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• Comprehensive Analysis of Structural Variants in Breast Cancer Genomes Using Single Molecule Sequencing

  This study used the SKBR3 breast cell line and tumor/normal organoids derived from breast tissue to explore the utility of long read sequencing for detecting structural variants in complex samples. Three technologies were used to characterize the samples: Illumina/10X, Pacific Biosciences, and Oxford Nanopore. Methylation results were derived from the Oxford Nanopore data. It is hoped that this resource will better help researchers better understand the utility of long read sequencing in cancer samples.

  Study phs002210

• Egypt_Genome_Project___high_coverage_whole_genome_sequencing

  All humans outside Africa are descendants of the same single exit, usually dated at 50-70 thousand years ago. However, the route taken out of Africa is still debated. The two main candidates are a northern route via Egypt and the Levant, or a southern route via Ethiopia and the Arabian Peninsula. We are generating genetic data to evaluate these two possibilities. In this study we propose to generate high-coverage sequencing data for 3 Egyptian samples.

  Study EGAS00001000482

• Multi-omics analysis of primary glioblastoma cell-lines shows recapitulation of pivotal molecular features of parental tumors

  Glioblastoma (GBM) is the deadliest primary brain cancer in adults. Emerging innovative therapies hold promise for personalized cancer treatment. Improving therapeutic options depends on research relying on relevant preclinical models. In this line we have established in the setting of the GlioTeX project (GBM and experimental therapeutics), a GBM-patient derived cell line library (GBM-PDCL). Multi-OMIC approach was used to determine the molecular landscape of PDCL and the extent to which they represent GBM tumors.

  Study EGAS00001001871

• Functional Significance of Prostate Cancer Risk-SNPs

  Prostate Cancer (PrCa), the most frequently diagnosed solid tumor in men in the U.S., results in ~192,000 new cases and ~27,000 deaths per year. Although the variation of PrCa incidence is likely to be the result of several factors, there is a large body of literature that strongly implicates a genetic etiology. Genome-wide association studies (GWAS) have emerged as the most widely used contemporary approach to identify genetic variants (in particular SNPs) that are associated with increased risk of human disease. For PrCa, at least five GWAS have now been performed yielding a substantial number of well-validated SNPs that are associated with an increased risk of PrCa, and that number continues to grow. A significant problem for many of the PrCa risk-SNPs identified so far, however, is that they do not lie within or near a known gene and they have no obvious functional properties. These findings suggest that many (if not most) of these risk-SNPs will be located in regulatory regions that control gene expression rather than in coding regions that may directly affect protein function. Therefore, in order to define the functional role of currently known risk-SNPs, the target genes must first be identified. A promising strategy to address this problem involves the use of expression quantitative trait loci (eQTL) analysis. Unfortunately, most of the publically available SNP-Transcript eQTL datasets utilize lymphoblastoid cells with only a handful using tissue from target organs. Although useful, these datasets alone are unlikely to be sufficient. Recent studies have demonstrated that gene expression and gene regulation occur in both a tissue-specific and tissue independent fashion and suggest that a complete repertoire of regulatory SNPs can only be uncovered in the context of cell type specificity. To date, such a tissue-specific dataset for normal prostate tissue does not exist. In this study, we have constructed a normal prostate tissue specific eQTL data set.

  Study phs000985

• Hereditary Cancer Diagnostics with I2HCP gene panel

  Germline blood DNA sequencing data generated in routine diagnostics of hereditary cancer using the I2HCP gene panel (~135 genes). There are 130 samples sequenced in a MiSeq machine and 108 sequenced in a HiSeq machine. There is a partial overlap between those two sets, meaning that some samples were sequenced in both machines. There is a strong enrichment in samples with copy-number variants (CNV), both single- and multi-exon, since this dataset was compiled for a benchmarking effort of CNV calling tools for genetic diagnostics.

  Dataset EGAD00001006171

• Genomic characterization of co-existing biliary tract intraepithelial neoplasia and carcinoma lesions reveals distinct evolutionary paths of gallbladder cancer

  Gallbladder carcinoma is the most common cancer of the biliary tract with dismal survival largely due to delayed diagnosis. Biliary tract intraepithelial neoplasia (BilIN) is the common benign tumor that is suspected to be precancerous lesions. However, the genetic and evolutionary relationships between BilIN and carcinoma remain unclear. Here we performed whole-exome sequencing of coexisting low-grade BilIN (adenoma), high-grade BilIN, and carcinoma lesions, and normal tissues from the same patients.

  Dataset EGAD00001007792

• Single Cell Transcriptomics of peripheral immune cells pre- and post-Immune Checkpoint Blockade

  This is raw sequencing data, analysis of which is presented in the paper "Sensitivity to Immune Checkpoint Blockade and Progression-Free Survival is associated with baseline CD8+ T cell clone size and cytotoxicity", DOI: https://doi.org/10.1101/2020.11.15.383786

  Dataset EGAD00001007942

• Emergence of oncofetal plasticity is ubiquitous in early colorectal cancers

  Metastasis formation is classically considered a late-stage event in colorectal cancer (CRC) evolution. Yet, the time and patterning by which metastatic competence is acquired remain poorly understood. Here, we show that metastasis-associated oncofetal cell states already emerge at the earliest stages of CRC, concurrent with invasive front formation. However, while necessary for metastasis, we detect them ubiquitously among early non-metastatic cancers, highlighting additional bottlenecks like immune evasion. To understand how oncofetal cells first emerge, we generated multiregional organoid models that reflect successive tumor progression stages within individual early-stage CRCs. Whole-genome sequencing and growth factor-dependency assays exclude tumor cell-intrinsic acquired traits. In contrast, single-cell spatial atlases of the tumor-microenvironment before and after malignant transformation revealed stereotypic patterning of fibroblast subtypes resembling normal tissue architecture, resulting in distinct regional microenvironments. At the onset of malignant growth into the submucosa, the first cancer-associated fibroblasts (CAFs) to appear strongly resemble submucosal trophocytes and colocalize with oncofetal cell states at invasive fronts. Functionally, fibroblast-organoid co-cultures confirm that these trophocyte-like CAFs induce plastic transitioning to oncofetal states. Thus, interactions between tumor and submucosal fibroblasts directly following malignant transformation dictate the timing and location at which oncofetal plasticity first occurs during CRC progression.

  Study EGAS50000001532

• Pharmacogenomics of Rheumatoid Arthritis Therapy

  Rheumatoid arthritis (RA) is the most common autoimmune inflammatory arthritis worldwide and affects 1.3 million adults in the USA. It has previously been studied using phenotype algorithms to identify electronic health records (EHR) case cohorts. Early genetic studies of EHR-linked cohorts of RA patients have been replicated in known associations. Further development of collections of EHR-linked cohorts for RA and other phenotypes may enable not only enhanced understanding of disease risks but also the investigation of outcomes and treatment responses.

  Study phs000983

• Aneurysmal Subarachnoid Hemorrhage patients with or without vasospasm

  Cerebellar vasospasm is a severe complication of aneurysmal subarachnoid hemorrhage (aSAH) occurring for 30% of aSAH patients. To date, no biomarker of vasospasm occurrence exists and thus all aSAH patients undergo a preventive and dangerous treatment. In this study, we explored the miRNome of aSAH patients to detect potential expression differences between the patients developing a vasospasm (VSP+) or not (VSP-). The shared data include raw and normalized count miRNA data in aneurysmal subarachnoid hemorrhage patients with or without vasospasm.

  Study EGAS00001003092