characterization of relapse neuroblastoma and show that RAS-MAPK pathway mutations may function as a biomarker for new therapeutic approaches to refractory disease.

  Dataset EGAD00001001360

• Rare Disease Synthetic Dataset

  The purpose of this project is to provide public human datasets for the study of rare diseases. The use of public human genomic background combined with the in-silico insertion of real disease-causing variants enable to have a representative dataset for testing purposes without facing ethical and legal issues associated with the use of human sensitive data. This project aims to help development of technical implementations for rare disease data integration, analysis, discovery, and federated access.

  Dataset EGAD00001008392

• Whole Genome Study for De Novo Mutation Rates

  Germline mutations are the source of evolution and contribute substantially to many health-related processes. In this study, we use whole genome deep sequencing data from parents-offspring trios to examine the de novo point mutations (DNMs) in the offspring. We studied correlation between parental ages with de novo mutation rates. This study is published in Wong WS, Solomon BD, Bodian DL, Kothiyal P, Eley G, Huddleston KC, Baker R, Thach DC, Iyer RK, Vockley JG, Niederhuber JE. New observations on maternal age effect on germline de novo mutations. Nat Commun. 2016 Jan 19;7:10486 (PMID: 26781218. Also, we studied differences in molecular signatures in paternal versus maternal origin of de novo mutations. This study is published in Jakob M. Goldmann, Wendy S.W. Wong, Michele Pinelli, Terry Farrah, Dale Bodian, Anna B. Stittrich, Gustavo Glusman, Lisenka E.L.M. Vissers, Alexander Hoischen, Jared C. Roach, Joseph G. Vockley, Joris A. Veltman, Benjamin D. Solomon, Christian Gilissen, John E. Niederhuber. Parent-of-origin specific signatures of de novo mutations. Nat Genet. 2016 Aug;48(8):935-9, PMID: 27322544.

  Study phs001055

• Acute Respiratory Distress Network (ARDSNet) Studies 01 and 03 Lower Versus Higher Tidal Volume, Ketoconazole Treatment and Lisofylline Treatment (ARMA/KARMA/LARMA) (ARDSNet-ARMA/KARMA/LARMA-BioLINCC)

  Data Access NOTE: Please refer to the “Authorized Access” section below for information about how access to the data from this accession differs from many other dbGaP accessions. Biospecimens Access to Biospecimens is through the NHLBI Biologic Specimen and Data Repository Information Coordinating Center (BioLINCC). Biospecimens from ARDSNet-ARMA/KARMA/LARMA include plasma, serum and urine. Please note that use of biospecimens in genetic research is subject to a tiered consent. Objectives The ARDS Network is a consortium of clinical centers and a coordinating center to design and test novel therapies for the treatment of Acute Lung Injury (ALI) and Acute Respiratory Distress Syndrome (ARDS). The primary objective of the KARMA trial was to investigate the efficacy and safety of Ketoconazole and Respiratory Management in the treatment of ALI and ARDS. The Ketoconazole arm of the study was later stopped due to an inability to show efficacy. Participants continued to be randomized to the respiratory management arms of the study (ARMA), which compared two ventilator strategies: a tidal volume of 6 mL/kg versus 12 mL/kg. The LARMA phase of the study investigated the efficacy of Lisofylline and Respiratory Management. Background Participants suffering from ARDS are extremely ill, require mechanical ventilation and, despite improvements in medical care and technology, had a mortality rate as high as 50 percent. An excessive inflammatory response is characteristic of ALI of which ARDS represents the most severe end of the pathophysiologic spectrum. The inflammatory response includes increased numbers of neutrophils activated to produce cytokines, proteases, and reactive oxygen intermediates. Pulmonary injury may also be enhanced by alveolar and tissue macrophages as a producer of vasoactive substances, neutrophil chemoattractants, and procoagulant substances. Ketoconazole, a synthetic antifungal imidazole, also has anti-inflammatory activities and may inhibit neutrophil recruitment via several different pathways known to be involved in the development of ALI and ARDS. Lisofylline causes a marked decrease in the circulating levels of the major oxidizable species of free fatty acids and also inhibits proinflammatory intracellular signaling. Mechanical ventilation in participants with ALI and ARDS have traditionally used tidal volumes of 10 to 15 ml per kilogram of body weight. These large tidal volumes are often necessary to achieve normal partial pressure of arterial carbon dioxide and pH, but may induce inflammatory responses through disruption of pulmonary epithelium and endothelium. Mechanical ventilation at lower tidal volumes may reduce injurious lung stretch and decrease the inflammatory response. Participants The Ketoconazole and Lisofylline trials were designed as 2 x 2 factorials and included 220 participants in each trial. A total of 860 participants were randomized into the ventilator management trial. Participants enrolled in the Lisofylline or Ketoconozole studies had to be concurrently enrolled in the ventilator management study and were first randomized into a ventilator strategy and then to drug or placebo. Conclusions Ketoconazole was found to be safe but did not reduce mortality, duration of mechanical ventilation, or improve lung function. Lisofylline was also found to be safe and to have no beneficial effect for participants with ALI or ARDS. Ventilation at lower tidal volumes resulted in reduced mortality and an increase in the number of days without ventilator support. (PMIDs: 10789668, 11902249, 10793162).

