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• Reference epigenomes generated as part of the International Human Epigenomics Consortium (IHEC)

  The Centre for Epigenome Mapping Technologies (CEMT) is an epigenome sequencing platform funded by the Canadian Institutes of Health Research (CIHR) and Genome BC as part of the Canadian Epigenetics, Environment and Health Research Consortium (CEEHRC). CEMT aims to produce 100 human reference epigenomes, each comprising the following datasets: whole genome; whole genome bisulfite and oxidative bisulfite; transcriptome; microRNA; and chromatin immunoprecipitation (ChIP)-seq for the core chromatin marks (H3K4me1, H3K4me3, H3K9me3, H3K27me3, H3K36me3, and H3K27ac).CEEHRC is a full member of the International Human Epigenomics Consortium (IHEC), which aims to coordinate the production of 1,000 reference maps of human epigenomes for key cellular states relevant to health and diseases. As such, all datasets submitted by the CEMT platform conform to IHEC assay standards and metadata guidelines.

  Study EGAS00001000552

• Michigan Polybrominated Biphenyl (PBB) Exposure Registry

  Humans are exposed to chemicals such as brominated flame retardants (BFRs) at unprecedented levels, and a wide variety of health effects are attributed to such exposures. However, the biological mechanisms that link exposures to its consequences remain unknown. An industrial accident in the 1970's exposed over 4000 individuals in rural Michigan to polybrominated biphenyl (PBB), a BFR that was present in the food supply for years prior to detection and management. Health effects are still evident in these individuals and their children. Because this population has been assessed regularly since the exposure, it is an ideal group in which to examine the molecular mechanisms that contribute to susceptibility, vulnerability and health effects. The goal of this project is to identify the genetic variants that associate with the rate of PBB elimination over time and integrate genetic and epigenetic datasets and identify complex gene-environment relationships in PBB exposed individuals. We will leverage data generated as part of past and ongoing studies in the Michigan Polybrominated Biphenyl Registry. We anticipate that this study will provide insight into how genetic variants and the environment interact in relation to PBB exposure and its health effects. We also anticipate the results of this study will be informative for studies of BFRs and other endocrine disrupting compounds with similar chemical properties. Note that methylation array data is available from NCBI GEO under GSE116339: Exposure to Polybrominated Biphenyl (PBB) Associates with DNA Methylation Differences Across the Genome

  Study phs001862

• Multi-layered molecular characterization defines prognostic subtypes of lung adenocarcinoma in Asian never-smokers

  Multi-layered genomic studies such as the TCGA project have greatly advanced our understanding on molecular pathogenesis of lung cancer. For Asian nonsmoker patients, however, majority of studies have been limited to mutational analyses, emphasizing ethnic differences in driver mutations (e.g. more frequent EGFR mutations and ALK fusions). In essence, a comprehensive multi-layered characterization that could lead to molecular etiology and patient stratification scheme to be translated into clinical applications for this patient group is still missing. Here we report molecular profiling of tumor and matched normal tissues from 114 non-small-cell lung adenocarcinoma patients using whole exome sequencing, transcriptome sequencing, and array comparative genomic hybridization (CGH).

  Study EGAS00001003705

• Thymic epithelial transplantation for complete DiGeorge syndrome Spatial (2026-01-19)

  Spatial transcriptome analysis of thymic cells from children with syndromic diseases such as Trisomy 21 and inflammatory/autoimmune diseases such as myasthenia gravis. . This dataset contains all the data available for this study on 2026-01-19.

  Dataset EGAD00001015798

• 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

• Paired-WGS Sequencing of Primary lymphomas of the central nervous system (PCNSL)

  26 Tumor/Control pairs of WGS data of PCNSL tumors, sequenced on either Illumina HiSeq2000/2500 instruments or HiSeq X Ten. The controls are blood or buffy coat samples in most cases.

