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• Data Quality Control

  Data Quality Control High-throughput sequencing techniques have become the leading method to study, decode and discover the genomic origins of biological phenomenons. EGA provides a secure archival of such identifiable genomics data with the purpose of data-upcycling, i.e. to re-use these data for research. High-quality data standards are essential to ensure the quality and credibility of the research. Moreover, a quality check report can assure a researcher beforehand about the data that they will request access, therefore saving time and effort. The EGA has developed a File Quality Control Report (QC Report) to provide generic quality control reports for Fastq, SAM/BAM/CRAM, and VCF files deposited at EGA. This QC Report will allow users to get information regarding the files submitted within a specific dataset. The data requesters will obtain information such as the quality of reads, mapped reads, number of variants, and other features before starting the requesting process, which will save the efforts and time.Accessing file quality control reportsIn each dataset page, the user can explore the files that it contains by clicking the "files" tab. The Quality Control report of a file has two sections. The first one, contains general information about the file, such as the inferred assembly, total reads, the dataset or study where it comes from, etc. The second section contains plots that summarise interesting information about the file, for example, the base coverage distribution, base quality or mapped reads. The description of each plot is accessible by clicking the "i" button at the top-right corner of each plot box. Technical Description For analysing the fastq, SAM/BAM/CRAM and VCF files, the EGA applies a set of tools widely used in the bioinformatics community. FASTQ: FastQC, recognised as the gold standard tool by the community.Per base sequence quality, per sequence quality scores, per base sequence content, per sequence GC content, sequence duplication levels, etc.SAM/BAM/CRAM: samtools, also the gold standard, generates results plots useful to get an overall idea of the quality of the file.base coverage distribution, base quality, % of mapped reads, % of both mates mapped, singletons, duplicates, etc.VCF: vcftools and bcftools, combined with a custom script to infer the genome assembly.site frequency distribution, Ts/Tv, base changes, indel distribution, etc.

  Documentation access/request-data/quality-control-reports

• Sequence data for study: Mobilization of tissue-resident memory CD4+ T lymphocytes from bone marrow and their contribution to a systemic secondary immune reaction

  Resident memory T lymphocytes (TRM) of epithelial tissues and the bone marrow protect their host tissue. To what extent these cells are mobilized and contribute to systemic immune reactions is less clear. Here we show that in secondary immune reactions to the measles-mumps-rubella (MMR) vaccine, CD4+ TRM are mobilized into the blood within 16 to 48 hours after immunization. This mobilization of TRM is cognate: TRM recognizing other antigens are not mobilized, unless they cross-react with the vaccine. We also demonstrate through methylome analyses that TRM are mobilized from the bone marrow. These mobilized cells make significant contribution to the systemic immune reaction, as evidenced by their T-cell receptor Vβ clonotypes represented among the newly generated circulating memory T-cells, 14 days after vaccination. Thus, TRM of the bone marrow confer not only local, but also systemic immune memory.

  Study EGAS00001005475

• The mission of the BIOS Consortium is to create a large-scale data infrastructure and to bring together BBMRI researchers focusing on integrative omics studies in Dutch Biobanks.

  The advent of the genome-wide association study (GWAS) led to the successful identification of thousands of variants that are robustly associated with complex disease phenotypes. Dutch biobanks played a substantial role in these discoveries. For most of these variants, however, the mechanisms through which they contribute to these phenotypes remain unknown. The BIOS Consortium applies a functional genomics approach that integrates genome-wide genetic data with data on the epigenome and transcriptome to elucidate these mechanisms. Over 4000 samples from BBMRI-NL biobanks with in-depth information on disease phenotypes and GWAS data are being enriched with RNA-sequencing and genome-wide DNA methylation data. The same is true for samples with whole-genome sequencing data from GoNL. This unique data infrastructure provides a powerful platform to evaluate key questions in integrative omics from establishing comprehensive eQTL and meQTL catalogues to linking molecular pathways across omics levels to phenotypic outcomes.

  Study EGAS00001001077

• A Retrospective and Cross-Sectional Analysis of Patients Treated for SCID Since January 1, 1968

  Individuals with a past diagnosis of severe combined immune deficiency (including many cases of "leaky SCID", Omenn syndrome, and reticular dysgenesis) who have undergone blood and marrow transplant, gene therapy, or enzyme replacement in the past may be eligible for 6902. The purpose of 6902 is very similar to 6901, except 6902 is looking backwards at what has already been done in the past (compared to 6901 which is looking into the future). Over 800 patients with SCID are expected to be enrolled on 6902. This makes 6902 the largest study ever to describe outcomes for patients with SCID treated at many different hospitals around North America. One of the most important components of the 6902 study is the "cross sectional" study. Patients who have received their treatments (BMT, gene therapy, enzyme replacement) many years ago are asked to come back to the hospital where they were treated. During this visit, additional research blood work is drawn and information is gathered regarding long-term transplant outcomes such as infections, graft-versus-host disease, autoimmune diseases, and quality of life. This will allow PIDTC researchers to better understand long-term outcomes from procedures that occurred many years ago (sometimes over 30 years ago) - something that is not possible at the present time with 6901. This will help researchers to best design new treatments and clinical trials in the future for children with SCID.

