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• Foregut Microbiome and Risk of Gastric Intestinal Metaplasia, and Gastric Cancer Risk

  The study is composed of two sub-studies. The first study, conducted by NYU Grossman School of Medicine, is a case-control study of 89 cases with gastric intestinal metaplasia (IM) and 89 matched controls who underwent upper gastrointestinal endoscopy at three sites affiliated with NYU Langone Health. Shotgun metagenomic sequencing using oral wash samples from the 89 case-control pairs and antral mucosal brushing samples from 55 case-control pairs were conducted. The other study, conducted by Vanderbilt University Medical Center, is a prospective case-control study on the oral microbiome and gastric cancer risk, utilizing shotgun metagenomic sequencing data of pre-diagnostic buccal samples from 319 Asians, 118 African Americans and 51 European Americans. This study includes data from three population-based studies: the Southern Community Cohort Study (SCCS), the Shanghai Women's Health Study (SWHS), and the Shanghai Men's Health Study (SMHS). The SWHS and SMHS include 74,941 women aged 40-70 years and 61,480 men aged 40-74 years, respectively, who were permanent residents of Shanghai and recruited to the cohorts between 1997 and 2006. The SCCS is an ongoing prospective cohort study, including ~86,000 participants recruited during 2002 and 2009 from 12 Southeastern states. Nearly 67% of study participants are African Americans (AAs) and the remaining are European American (EA) subjects.

  Study phs002566

• Study to investigate the prevalence of leukaemic mutations in whole blood DNA in a cohort of blood donors

  The aim of this study is to ascertain whether leukaemic mutations exist within the blood of people with otherwise normal haematopoeisis. To satisfy this aim we plan to look for 7 known leukaemic mutations in the whole blood DNA of a large cohort of blood donors who have normal haematopoesis. Genomic regions around mutational sites have been amplified using a 2 step PCR process which involves barcoding of individual patients

  Dataset EGAD00001001319

• Exome sequencing of uterine leiomyosarcomas

  Uterine leiomyosarcomas (ULMSs) are aggressive smooth muscle tumors associated with poor clinical outcome. Despite previous cytogenetic and molecular studies, their molecular background has remained elusive. To examine somatic variation in ULMS, we performed exome sequencing on 19 tumors. Altogether 43 genes were mutated in at least two ULMSs. Most frequently mutated genes included tumor protein P53 (TP53; 6/19; 33%), alpha thalassemia/mental retardation syndrome X-linked (ATRX; 5/19; 26%), and mediator complex subunit 12 (MED12; 4/19; 21%). Unlike ATRX mutations, both TP53 and MED12 alterations have repeatedly been associated with ULMSs. All the observed ATRX alterations were either nonsense or frameshift mutations. ATRX protein levels were reliably analyzed by immunohistochemistry in altogether 44 ULMSs, and the majority of tumors (23/44; 52%) showed clearly reduced expression. Loss of ATRX expression has been associated with alternative lengthening of telomeres (ALT), and thus the telomere length was analyzed with telomere-specific fluorescence in situ hybridization. The ALT phenotype was confirmed in all ULMSs showing diminished ATRX expression. Exome data also revealed one nonsense mutation in death-domain associated protein (DAXX), another gene previously associated with ALT, and the tumor showed ALT positivity. Aberrant expression of both TP53 and ATRX were associated with poor overall survival. In conclusion, exome sequencing revealed that TP53, ATRX, and MED12 are frequently mutated in ULMSs. ALT phenotype was commonly seen in tumors, indicating that ATR inhibitors, which were recently suggested as possible new drugs for ATRX-deficient tumors, could provide a potential novel therapeutic option for ULMS.

  Study EGAS00001001612

• Mitochondrial DNA deletion detection in POLG patients

  Accumulation of deletions in the mitochondrial genome is a pathological hallmark of both aging and a broad range of neurometabolic disorders. Prior mtDNA deletion studies have been limited by reliance upon either long range PCR or NGS strategies that target specific regions of the mitochondrial genome. We developed an ultrasensitive high throughput sequencing process (LostArc) to identify and quantify all deletions in circular DNA molecules while minimizing interference from linear DNA and PCR artefacts. We applied this process to skeletal muscle biopsies from 19 unaffected individuals (aged 17 to 93 years) and from 22 patients with heritable mitochondrial disease (17 to 80 years) bearing pathogenic variants in POLG, the nuclear gene encoding the catalytic subunit of the mitochondrial replicative DNA polymerase ɣ (Pol ɣ). To our astonishment, LostArc revealed 35 million mtDNA deletions with ~470,000 unique deletion spans. This unprecedented volume of data enabled detailed and highly informative bioinformatics analyses. We show that ablation of mtDNA is sufficient to explain skeletal muscle phenotypes associated with aging and POLG-derived disease, with a clear threshold separating symptomatic and asymptomatic individuals. Unsupervised hierarchical clustering and principle component analysis reveal distinct age- and disease-correlated deletion patterns that implicate DNA replication by Pol ɣ in the formation of mtDNA deletions. Deletion patterns also point to active mtDNA replication but little or no purifying selection against deleted mtDNA by mitophagy in postmitotic muscle fibers. Monte Carlo simulations of varied hypotheses for deletion formation, based in part on competing models of mtDNA replication, suggest the observed patterns are most consistent with deletions initiated by replication fork stalling during strand displacement mtDNA synthesis. Note that sequence data for HEK293 can be found under BioProject PRJNA642884.

