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• Circulating RNA profiles of healthy and preeclamptic pregnancies

  This prospective study investigated whether circulating RNA (C-RNA; cell free RNA present in the bloodstream) measurements could non-invasively monitor pregnancy status, with emphasis on detecting molecular markers associated with preterm preeclampsia. Whole blood samples were collected from pregnant women at the time of diagnosis with early-onset preeclampsia with severe features. Blood samples were also obtained normotypical control pregnancies and from patients diagnosed with late-onset preeclampsia for comparison. For all samples, C-RNA was extracted from 4 mL blood and whole transcriptome enrichment performed on cDNA libraries prior to sequencing to a target depth of 50M reads on an Illumina HiSeq 2000 platform. Throughout the course of this work, whole transcriptome RNA sequencing data was obtained from 289 C-RNA samples collected from 178 subjects. The complete dataset consists of samples from the following cohorts: Illumina Preeclampsia Cohort (iPEC): 40 pregnancies at the time of early-onset preeclampsia diagnosis and 73 gestational age-matched controls PEARL preeclampsia cohort: 12 early-onset and 12 late-onset preeclampsia patients PEARL healthy control cohort: 152 longitundinal samples collected from 41 healthy pregnancies

  Study phs002017

• Whole-Exome Sequencing Study of Diabetic Nephropathy

  To identify rare variants of diabetic kidney disease (DKD), we conducted a whole-exome sequencing (WES) study. This study employed an extreme case–control design, which included a selection of the 593 most rapidly progressing DKD cases from the Chronic Renal Insufficiency Cohort (CRIC) Study (phs000524). In this two-stage WES study of DKD, participants with DKD from the CRIC were compared with control groups of participants without DKD from another cohort in the first stage. Suggestive signals identified in the first stage were confirmed in the second stage analysis among a diverse population with existing whole-genome sequencing (WGS) data. Generalized linear mixed models, which accounted for genetic relatedness and adjusted for age, sex and ancestry, were used to test associations between single variants and DKD. Gene-based aggregate rare variant analyses were conducted using an optimized sequence kernel association test implemented within our mixed model framework. As a result, we identified four novel gene loci, DIS3L2, KRT6B, ERAP2 and NPEPPS, that achieved exome-wide significance and may play an important role in the DKD disease course. This large WES study provides novel insights into DKD's molecular mechanisms.

  Study phs003429

• Pre-activated anti-viral innate immunity in the upper airways controls early SARS-CoV-2 infection in children

  Children have reduced SARS-CoV-2 infection rates and a substantially lower risk for developing severe COVID-19 than adults. However, the molecular mechanisms underlying protection in younger age groups remain unknown. Here, we characterize the single-cell transcriptional landscape in the upper airways of SARS-CoV-2-negative (n=18) and age-matched SARS-CoV-2–positive children (n=24) and corresponding samples from adults (n=44), covering an age range of four weeks to 77 years. Children displayed higher basal expression of the relevant pattern recognition receptors (PRR) such as MDA5 (IFIH1) and RIG-I (DDX58) in upper airway epithelial cells, macrophages, and dendritic cells, resulting in stronger innate antiviral responses upon SARS-CoV-2 infection than adults. We further detected distinct immune cell subpopulations including KLRC1 (NKG2A)+ cytotoxic T cells and a CD8+ T cell population with a memory phenotype occurring predominantly in children. Our study provides evidence that the airway immune cells of children are primed for virus sensing, resulting in a stronger early innate antiviral responses to SARS-CoV-2 infection than adults.