  Dataset EGAD00001007806

• Whole genome and transcriptome analysis of medullary thyroid cancer

  Medullary thyroid cancer is the neoplasm of the calcitonin-producing parafollicular cells of the thyroid gland. The hormone calcitonin acts to lower the blood calcium level, counteracting the effects of the parathyroid hormone; it can also serve as a biomarker for the presence or recurrence of medullary thyroid cancer. Surgery is the only curative treatment for this cancer. Targeted therapeutics vandetanib and cabozantinib are approved for the treatment of aggressive and metastatic tumors that are not amenable to surgery. The use of these multikinase inhibitors are supported by the observed overactivation of the RET oncoprotein in a large sub-population of medullary thyroid cancers; however, not all patients carry oncogenic alterations of this kinase. Hence, there is a need for molecular characterization of medullary tumors on the genomic scale with the aim of identifying targetable mutations. Here, we describe the genomic profiles of two medullary thyroid cancers and report the presence of a putative oncogenic BRAF fusion in one. Such alterations previously observed in other malignancies and known targets of available drugs, can benefit patients who currently have no therapy options.

  Study EGAS00001001473

• From research to data sharing: exploring EGA user's experiences

  The Cell Plasticity and Regeneration Group at the Bellvitge Biomedical Research Institute-IDIBELL focuses on the process of recruitment of macrophages that takes place in the small intestine during injury and healing. They recently published a paper titled “Mucosal Macrophages Govern Intestinal Regeneration in Response to Injury" in Gastroenterology Journal. As part of the research, some experiments were conducted using human intestinal organoid lines. These cells were processed for RNA sequencing, and the sequencing data were deposited at the EGA to be made available to the scientific community. When dealing with human genomic information, repositories must ensure the availability of the datasets while ensuring data protection. In this context, the European Genome-phenome Archive stands as a service for secure archiving and sharing of genetic, phenotypic and clinical data resulting from biomedical research. Following the recent publication of their paper, we took the opportunity to talk to Ilias Moraitis, first author, and Jordi Guiu, group leader, to find out about their experience with data sharing. Could you explain the focus of your research? In the lab, we study intestinal regeneration and how immune cells participate in this process. We use several techniques: engineered mouse models, image tracing, as well as mouse and human cells intestinal organoids. What challenges do you face regarding data management? We didn’t have a lot of problems. Always the informatic part, the data analysis, can give problems. But everything was smooth and working. We think it’s very important to deposit the data in repositories. For the mouse data it is very straightforward, but for us it was the first time depositing human data, which is sensitive because it comes from patients, and this is legally regulated. That’s why we thought about the EGA, and it was our first time. Why do you think it is important to submit data to repositories such as EGA? Because we think data is important for the science. Nowadays, we are sequencing a lot everywhere worldwide and having these resources shared with the scientific community it’s not only good for science, but it is also saving money and reducing costs. And there is so much data in there that can be used for other projects and for other questions. And it saves time! How was the process of submitting the data to the EGA? The communication worked very well but it was slower than we would like. But I think this is something we learn on the way. People usually wait until the last minute to do this before publication but if you know it in advance, you can start the process earlier. If you had to repeat the process, would you do anything differently? It’s like everything, isn’t it? For the first time you don’t know, you aren’t sure, but for the second time you know the steps, you know what to do and it’s faster. Of course, we would to do it earlier. Also, there were some things related to the control access that we didn’t know how to manage, but it was something more internal to us. Who is going to receive the communications and when, is our ethical committee going to evaluate this? All these technicalities that we didn’t know before starting this process, so we had to think about all these things. Next time it will be faster on our side. Do you have any suggestions for us to improve the submission process? Maybe we’ll need to ask our bioinformatician who did it! He was in charge of this part. Besides that, we think if the process were faster, it would be better for everyone. Also, in science a lot of times you have to do a lot of things at the very last minute, because of the nature of the experiments, or the need to accomplish for submitting a paper. Being faster in the process would be a plus. On your side, we went through the process and were able to find some information, but there were aspects we weren't aware of and weren't sure how to handle. I'm not sure if other institutes have different protocols for managing data requests or how they handle these internally. We believe the main issue lies in how the forms are filled out. Do you have any recommendations for other submitters? The main advice is to do this with enough time. Submit the data when you have the sequences, and don’t wait until the last minute. And then it can be under embargo, so you don’t need to make it public at that moment. As soon as you sequence, upload it and then it will be there for whenever you need to publish. How do you think we could encourage other researchers to submit their data? There are different layers here. One is that it is mandatory. You have to do this. The other is that we belong to a research community, to the same community and sharing this is making our research community stronger and more efficient. And then, also because this gives you visibility. The data is there, other people can analyse your data, and this also will bring citations to your papers. It has many advantages.

