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• The_effects_of_chemotherapy_and_radiation_in_human_oesophageal_epithelium__low_input

  Human oesophagus is a patchwork of competing mutant clones. We wish to see how this patchwork is altered under the extreme selection pressures of chemotherapy and radiotherapy both individually and combined. We will sequence 0.25mm diameter punch biopsies from patients who have undergone chemotherapy and radiotherapy to assess how the mutational landscape has changed.

  Study EGAS00001007416

• The_effects_of_chemotherapy_and_radiation_in_human_oesophageal_epithelium

  Human oesophagus is a patchwork of competing mutant clones. We wish to see how this patchwork is altered under the extreme selection pressures of chemotherapy and radiotherapy both individually and combined. We will sequence 2mm2 contiguous pieces of oesophageal epithelium from patients who have undergone chemotherapy and radiotherapy to assess how the mutational landscape has changed.

  Study EGAS00001007417

• RNA seq on 19 samples of Radiation-Induced Meningiomas

  Purpose: Majority of pediatric cancers require the irradiation of the central nervous system (CNS), and as more patients survive into adulthood from improved oncological therapy the sequelae of brain radiation are increasing in prevalence. Radiation-induced meningiomas (RIMs), one such secondary effect, demonstrate a clinically more aggressive behaviour than sporadic meningiomas (SMs). We aimed to describe the genomic mutational landscape of RIMs.Methods: We analyzed a principal cohort of 18 RIMs, with 31 RIMs overall, from patients who received childhood radiation therapy and 30 SMs, as a comparator population. We performed a multiplatform integrative genomic analysis; including methylation, whole exome and RNA sequencing. Results: RIMs exhibited a five-fold increase in copy number alterations, commonly the loss of chromosome 1p (17/18 RIMs) and 22q (17/18 RIMs), which was significantly more than observed in sporadic meningiomas. Furthermore, RNA sequencing data revealed an NF2 gene fusion event in 35.3% of RIMs. In all 6 cases, there was a complete NF2 exon spliced into a complete exon of a reciprocal gene, suggesting that the breakpoints of genomic rearrangement are intronic. All tumours with the NF2 fusion also possessed monosomy of chromosome 22q, rendering the cells with homozygous disruption of NF2. Clinically, RIMs with the NF2 fusion exhibited ill-defined borders and a tendency to develop in anatomic frontal location. Also, targeted sequencing panel confirmed that RIMs had fewer nonsynonymous NF2 mutations (6.5% vs. 30% in SM) and absence of mutations in TRAF7, SMO, KLF4, PIK3CA and AKT1, genes traditionally involved in SMs.Conclusion: Our study demonstrates that RIMs have distinct genomic drivers of oncogenesis as compared to SMs, specifically NF2 inactivation through fusion event. Radiation therapy possibly triggers genomic structural rearrangements through error-prone repair of double-stranded DNA breaks.

  Study EGAS00001002318

• Identifying New Genetic Subtypes in Follicular Lymphoma

  Follicular lymphoma (FL) exhibits considerable variability in biological features and clinical trajectories across patients. To dissect the diversity of FL, we utilized a Bernoulli mixture model to identify genetic subtypes in 713 pre-treatment tumor tissue samples. Our analysis revealed the existence of five subtypes with unique genetic profiles that correlated with clinicopathological characteristics. The clusters were enriched in specific mutations as follows: CS (CREBBP and STAT6), TT (TNFAIP3 and TP53), GM (GNA13 and MEF2B), Q (quiescent, for low mutation burden), and AR (mutations of mTOR pathway-related genes). The subtype Q was enriched for patients with stage I disease and was associated with a lower proliferative history compared to the other subtypes. The AR subtype was unique in its enrichment for IgM-expressing FL cases and was associated with advanced-stage and more than 4 nodal sites. The existence of subtypes was validated in an independent cohort of 418 samples from the GALLIUM trial. Notably, patients assigned to the TT subtype consistently experienced inferior progression-free survival when treated with immunochemotherapy. Collectively, our findings offer insight into core pathways distinctly linked with each FL cluster and are expected to be informative in the era of targeted therapies.