  Study EGAS00001005461

• DNA Methylation Characterization of Fusion-Positive and Fusion-Negative Rhabdomyosarcoma

  Rhabdomyosacoma (RMS) is a common pediatric soft tissue tumor that is associated with the skeletal muscle lineage. RMS comprises two major subtypes: fusion-positive (FP, most commonly PAX3- FOXO1 or PAX7-FOXO1) and fusion-negative (FN, frequently associated with mutations in RAS pathway). Our previous study demonstrated that FP and FN tumors exhibit distinct DNA methylation profiles. In this study, further investigation of genome-wide DNA methylation profiles in RMS tumors revealed DNA methylation differences between AX3-FOXO1 and PAX7-FOXO1 subsets in FP RMS, and between RAS mutation and RAS wild-type subsets in FN RMS. These data provide new insight into the relationship of DNA methylation with mutational changes and transcriptional organization in FP and FN RMS.

  Study phs001970

• M116 scRNA-seq

  scRNA-seq was performed using Chromium Next GEM Single Cell 3’ Kit v3.1 (10X Genomics) according to the manufacturer’s instructions. Briefly, M116's PBMCs were thawed and quantified in order to calculate the number of cells to be loaded. Then, barcoded Single Cell 3ʹ Gel Beads, a master mix containing PBMCs, and Partitioning Oil were combined onto the Chromium Next GEM Chip G to generate Gel Beads-In-Emulsion (GEMs), where polyadenylated mRNAs were reverse transcribed. This way, all generated cDNAs from the same cell shared a common 10X Barcode. Following the reverse transcription, GEMs were broken and cDNAs were amplified and cleaned up with SPRIselect beads (Beckman Coulter®). Next, a portion of these cDNAs were enzymatically fragmented and subjected to adaptor ligation before using them as a PCR template for the incorporation of i5/i7 indexes. Finally, libraries were purified with SPRIselect beads, quantified and quality checked by using the 2200 TapeStation (Agilent®), and subjected to paired-end 150-bp sequencing (Novaseq systems, Illumina®) following standard practices at external facilities (Novogene®). Files types included in this dataset are raw Fastq files.

  Dataset EGAD50000001289

• Somatic L1 retrotransposition in normal colorectal epthelium

  Throughout an individual’s lifetime, genomic alterations accumulate in somatic cells. However, the mutational landscape induced by retrotransposition of long interspersed nuclear element-1 (L1), a widespread mobile element in the human genome, is poorly understood in normal cells. Here, we explored the whole-genome sequences of 406 normal colorectal clones, 12 MUTYH-associated adenomatous clones, and 19 matched colorectal cancer tissues. In addition, we analyzed promoter DNA methylation status of retrotransposition-competent L1 (in 139 clones) and read-through RNA expression profiles (in 116 clones) to investigate the epigenetic regulation of L1 activity.

  Dataset EGAD00001010183

• Catalogue Statistics

  EGA Statistics Bibliography Growth Community Archive Distribution Catalogue What is in the EGA? The European Genome-phenome Archive (EGA) overview The EGA archives and distributes the results of several types of studies. Such studies include genome-wide association studies (GWAS), different purpose sequencing and molecular diagnosis assays among others. Moreover, these studies target many different kind of diseases from cancer to neurodegenerative alterations. We summarised all this data in the charts below. The statistics are computed daily based on an updated list of studies. Each pie chart depicts a different aspect of the studies: which disease type was studied, which type of sampling method was used and what was the scope of the genomic analysis. Number of studies per disease type Studies in the EGA by disease barHorizontalChart('disease-graph', 'https://stats.ega-archive.org/catalog/by_disease') Number of studies per technology type Studies in the EGA by technology barHorizontalChart('technology-graph', '/stats/studies/technology', 'Include dbGaP') Number of studies per sample type Studies in the EGA by samples barChart('samples-graph', '/stats/studies/sample-types', 'Include dbGaP')

