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• Expression quantitative trait loci analysis using human immune cells in a Japanese population

  Recent evidence suggests that a substantial portion of complex disease risk alleles modify gene expression in a cell-specific manner. Therefore, it is reasonable to expect that cell-specific expression quantitative trait loci (eQTL) analysis can identify the candidate causal mechanisms of complex diseases (an eQTL is a variant whose polymorphism affects gene expression). We fractionated peripheral blood from 105 healthy Japanese volunteers into five major immune cell subsets (CD4+ T cells, CD8+ T cells, B cells, NK cells, and monocytes). We quantified gene and exon expression by RNA sequencing, and tested associations with neighboring common variants (MAF ? 0.05).

  Study JGAS000085

• genome-wide cfDNA methylation analysis

  To characterise cfDNA methylome in metastatic prostate cancer

  Study EGAS00001003958

• Anaplastic Oligodendroglioma AO Exome-seq data

  Anaplastic oligodendrogliomas (AOs) are rare primary brain tumors which are generally incurable, with heterogeneous prognosis and few treatment targets identified. Most oligodendrogliomas have chromosome 1p/19q co-deletion and IDH mutation. We analyzed 51 AOs by whole-exome sequencing, identifying previously reported frequent somatic mutations in CIC and FUBP1. We also identified recurrent mutations in TCF12 and in an additional series of 83 AO. Overall 7.5% of AO are mutated for TCF12, which encodes an oligodendrocyte-related transcription factor. 80% of TCF12 mutations identified were in either the bHLH domain, which is important for TCF12 function as a transcription factor, or were frame shift mutations leading to TCF12 truncated for this domain. We show that these mutations compromise TCF12 transcriptional activity and are associated with a more aggressive tumor type. Our analysis provides further insights into the unique and shared pathways driving AO.

  Dataset EGAD00001001452

• NOUS-209 off-the-shelf immunotherapy has the potential to hit primary and metachronous colorectal and urothelial cancer in Lynch syndrome

  Lynch syndrome is an inherited cancer predisposition characterized by the development of microsatellite-instable tumors, most commonly colorectal and urothelial cancers. These cancers harbor recurrent frameshift mutations (FSMs) that generate shared neoantigens, creating opportunities for targeted immunotherapy. NOUS-209 is a viral-vector–based cancer vaccine encoding 209 of these shared neoantigen peptides. This study investigated the presence and evolution of NOUS-209 target FSMs in Lynch syndrome–associated tumors, revealing their persistence across primary and metachronous cancers and supporting the rationale for NOUS-209 as a preventive immunotherapy.

  Study EGAS50000001336

• Multi-region RNA-Seq data of 10 neuroblastoma cases

  To investigate intratumour heterogeneity and to better understand tumour evolution in neuroblastoma, we have performed a multi-region RNA sequencing on a total of 51 spatially separated tumor samples from 9 primary neuroblastomas (2 low-risk, 1 intermediate-risk and 6 high-risk) and 1 relapsed neuroblastoma. We also assessed the impact of chemotherapy on the clonal expansion by sequencing tumour regions from one medium risk and one high-risk tumour for which we had matched samples obtained at diagnosis and after chemotherapy.

  Dataset EGAD00001008133

• SARS-CoV-2 host genetics and COVID-19 outcomes in admixed Brazilians with extreme phenotypes

  COVID-19 comprises clinical outcomes of SARS-CoV-2 infection and is highly heterogeneous, ranging from asymptomatic individuals to deceased young adults without comorbidities. There is growing evidence that host genetics play an important role in COVID-19 severity, including inborn errors of immunity, age-related inflammation and immunosenescence. This study proposes a strategy of subject’s ascertainment based on phenotypic extremes to take part in genomic studies and elucidate intrinsic risk factors involved in COVID-19 severe outcomes. Different cohorts were collected and submitted to Next-Generation Sequencing (Whole exome and whole genome sequencing).

  Study EGAS00001006376

• Chordoma_Extension_Study

  Extension analysis to pursue candidate genes of interest in chordoma

  Study EGAS00001000892

• Chordoma_Extension__known_cancer_genes_

  Extension analysis to pursue candidate genes of interest in chordoma

  Study EGAS00001000895

• Enrichment of Lung Microbiome with Supraglottic Taxa which is Associated with Increased Pulmonary Inflammation

  Background: The lung microbiome of healthy individuals frequently harbors oral organisms. Despite evidence that micro-aspiration is commonly associated with smoking-related lung diseases, the effects of lung microbiome enrichment with upper airway taxa on inflammation has not been studied. We hypothesize that the presence of oral microorganisms in the lung microbiome is associated with enhanced pulmonary inflammation. Methods: We sampled bronchoalveolar lavage (BAL) from the lower airways of 29 asymptomatic subjects (9 never-smokers, 14 former-smokers and 6 current-smokers). We quantified, amplified, and sequenced 16S rRNA genes from BAL samples by qPCR and 454 sequencing. Pulmonary inflammation was assessed by exhaled nitric oxide (eNO), BAL lymphocytes and neutrophils. Results: BAL had lower total 16S than supraglottic samples and higher than saline background. Bacterial communities in the lower airway clustered in two distinct groups that we designated as pneumotypes. The rRNA gene concentration and microbial community of the first pneumotype was similar to that of the saline background. The second pneumotype had higher rRNA gene concentration and higher relative abundance of supraglottic-characteristic taxa (SCT), such as Veillonella and Prevotella, and we called it pneumotypeSCT. Smoking had no effect on pneumotype allocation, alpha or beta diversity. PneumotypeSCT was associated with higher BAL lymphocyte-count (p = 0.007), BAL neutrophil-count (p = 0.034) and eNO (p = 0.022). Conclusion: A pneumotype with high relative abundance of supraglottic-characteristic taxa is associated with enhanced subclinical lung inflammation.

  Study phs000633

• Whole genome analysis of mutation hotspots in gastric cancer

  Tissue-specific driver mutations in non-coding genomic regions remain undefined for most cancer types. In this study, we unbiasedly analysed 212 gastric cancer whole genomes to identify recurrently mutated non-coding regions in gastric cancer. Applying comprehensive statistical approa- ches to accurately model background mutational processes, we observe significant enrich- ment of non-coding indels (insertions/deletions) in three gastric lineage-specific genes. We further identify 34 mutation hotspots, of which 11 overlap CTCF binding sites (CBSs).

  Study EGAS00001002872