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• Genome_wide_CRISPR_Cas9_screening_of_Human_Organoids

  In this study we will exploit the bacterial clustered regularly interspaced short palindromic repeats (CRISPR) system to perform a genome-wide single-guide RNA (sgRNA) library to screen for genes required for proliferation and survival in human organoids.

  Study EGAS00001001932

• A fast, affordable and minimally-invasive diagnostic test for Cancer of Unknown Primary (CUP) using DNA methylation profiling

  CUP diagnosis on FFPE tissue and liquid biopsies (blood, pleural and peritoneal effusions) using cfRRBS (cell-free reduced representation bisulfite sequencing), a technique that allows for identification of the methylation profile starting from minimal amounts of highly fragmented DNA.

  Study EGAS50000000257

• A Pilot Trial of Complement Inhibition Using Eculizumab to Overcome Platelet Transfusion Refractoriness in HLA Allo-Immunized Patients

  Platelet transfusion can be a life-saving procedure in preventing or treating serious bleeding in patients who have low and/or dysfunctional platelets. Heavily transfused patients frequently develop human leukocyte antigen (HLA) allo-immunization resulting in platelet transfusion refractoriness and a high risk for life-threatening thrombocytopenia. Data suggest complement activation leading to the destruction of platelets bound by HLA allo-antibodies may play a pathophysiologic role in platelet refractoriness. We conducted a pilot trial to investigate the use of eculizumab to treat platelet transfusion refractoriness in allo-immunized patients with severe thrombocytopenia. We hypothesized that when we treated patients having platelet refractoriness with eculizumab, platelet counts would increase to higher numbers after platelet transfusions, decreasing the risk of bleeding complications associated with having a low platelet count. The response of the treatment was assessed by the corrected platelet count increment (CCI) 10 - 60 min and 18 - 24 h post transfusion, and any requirement for subsequent platelet transfusions following eculizumab. Reference 1 (PMID: 32086819) contains the main results for this trial.

  Study phs003212

• Whole Exome Sequencing in Familial Parkinson Disease

  We have an ongoing study that has recruited families having at least a sibling pair with Parkinson disease (PD). Families have been screened for mutations in known PD causative genes (LRRK2, parkin, etc). Following review of families without a causative mutation, we selected families for whole exome sequencing that had the strongest history of PD and with the most definitive diagnosis. All families have at least 3 affected family members who were evaluated as part of this study. Only affected family members were included for whole exome sequencing.

  Study phs000376

• Maintenance of Genome Sequence Integrity in Long- and Short-lived Rodent Species

  In this study, we compared somatic mutation frequencies and spectra of bleomycin-treated and control fibroblasts of 5 species, i.e., mouse, guinea pig, blind mole-rat, naked mole-rat and humans, by using single-cell whole-genome sequencing. Sequencing data of the human cells are deposited here in the dbGaP. Sequencing data of the rodent cells are in the SRA database, under accession ID: PRJNA753541.

  Study phs002610

• Genomic characterization of germ-cell tumors in childhood

  Germ cell tumors (GCTs) are rare neoplasms affecting approximately 3.5% of pediatric patients, with diverse histological subtypes. Despite their low mutational burden, prevalent alterations in KIT, KRAS, and NRAS genes are observed, but molecular understanding of pediatric GCTs lags behind adult counterparts. We aimed to elucidate the genomic landscape of 16 pediatric GCT patients via whole exome sequencing (WES), which revealed somatic alterations resembling those in adult GCTs.

  Study EGAS50000000619

• WTCCC2 Pharmacogenomic Response to Statins study

  A WTCCC2 project genome-wide study for pharmacogenomic response to statins (PR) in individuals from Scotland.

  Study EGAS00000000121

• Metagenome shotgun sequencing of the Inflammatory Bowel Disease

  We performed a comprehensive metagenome-wide association study for inflammatory bowel disease by utilizing whole-genome shotgun sequencing.

  Study JGAS000530

• WTCCC2 BO (Barretts oesophagus) samples

  A WTCCC2 project genome-wide case-control association study for Barretts oesophagus in individuals from the UK.

  Study EGAS00001000628

• A method for multiplexed full-length single-molecule sequencing of the human mitochondrial genome

  A method for multiplexed full-length single-molecule sequencing of the human mitochondrial genome - cell line data

  Dataset EGAD00001008963

• Somatic variants in 344 colorectal cancer samples

  The dataset contains somatic variants in 344 colorectal cancer samples. Variants are called with Mutect2 (GRCh38). Important: VCF-files include also variants, which have been annotated as "str_contraction" and "panel_of_normals". Please, use only "PASS" variants in studies, which are not microsatellite repeat related. Samples are sequenced with Novaseq 6000, HiSeq 2000, and HiSeq X Ten instruments (average coverage depth ~30+). The dataset consists of 257 MSS, 58 MSI, 25 MSS IBD, and 4 POLE mutant CRCs.