  Study phs001326

• RNA-seq analysis of transcriptome variation with human ESC subclones

  Many studies over the past 10 years, culminating in the recent report of the International Stem Cell Initiative (ISCI, 2011) have shown that hPSC acquire genetic and epigenetic changes during their time in culture. Many of the genetic changes are non-random and recurrent, probably because they provide a selective growth advantage to the undifferentiated cells. Some are shared by embryonal carcinoma cells, the malignant counterparts of ES cells. The origins of these growth advantages are poorly understood, but may come from altered cell cycle dynamics, resistance to apoptosis or altered patterns of differentiation. Less is known about the nature and consequences of epigenetic changes, but it is likely that these similarly affect hPSC behaviour; e.g., enhanced expression of DLK1, an imprinted gene, is associated with altered hPSC growth (Enver et al 2005). Inevitably, these genetic and epigenetic changes will impact on our ability to use hPSC for regenerative medicine, either because malignant transformation of the undifferentiated cells or their differentiated derivatives to be used for transplantation compromises safety, or because they impede the function of those differentiated derivatives, or because they affect the efficiency with which the undifferentiated cells can be expanded and differentiated into desired cell types. Focusing initially upon the existing clinical grade hESC lines, later moving to iPSC, we will Consolidate and extend knowledge of the rate, type and functional impact of the genetic variations that occur during hPSC culture. We will use whole genome and exome sequencing as well as SNP arrays, together with clonal analysis and other cytogenetics techniques. Common changes will be compared with those found in the normal human population, at low frequency in the original cell population or observed during iPSC generation in the HIPSCI project currently based at the WTSI. These studies will provide a better understanding of the range of genetic changes that occur in hPSC beyond the CNVs already identified. In conjunction with cancer genome resources and expertise at WTSI, bioinformatic analyses of these hPSC data will allow us to assess potential impact on hPSC behaviour pertinent to applications in regenerative medicine, notably the likelihood that specific changes arising in undifferentiated PSC cultures may be associated with potential malignant transformation of differentiated progeny 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/ .

  Dataset EGAD00001004266

• PSCP_mutation analysis in hESCs

  Many studies over the past 10 years, culminating in the recent report of the International Stem Cell Initiative (ISCI, 2011) have shown that hPSC acquire genetic and epigenetic changes during their time in culture. Many of the genetic changes are non-random and recurrent, probably because they provide a selective growth advantage to the undifferentiated cells. Some are shared by embryonal carcinoma cells, the malignant counterparts of ES cells. The origins of these growth advantages are poorly understood, but may come from altered cell cycle dynamics, resistance to apoptosis or altered patterns of differentiation. Less is known about the nature and consequences of epigenetic changes, but it is likely that these similarly affect hPSC behaviour; e.g., enhanced expression of DLK1, an imprinted gene, is associated with altered hPSC growth (Enver et al 2005). Inevitably, these genetic and epigenetic changes will impact on our ability to use hPSC for regenerative medicine, either because malignant transformation of the undifferentiated cells or their differentiated derivatives to be used for transplantation compromises safety, or because they impede the function of those differentiated derivatives, or because they affect the efficiency with which the undifferentiated cells can be expanded and differentiated into desired cell types. Focusing initially upon the existing clinical grade hESC lines, later moving to iPSC, we will Consolidate and extend knowledge of the rate, type and functional impact of the genetic variations that occur during hPSC culture. We will use whole genome and exome sequencing as well as SNP arrays, together with clonal analysis and other cytogenetics techniques. Common changes will be compared with those found in the normal human population, at low frequency in the original cell population or observed during iPSC generation in the HIPSCI project currently based at the WTSI. These studies will provide a better understanding of the range of genetic changes that occur in hPSC beyond the CNVs already identified. In conjunction with cancer genome resources and expertise at WTSI, bioinformatic analyses of these hPSC data will allow us to assess potential impact on hPSC behaviour pertinent to applications in regenerative medicine, notably the likelihood that specific changes arising in undifferentiated PSC cultures may be associated with potential malignant transformation of differentiated progeny. This data is part of a pre-publication release. For information on the proper use of pre-publication data shred by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/