  Study phs002052

• Evolution of Chronic Lymphocytic Leukemia to Richter's Syndrome (RS)

  Richter's syndrome arising from chronic lymphocytic leukemia is a striking example of an aggressive malignant histology that emerges from indolent cancer. To understand this process, we reconstructed phylogenies based on whole exome sequencing of matched normal, CLL and RS samples. We computationally deconvoluted CLL and RS clones and identified drivers of transformation. We additionally performed whole genome sequencing, whole transcriptome sequencing and single-cell transcriptome sequencing to understand the mutational signatures, genome-wide events and gene expression changes associated with transformation.

  Study phs002458

• EGA submission account terms

  Submission account terms Each EGA submission account has a dedicated submission box. To ensure continued service to all submitters EGA submission boxes should not exceed 8Tb in size, and cannot exceed 12Tb. Those that are near to or exceeding this value will be monitored on a weekly basis by the helpdesk team and the submitter will be contacted and guidance provided accordingly on completing their metadata registration. You will be able to register your metadata associated with the files in your submission account via EGA Submitter Portal, Webin or the EGA REST API. EGA also requests that metadata is submitted within 60 days of upload data to a submission box. When we detect files that are over 60 days old in a submission box we will notify the submitter requesting that metadata be submitted or the files removed from the submission box. It is important to note that data is not archived at the EGA until the metadata describing the files has been associated and the archival process has completed. It is only when associated metadata has been submitted that the archival process into EGA is fully triggered. EGA removes files from the submission box once they have been successfully archived, so no action is required by a submitter to remove successfully archived files. Files over 90 days old will be deleted from the submission box unless EGA Helpdesk has been contacted and confirmed an exemption with the submitter.

  Documentation submission/terms

• Single cell sequencing of a post-PD-1 inhibitor metastatic melanoma mass

  Three technical replicates of FACS-sorted T cells (CD45+CD3+) and one replicate of FACS-sorted tumor cells (MCSP+) were loaded to a targeted 10,000 cells per lane on the 10X Genomics Chromium Controler with the single cell 5’ Immune Repertoire and Gene Expression profiling kit. In total, we loaded ~30,000 individual tumor infiltrating lymphocytes (TILs) and ~10,000 melanoma cells on the 10X platform (10X Genomics, CA, USA). Reverse transcription, TCR enrichment, and library preparations were performed according to the 10X Genomics 5’ V(D)J protocol revision C. Transcriptome libraries were pooled and sequenced on the Illumina NovaSeq 6000 S2 flow cell with 26 R1, 8 i7, and 91 R2 cycles respectively. The TCR libraries were pooled and sequenced on the Illumina MiSeq V2 150 cycles paired-end. Single cell transcriptomic and TCR data was processed with the 10X Genomics Cell Ranger Pipeline version 2.2.0 with the software-provided GRCh38 reference transcriptomes. After quality control, there was RNAseq profile data available from 6267 immune and 4303 melanoma cells. Downstream processing and visualization was encompassed through Seurat and tSNE plots.

  Dataset EGAD00001006013

• The variable genomic landscape during osteosarcoma progression: insights from a longitudinal WGS analysis

  Osteosarcoma is a primary bone tumor that exhibits a complex genome characterized by gross chromosomal abnormalities. Osteosarcoma patients often develop metastatic disease, resulting in limited therapeutic options and poor survival rates. To gain knowledge on the mechanisms underlying osteosarcoma heterogeneity and metastatic process, it is important to obtain a detailed profile of the genomic alterations that accompany osteosarcoma progression. Therefore, in this study we performed WGS on multiple tissue samples from six patients with osteosarcoma, including the treatment naïve biopsy of the primary tumor, resection of the primary tumor after neoadjuvant chemotherapy, local recurrence and distant metastases.

  Study EGAS50000000329

• Ultra-fast multiplex small DNA sequencing on the MinION nanopore sequencing platform

  Here, we developed an ultra-rapid multiplexed library preparation and sequencing method for the MinION and applied this method to accurately test euploid and aneuploid genomic DNA samples in under three hours, including library preparation and sequencing. This novel method shows great promise as a clinical diagnostic test for applications requiring rapid short-read DNA sequencing.

  Study EGAS00001002650

• Policy Documentation

  Policy Documentation The following policy documentation is required to be prepared and submitted to the EGA, together with your data files and associated metadata. Data Access Agreement (DAA) The Data Access Agreement is a contract made between Data User and Data Access Committee. The agreement should be drafted by the DAC and includes, but is not limited to, details of data use, publication embargoes and storage. Completion of a DAA by the applicant/s should form part of the application process to the DAC. NOTICE The data access agreement template below is provided for guidance only and should be adapted as you see fit to suit your own purpose. In the interest of promoting data sharing, we suggest that if an agreement cannot be met around clause 19 in this example that both parties should agree to remain silent, and that the clause should be removed from the agreement. Example DAA template Alternate (harmonised) DAA template

  Documentation access/data-access-committee/policy-documentation