  Dataset EGAD00001006572

• Evaluation of the Efficacy and Safety of a Clinical Grade Human Induced Pluripotent Stem Cell-Derived Cardiomyocyte Patch: A Pre-Clinical Study

  Cardiomyocyte-derived induced pluripotent stem cells (iPSCs) may represent a promising therapeutic strategy for severely damaged myocardium. This study aimed to assess the efficacy and safety of clinical grade human iPSC-derived cardiomyocyte (hiPSC-CM) patches and conduct a pre-clinical proof-of-concept analysis.

  Study EGAS50000000189

• Germline genome sequencing samples from the Hereditary Cancer Syndromes (ICCon) Cancer Flagship

  A prospective study of individuals with suspicion of a hereditary cancer syndrome for whom previous clinical targeted genetic testing was either not informative or was not available. To identify pathogenic disease-causing variants explaining participant presentation, germline whole-genome sequencing and a comprehensive cancer virtual gene panel analysis were undertaken.

  Study EGAS00001007045

• Whole Exome Sequencing for Colorectal Cancer

  This project was designed to use next generation sequencing technology to screen the protein coding regions of the genome for low frequency variants in a panel of high-risk colorectal adenocarcinoma cases. Blood and cell-line DNA for colorectal cancer patients and a subset of quality control samples that had existing whole exome sequence data were analyzed using Illumina HiSeq sequencers. Samples from this project were from participants in the Women's Health Initiative (WHI) and the Diet, Activity, and Lifestyle Study (DALS).

  Study phs000410

• Investigation of different library preparation and tissue of origin deconvolution methods for urine and plasma cfDNA methylome analysis

  In this study, a single- and a double-stranded library preparation approach was evaluated with respect to their technical biases when applied on cfDNA from plasma and urine. This study thus outlines potential limitations of double-stranded library preparation for methylation analysis of cfDNA especially for urinary cfDNA. While the double-stranded method allows jagged end analysis in addition to TOO analysis, it leads to significant methylation bias in urinary cfDNA, which single-stranded methods can overcome.

  Study EGAS00001007314

• Single-cell study of 14 childhood medulloblastoma patients

  Medulloblastoma intra-tumoural genetic heterogeneity and clonal evolution, and their role in disease pathogenesis and clinical behaviour, are poorly understood. We used single-cell whole-genome sequencing (sc-WGS) to reconstruct the natural history and temporal evolution of 14 medulloblastomas, representing its major clinico-molecular sub-classes. We identified wholly-clonal tumours which displayed single-clone expansion (i.e. linear evolution); all were observed in favourable-outcome sub-classes (i.e. MBWNT and infant MBSHH). In contrast, remaining tumours harboured sub-clonal structures which displayed punctuated or gradual trajectories; highest-risk sub-classes, typically characterised by MYC-amplification (MBGroup3) or TP53-mutation (MBSHH), and linked to genomic instability and LCA pathology, were most clonally-diverse. Clinically-adopted biomarkers were typically early-clonal/initiating events, representing exploitable targets for early-disease detection; in analyses of spatially-distinct tumour regions, a single biopsy was sufficient to assess their status. sc-WGS revealed events not previously appreciated in bulk tumour analysis, which arose later and/or sub-clonally and more commonly displayed spatial diversity; their clinical significance and role in disease evolution post-diagnosis now require establishment. In summary, our findings reveal diverse modes of tumour initiation and clonal evolution in the major medulloblastoma sub-classes, highlighting their pathogenic relevance and clinical potential.

  Dataset EGAD00001009057

• Study on rectal mucus sampling for colorectal cancer diagnostics

  DAC for a study on rectal mucus sampling for colorectal cancer diagnostics

  Dac EGAC50000000643

• Evaluation_of_size_selection_on_cancer_specific_sequencing_libraries

  A couple of previously characterized and sequenced libraries will be repeated using a couple of differing size selection criteria and skim sequenced using an Illumina HiSeq. The resulting sequence will be analyzed to determine the optimal DNA library size for our specific downstream analysis.

  Study EGAS00001000293

• Improved Sezary cell detection and novel insights into immunophenotypic and molecular heterogeneity in Sézary syndrome

  We performed a prospective investigation in Sézary syndrome by the application of a standardized multiparameter flow cytometry, FACS-cell sorting, and RNA-sequencing for an in-depth immunophenotypic and transcriptional profiling of Sézary cells.