  Study phs003734

• Washington University PDX Development and Trial Center

  This data set is a collection of patient specimens from common and rare cancers that have been developed into patient-derived xenograft (PDX) models at the Washington University PDX Development and Trial Center (WU-PDTC). The goal of the PDTC is to develop and characterize PDX models, gaining insight into tumor biology, and validating biomarkers across all major tumor types. Pre-clinical experiments in these PDX models will be used to advance our ability to predict clinical responses to new molecularly targeted agents under development.

  Study phs002305

• Ballett

  TSO500 study: The project, called "BALLETT" (Belgian Approach of Local Laboratory Extensive Tumor Testing), has a double goal: (1) show the relevance of broad molecular profiling to improve oncological patients care, (2) demonstrate that broad molecular testing can be performed in a decentralized setting by local diagnostics laboratories in a fully standardized and uniform way while complying with the highest quality standards. NCT05058937 The publication number is: Your manuscript ID is bcr-2023-256124. Title: CUP and BRAF V600E meeting the BEACON combination.

  Study EGAS50000000478

• Transcriptome and epigenomic landscape of cytotrophoblasts from normal and HDP placentas

  Hypertensive isorders of pregnancy (HDP) is a severe pregnancy-related disorder that poses significant risks to both maternal and fetal health. Dysfunctional placental development is one of the major contributors to the onset of HDP. In this study, we investigated the gene expression and epigenomic modifications in cytotrophoblasts from normal and HDP placentas. The information obtained in this study contributes to the growing body of knowledge aimed at improving the diagnosis, management, and treatment of HDP.

  Study JGAS000667

• PEVOsq

  The PEVOData PEVOsq basket trial is an open-label, multi-center, phase II trial investigating the combination of pembrolizumab (an immune checkpoint inhibitor) with vorinostat (a histone deacetylase inhibitor). This trial focuses on treating patients with recurrent or metastatic squamous carcinomas, including cancers of the cervix, head and neck, anus, vulva/vagina, penis, and lung. The aim is to evaluate the efficacy and safety of this combination, with pembrolizumab administered every 3 weeks and vorinostat daily. Outcomes include overall response rate and progression-free survival.

  Study EGAS50000000731

• Metabolomic and transcriptomic analyses identify metabolic alterations and immune suppression in ovarian cancer

  The objective of this study is to identify metabolic alterations and related phenotypes specific to ovarian cancer by performing metabolomic analysis of plasma and tissue samples. In addition, transcriptomic analysis is conducted to investigate the relationship between metabolic status and immune-related gene expression. By integrating metabolomic and transcriptomic data, this study aims to clarify how metabolic reprogramming contributes to tumor progression and immune suppression, particularly the reduction of natural killer (NK) cell activity, in ovarian cancer.

  Study JGAS000831

• Regions of common inter-individual DNA methylation differences in human monocytes.

  Based on whole genome bisulfite sequencing of five human monocytes from unrelated individuals, we have identified regions of common inter-individual DNA methylation differences, where methylation is inversely correlated with active histone marks, but not with the expression of the associated genes. Genome-wide association studies in 1128 individuals show that allelic DNA methylation is caused by genetic variation in cis. At some loci, DNA methylation appears to be affected also by genetic variation in trans.

  Study EGAS00001002265

• Next generation sequencing of sporadic schwannomatosis samples

  Schwannomatosis (MIM #162091) is characterized by the development of multiple schwannomas without vestibular nerve involvement (which is a characteristic of neurofibromatosis type 2 - NF2). In an effort to detect novel genetic alterations predisposing to schwannomatosis, we sequenced eight tumor-blood DNA pairs from de novo schwannomatosis patients. The results of our study are present in the paper "Whole exome sequencing reveals that the majority of schwannomatosis cases remain unexplained after excluding SMARCB1 and LZTR1 germline variants" published in Acta Neuropathologica (PMID:25008767)

  Study EGAS00001000767

• Genetic landscape of relapsed DLBCL

  Diffuse large B-cell lymphoma is a heterogenous malignancy that can arise de novo or can result from histologic transformation from indolent lymphomas. Considerable sequencing effort has been placed on determining the mutations that are common at the time of diagnosis in DLBCL but little is known about the nature of relapsed disease. We have sequenced tumour and matched normal exomes of 38 rrDLBCL patients including 25 de novo DLBCLs and 13 transformed lymphomas to identify somatic mutations and copy number alterations associated with relapse.

  Study EGAS00001001553

• Assessment_of_genetic_and_epigenetic_variation_in_human_IPS_cells

  In 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 but it is unclear whether some cell types carry through fewer mutations through reprogramming (either due to mutations present in the primary cells, or mutations accumulated during reprogramming). Through in depth analysis of hiPSCs generated from different somatic cells, it will be possible to assess the variation in genetic stability of different cell types.

  Study EGAS00001000231

• Celiac disease-specific intestinal T cells analyzed with HLA-class II tetramers, RNA-seq and mass cytometry have a narrow, autoimmune-associated phenotype

  Celiac disease (CD) is an HLA-DQ2/8-associated autoimmune enteropathy driven by activation of gluten-specific CD4+ T lymphocytes upon gluten consumption. Much less is known about the phenotype and function of these cells or their correlation, if any, to disease-relevant cells in other autoimmune disorders. Here we use mass cytometry and RNA seq to show that gluten-specific blood and gut T cells occupy a small and phenotypically distinct T-cell subset.

  Study EGAS00001003017