  Dataset EGAD00001002231

• PSCP_bisulphite analysis in hESCs

  Many studies over the past 10 years, culminating in the recent report of the International Stem Cell Initiative (ISCI, 2011) have shown that hPSC acquire genetic and epigenetic changes during their time in culture. Many of the genetic changes are non-random and recurrent, probably because they provide a selective growth advantage to the undifferentiated cells. Some are shared by embryonal carcinoma cells, the malignant counterparts of ES cells. The origins of these growth advantages are poorly understood, but may come from altered cell cycle dynamics, resistance to apoptosis or altered patterns of differentiation. Less is known about the nature and consequences of epigenetic changes, but it is likely that these similarly affect hPSC behaviour; e.g., enhanced expression of DLK1, an imprinted gene, is associated with altered hPSC growth (Enver et al 2005). Inevitably, these genetic and epigenetic changes will impact on our ability to use hPSC for regenerative medicine, either because malignant transformation of the undifferentiated cells or their differentiated derivatives to be used for transplantation compromises safety, or because they impede the function of those differentiated derivatives, or because they affect the efficiency with which the undifferentiated cells can be expanded and differentiated into desired cell types. Focusing initially upon the existing clinical grade hESC lines, later moving to iPSC, we will Consolidate and extend knowledge of the rate, type and functional impact of the genetic variations that occur during hPSC culture. We will use whole genome and exome sequencing as well as SNP arrays, together with clonal analysis and other cytogenetics techniques. Common changes will be compared with those found in the normal human population, at low frequency in the original cell population or observed during iPSC generation in the HIPSCI project currently based at the WTSI. These studies will provide a better understanding of the range of genetic changes that occur in hPSC beyond the CNVs already identified. In conjunction with cancer genome resources and expertise at WTSI, bioinformatic analyses of these hPSC data will allow us to assess potential impact on hPSC behaviour pertinent to applications in regenerative medicine, notably the likelihood that specific changes arising in undifferentiated PSC cultures may be associated with potential malignant transformation of differentiated progeny. 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/

  Dataset EGAD00001002235

• The epigenomic response of skeletal muscle in life-long high-level trained and untrained men and women after acute exercise

  To investigate the influence of lifelong exercise training on the response of skeletal muscle to a bout of acute exercise we generated targeted epigenomic data from long-term endurance (8 men) and strength (8 men) trained individuals and healthy age-matched untrained controls (8 men). Skeletal muscle biopsies were taken from M. vastus lateralis before, directly after, and 3hrs following acute exercise. Control subjects completed one bout of acute endurance exercise and one bout of acute resistance exercise, separated by 4-8 weeks, athletes completed one bout in their respective form of sports. All 96 samples were used for DNA extraction and targeted library construction using a custom Twist Biosciences panel and following EM-methylation tranformation were sequenced (2x150bp paired end) on the Illumina NovaSeq 6000.

  Dataset EGAD50000000512

• eMERGE Phase III Clinical Center at Partners HealthCare

  The Partners HealthCare Biobank is a large research data and sample repository working within the framework of Partners Personalized Medicine. It provides researchers access to high quality, consented samples to help foster research, advance understanding of the causes of common diseases, and advance the practice of medicine. The Partners Biobank provides banked samples (plasma, serum and DNA) collected from consented patients. These samples are available for distribution to Partners HealthCare investigators with appropriate approval from the Partners Institutional Review board (IRB). They are linked to clinical data that originates in the Electronic Medical Record (EMR), as well as additional health information collected in a self-reported survey. The Partners Biobank will be genotyping 25,000 subjects with the Illumina Multiethnic Beadchip 1.6 million SNPs with exome and custom content (> 60,000 LoFs). Of the participants genotyped so far, 4929 of 4962 (99.3%) individuals have genotype data that passed the default quality thresholds for the Infinium array (call rate >= 0.99). We are submitting the genotype data to dbGaP for 4929 subjects with 12 phenotypes (based on icd9 codes). We will do annual releases until we reach the full 25,000 genotyped subjects.

  Study phs000944

• Barcoding reveals complex clonal dynamics of de novo transformed human mammary cells

  Most human breast cancers have already diversified genomically when they first become clinically evident, by which time extensive heterogeneous histopathologies, transcriptomes and growth patterns are also apparent. Accordingly, important initial events and the cellular context in which they occur have been difficult to characterize. Using DNA barcoding, we now demonstrate the high efficiency with which both purified basal and luminal cells isolated directly from normal adult human mammary tissue can be rapidly transformed by a single oncogene (KRASG12D) resulting in the production within 8 weeks in vivo of serially transplantable, polyclonal, invasive ductal carcinomas that are phenotypically heterogeneous and transcriptionally distinct from the initial cells transduced. Barcoding also revealed a consistent dramatic change in the clonal content of passaged tumours. This system thus provides a powerful new platform for examining early events in the genesis, evolution and treatment response of malignant human mammary cells generated using defined mutations.

  Study EGAS00001001310