  Study EGAS50000000435

• CRUK-ICGC Prostate Cancer Group Study

  Prostate cancer somatic genomic sequencing data generated from 2011 onwards under auspices of the International Cancer Genome Consortium Prostate Cancer UK consortium (CRUK-ICGC Prostate Group), co-led by Colin Cooper and Ros Eeles, with other Principal Investigators (Brewer, Neal, Bova, McDermott, Wedge, Lynch, Massie, and Foster) and others as listed in study publications. Funded by Cancer Research UK and other funders as listed in study publications. Contents and publications related to each dataset are described with each dataset (EGAD) entry. Our study was funded with the ambition of collecting Whole Genome DNA sequence data from 250 prostate cancers, with matching transcriptome and methylome data. The original aims of the project were: 1.To understand the significance of multifocal prostate cancer. 2.To understand the clinical heterogeneity of prostate cancer to devise markers for predicting outcome and for drug targeting. 3.To understand the molecular basis of development and spread of castration-resistant and metastatic disease 4.To understand the aetiology of prostate cancer particularly the large variation in incidences that occur in different populations and ethnic groups. Please see https://doi.org/10.5281/zenodo.4022439 for links between sample IDs reported in literature and EGA IDs.

  Study EGAS00001000262

• NHLBI TOPMed: Pharmacogenomics of Hydroxyurea in Sickle Cell Disease (PharmHU)

  Sickle cell disease (SCD) is characterized by the presence of sickle hemoglobin (HbS) within circulating erythrocytes resulting in hemolytic anemia, vascular occlusion, and end organ damage due to alterations in the shape and deformability of the cell membrane. The disease is inherited in an autosomal recessive pattern, and is most commonly caused by a single nucleotide substitution in the hemoglobin subunit beta (HBB) gene located on chromosome 11. Participants in this study include children with SCD treated with hydroxyurea to pharmacologically increase fetal hemoglobin (HbF) levels and reduce disease severity. Therefore, the primary phenotype of interest in this study is the change in HbF levels in response to hydroxyurea treatment. Genetic factors have been shown to influence inter-individual variation in drug response, and identification of novel genes and variants associated with clinical outcomes in SCD will be achieved through collaboration between Baylor College of Medicine, Augusta University, Columbia University Medical Center, Emory University School of Medicine and Children's Healthcare of Atlanta, and St. Jude Children's Research Hospital. The NHLBI TOPMed Program is designed to generate scientific resources to enhance understanding of fundamental biological processes that underlie heart, lung, blood and sleep disorders (HLBS). It is part of a broader Precision Medicine Initiative, which aims to provide disease treatments that are tailored to an individual's unique genes and environment.

  Study phs001466

• NHLBI TOPMed: Pediatric Cardiac Genomics Consortium (PCGC)'s Congenital Heart Disease Biobank