  Study EGAS00001005229

• The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Genetics of Genetic Epidemiology of Metabolic Syndrome in an Island Population

  The major objective of this study was to conduct a systematic genetic study of metabolic traits involved in metabolic syndrome through collection and analysis of epidemiological, demographic, environmental, and relevant biological and clinical data from a relatively isolated island population of the eastern Adriatic coast of Croatia. The population was chosen for the following reasons: 1) in spite of practicing a largely traditional life style and dietary habits, high rates of obesity, arterial hypertension, dyslipidemia and related metabolic abnormalities were found in previous studies; 2) the population was established by a relatively small number of founders, predominantly of Slavic descent from the mainland during 15th to 18th century AD, a genetically homogeneous population living in a homogeneous environment; 3) sharing a common European ancestry, a relevant population for study in the context of the general US population; 4) Croatian collaborators have been conducting anthropological and genetic studies in these communities for over three decades. There were two major aims of the study: 1) to recruit ~1200 adult participants and collect blood samples together with demographic, anthropometric, environmental and clinical data from the island of Hvar; to perform biochemical tests to measure glucose, insulin, uric acid and lipid levels; 2) conduct a genome-wide association analysis of metabolic traits and phenotypes using genome-wide SNP arrays (Affymetrix Genome-Wide Human SNP Array 5.0).

  Study phs000737

• Mutational landscape and patterns of clonal evolution in relapsed pediatric acute lymphoblastic leukemia

  Relapse of acute lymphoblastic leukemia (ALL) remains a leading cause of childhood death. Prior studies have shown clonal mutations at relapse often arise from relapse-fated subclones that exist at diagnosis. However, the genomic landscape, evolutionary trajectories and mutational mechanisms driving relapse are incompletely understood. In an analysis of 92 cases of relapsed childhood ALL, incorporating multimodal DNA and RNA sequencing, deep digital mutational tracking and xenografting to formally define clonal structure, we identify 50 significant targets of mutation with distinct patterns of mutational acquisition or enrichment. CREBBP, NOTCH1, and Ras signaling mutations rose from diagnosis subclones, whereas variants in NCOR2, USH2A and NT5C2 were exclusively observed at relapse. Evolutionary modeling and xenografting demonstrated that relapse-fated clones were minor (50%), major (27%) or multiclonal (18%) at diagnosis. Putative second leukemias, including those with lineage shift, were shown to most commonly represent relapse from an ancestral clone rather than a truly independent second primary leukemia. A subset of leukemias prone to repeated relapse exhibited hypermutation driven by at least three distinct mutational processes, resulting in heightened neoepitope burden and potential vulnerability to immunotherapy. Finally, relapse-driving sequence mutations were detected prior to relapse using deep digital PCR at levels comparable to orthogonal approaches to monitor levels of measurable residual disease. These results provide a genomic framework to anticipate and circumvent relapse by earlier detection and targeting of relapse-fated clones.

  Study EGAS00001003975

• ESGI___Whole_Genome_Sequencing_of_samples_from_the_Cilentogen_isolates

  Deep whole genome sequencing of sampels from the Cilento isolates. The samples are sequenced using the Illumina HiSeq X Ten system.

  Study EGAS00001001116

• ESGI___Whole_Genome_Sequencing_of_samples_from_the_Croatian_isolated_populations_

  Whole genome sequencing of sampels from isolated populations from Croatia. The samples are sequenced using the Illumina HiSeq X Ten system.

  Study EGAS00001001119

• RNA sequencing of undifferentiated sarcomas

  mRNA sequencing of 50 undifferentiated sarcoma tumour samples and 5 adjacent muscle tissue samples. BAM files are provided, with metadata specifying which samples are tumour/normal.

  Dataset EGAD00001004439

• ExomeSeq Neoantigen Immunogenicity Landscapes

  Immune checkpoint blockade (ICB) therapy is a cornerstone of oncologic treatment for patients with advanced stage non-small cell lung cancer (NSCLC) and other malignancies. Neoantigen immunoediting drives ICB efficacy, yet the fundamental physiochemical characteristics of neoantigens and how neoantigen immunogenicity shapes treatment response remains poorly understood. To help address these questions, a prospective clinical trial of NSCLC patients treated with nivolumab was conducted. We assessed genomic alterations in tumors from 58 patients and performed large-scale neoepitope immunogenicity analyses, before and during treatment (CheckMate153, CA209-153). Tumors were analyzed by whole-exome and transcriptome sequencing. In responding patients, loss of mutation and neoantigen burden early during therapy associated with clinical benefit. We evaluated the immunogenicity of 1,453 candidate neoantigens and identified 502 neopeptides that bound to MHC I and 196 neopeptides that were immunogenically recognized by T cells in the setting of nivolumab treatment. These T cell reactive neoantigens were differentially present in clonal populations that underwent distinctive evolutionary trajectories across responders and nonresponders. Mapping these neoantigens to tumor clonal dynamics and clinical response revealed strong selection against immunogenic neoantigen harboring clones compared to non-immunogenic clones. Using this large collection of neoantigens, we identified position specific amino acid features related to immunogenicity, which we used to develop and validate an immunogenicity score. Changes in the genomic and neoantigen immunogenicity landscapes were accompanied by temporal changes in the tumor microenvironment. Nivolumab-induced microenvironmental evolution in NSCLC shared some similarities with that in melanoma, yet critical differences in immunologic programs were apparent from comparative network analysis between tumor types. This study provides unprecedented molecular portraits of the neoantigen landscapes underlying nivolumab’s mechanism of action.

  Study EGAS00001007508