  Documentation about/statistics/catalogue

• WES data (cfTrack study) from NSCLC patients and OC patients

  We also collected samples from 8 NSCLC patients and 4 ovarian cancer patients and. For all 8 NSCLC patients, a tumor biopsy sample, a WBC sample, and three plasma samples were collected. For all 4 ovarian cancer patients, a WBC sample and two serum samples were collected. We collected tumor tissue sample from one ovarian cancer patient (OV4). The cfDNA was extracted from their plasma samples using the QIAamp circulating nucleic acid kit from QIAGEN (Germantown, MD). For serum cfDNA, ampure XP beads size selection was further performed to eliminate gDNA contamination. In brief, 0.5 volume of beads were first added to the cfDNA samples. After incubation, the supernatant was transferred to a new tube and an additional 2.0 volume of beads were added. After 80% ethanol wash, cfDNA was eluted from the beads. FA assays (Agilent Technologies) were performed to rule out the contamination of gDNA in the size selected samples. The cfDNA WES library of all patients and the genomic DNA WES library of the 4 ovarian cancer patients were constructed with the SureSelect XT HS kit from Agilent Technologies (Santa Clara, CA) according to the manufacturer’s protocol. In brief, 10ng of cfDNA was used as input material. After end repair/dA-tailing of cfDNA, the adaptor was ligated. The ligation product was purified with Ampure XP beads (Beckman-Coulter, Atlanta, GA) and the adaptor-ligated library was amplified with index primer in 10-cycle PCR. The amplified library was purified again with Ampure XP beads, and the amount of amplified DNA was measured using the Qubit 1xdsDNA HS assay kit (ThermoFisher, Waltham, MA). 700-1000 ng of DNA sample was hybridized to the capture library and pulled down by streptavidin-coated beads. After washing the beads, the DNA library captured on the beads was re-amplified with 10-cycle PCR. The final libraries were purified by Ampure XP beads. The library concentration was measured by Qubit, and the quality was further examined with Agilent Bioanalyzer before the final step of 2x150bp paired-end sequencing at an average coverage of 200. Whole-exome capture libraries of genomic DNA from the 8 NSCLC patients were constructed via Roche SeqCap EZ Exome V6 (Roche). Enriched exome libraries were sequenced on the Illumina HiSeq 3000 platform (Illumina) to generate 2x100bp paired-end reads at an average coverage of 200.

  Dataset EGAD00001008454

• Plasma ctDNA is a tumor tissue surrogate and enables clinical-genomic stratification of metastatic bladder cancer

  Study EGAS00001004615

• Mortality and risk of progression to adult T-cell leukemia/lymphoma in patients with HTLV-1-associated myelopathy/tropical spastic paraparesis

  Human T-cell leukemia virus (HTLV)-1 causes the functionally debilitating disease HTLV-1-associated myelopathy/ tropical spastic paraparesis (HAM/TSP) as well as adult T-cell leukemia lymphoma (ATLL). Although there were concerns that the mortality of HAM/TSP could be affected by the development of ATLL, prospective evidence was lacking in this area. In this 5-year prospective cohort study, we determined the mortality, prevalence, and incidence of ATLL in 527 HAM/TSP patients. The standard mortality ratio of HAM/TSP patients was 2.25, and ATLL was one of the major causes of death (5/33 deaths). ATLL prevalence and incidence in these patients were 3.0% and 3.81 per 1,000 person-years, respectively. To identify patients at a high risk of developing ATLL, flow cytometry, Southern blotting, and targeted sequencing data were analyzed in a separate cohort of 218 HAM/TSP patients. In 17% of the HAM/TSP patients, we identified an increase in T-cells positive for cell adhesion molecule 1 (CADM1), a marker for ATLL and HTLV-1 infected cells. Genomic analysis of these patients revealed that somatic mutations of HTLV-1 infected cells were seen in 90% of the cases and 11% of them had dominant clone and developed ATLL in the longitudinal observation. In this study, we were able to demonstrate for the first time that the increased mortality in patients with HAM/TSP and a significant effect of ATLL on their prognosis. Having dominant clonal expansion of HTLV-1- infected cells with ATLL-associated somatic mutations may be important characteristics of patients with HAM/TSP who are at an increased risk of developing ATLL.

  Study JGAS000226