  The Pediatric Cardiovascular Genetics Consortium (PCGC) proposes to define genetic causes for congenital heart defects (CHD) as part of the TOPMed Program are the most common form of heart disease in childhood and are also the most prevalent form of birth defects, occurring in 2-3% of live births. The PCGC has recruited and clinically characterized = 10,000 CHD probands and parents (CHD trios). From whole exome sequencing (WES) of >2800 CHD trios, we identified a substantial enrichment of damaging de novo mutations in genes important for cardiogenesis, particularly implicating histone modifier enzyme gene defects. Analysis of whole genome sequencing (WGS) of 350 probands with CHD unexplained by WES and their parents preliminarily implicated de novo mutations in enhancers of genes previously shown to cause CHD in mouse knock out models. Sequencing of RNA (RNAseq) from discarded cardiac tissues from CHD probands has revealed likely causal allele-specific expression (ASE) as well as biallelic loss of expression (LOE). We have also discovered de novo epimutations, differentially methylated regions (DMRs), some with underlying de novo DNA variation, that are detectable in peripheral blood leukocytes and appear to underlie 10% of CHD. Of note, these assorted 'omic' approaches have enabled one another, both for attributing causality and assessing functional impact. Based on these extensive preliminary data, we hypothesize that PCGC probands with uninformative exomic analyses (WES-negative) harbor de novo genetic and/or epigenetic mutations in critical regulatory elements that participate in developmental expression of cardiac genes. To identify these etiologies, we propose analyses of WGS in 1000 WES-negative CHD trios, prioritizing those with probands with banked CHD tissues (n=78), one damaging variant in a recessive CHD gene, and older fathers (age>45). We also request WGS for 230 probands, for whom we have cardiac tissues but not parental DNAs. We request RNAseq for 308 cardiac tissues. For DNA methylation, which TOPMed will offer through the Illumina 850k array platform, we are requesting analysis of DNAs from peripheral blood leukocytes for all probands for whom WGS will be performed (1000 from trios, 230 singletons) as well as DNAs from cardiac tissues (n=308) to pair with the WGS, RNAseq and blood DNA methylation data. We will use existing resources and capabilities of the PCGC to confirm relevant mutations and those of its companion consortium in the Bench to Bassinet Program, the Cardiovascular Development Consortium, to inform analyses of non-coding mutations as well as to perform confirmatory functional genomics studies using cell and animal models. We expect that the studies resulting from data generated through TOPMed will provide novel insights into the molecular basis for CHD and fundamental knowledge about genes and pathways involved in cardiac development. Aside from being relevant to CHD, we anticipate that our findings will inform the understanding of later-onset cardiovascular diseases, including some arising in adulthood.

  Study phs001735

• Osteosarcoma_X10

  This is a continuation of the osteosarcoma work we have undertaken.

  Study EGAS00001002167

• Whole genome sequencing of neuroendocrine tumors of the small intestine

  This dataset contains whole genome sequences for 13 patients with neuroendocrine (unique/multiple) tumor(s) of the small intestine. There are in total 25 tumor and 12 matched normal genomes. Libraries were prepared using a Illumina DNA PCR Free kit following the manufacturer’s recommendations and sequencing was performed on Illumina Novaseq6000 machine with a 2x151bp paired-end fashion. It contains data for : - 1 patient with 4 tumors and 1 matched normal - 1 patient with 3 tumors and 1 matched normal - 1 patient with 2 tumors, 1 liver metastasis and 1 matched normal - 2 patients with 1 tumor, 1 mesenteric nodule and 1 matched normal - 7 patients with 1 tumor and 1 matched normal - 1 patient with 3 tumors and 1 mesenteric nodule

  Dataset EGAD50000000907

• Targeted Sequencing of 52 Genes for Severe COVID-19

  This dataset comprises targeted sequencing data of 52 genes previously implicated in severe COVID-19 outcomes. The study includes samples from 764 individuals with severe COVID-19 and 3,939 population-based controls from the GCAT cohort (Spain). Molecular Inversion Probes (MIPs) were utilized for cost-effective and precise sequencing of the selected genes. The targeted genes include: Inflammasome/IL-1/TNF Pathway: NLRP3, CASP1, CASP8, IL1B, TNF, RIPK1, RIPK3, MYD88, TNFRSF13B SARS-CoV-2 Entry/Replication: ACE2, TMPRSS2, FURIN, SLC6A20, DDX1, DDX58, TLR4, FYCO1, CTSB, CTSL, ADAM17 Complement System: MBL2, CFH, CFI, CFB, ADAM10, CD46 Interferon Signaling: TLR3, IFIH1, IFITM3, TBK1, TLR7, IL10RB, IFNAR1, IFNAR2, SIGLEC1, MYD88, IFNGR1 Chemokine Receptor Signaling: CCR1, CCR3, CCR2, CCR9, IL8, CXCL3, CXCL10, CXCR6, XCR1, CCL2, CCL20 Immunodeficiency Genes: CASP8, CD46, CFB, CFH, CFI, IFNAR1, IFNAR2, IFNGR1, IFIH1, MYD88, NLRP3, RIPK1, TBK1, TLR3, TLR7

  Dataset EGAD50000001378