  Blog from-research-to-data-sharing

• Development of Novel Chondrosarcoma Organoid Models for Drug Discovery

  Chondrosarcoma is a rare and aggressive malignant bone tumor characterized by resistance to conventional chemotherapy and radiotherapy. Its pathogenesis remains poorly understood, although recurrent mutations such as IDH1 have been implicated in tumor development. We treated patients with chondrosarcoma at the Osaka International Cancer Institute and established two organoid cultures from resected tumor specimens using a modified air-liquid interface method. After serial passaging, the organoids were successfully xenografted into NOD-scid IL2Rgnull (NSG) mice. The established organoids retained key histological features and genetic characteristics of the original tumors. These organoid models provide a novel and reliable platform for studying the biology of chondrosarcoma and may facilitate the development of effective therapeutic strategies for this treatment-resistant tumor.

  Study JGAS000834

• Common Fund (CF) Genotype-Tissue Expression Project (GTEx)

  Lay Description The aim of the Genotype-Tissue Expression (GTEx) Project is to increase our understanding of how changes in our genes affect human health and disease with the ultimate goal of improving health care for future generations. GTEx will create a database that researchers can use to study how inherited changes in genes lead to common diseases. GTEx researchers are studying genes in different tissues obtained from many different people. The GTEx project also includes a study of the GTEx donor consent process - this study will help ensure that the consent process and other aspects of the project effectively address the concerns and expectations of participants in the study. GTEx is a pioneering project that uses state-of-the-art protocols for obtaining and storing a large range of organs and tissues, and for testing them in the lab. Until now, no project has analyzed genetic variation and expression in as many tissues from the same person in such a large population as planned for GTEx. Scientific Description Understanding the role of variation in the human genome is crucial to elucidating genetic contributions to human health and disease. Despite the results of genome-wide association studies (GWAS) documenting strong statistical associations between genetic variation and human traits, the functional role for most of these variants is largely unexplained. Nearly 90% of these GWAS-implicated sites lie outside of protein-coding sequences, suggesting that these variants might regulate gene expression. The goal of the Genotype-Tissue Expression (GTEx) project is to establish a resource database and tissue biobank in which to study the relationship between genetic variation and gene expression and other molecular phenotypes in reference/non-diseased tissues. The ultimate resource will include approximately 960 post-mortem donors with several dozen tissues from each, a resource large enough to study both cis- and trans- gene expression quantitative trait loci (eQTLs). Some tissue will also be banked for additional molecular analyses. To request biosamples, please see the Biobank page for more information. GTEx was initially funded as a 2-year pilot project by the NIH Common Fund (CF) in 2010, and has been scaled up after demonstration of feasibility. The project will collect and analyze RNA levels in many different human tissues and each donor will be characterized for germline genetic variation through dense genotyping arrays and sequencing of either whole exomes or whole genomes. By treating RNA expression levels as quantitative traits, eQTLs will be identified as sites containing genetic variation that correlate with changes in RNA expression. Such eQTLs have been associated with 4%-12% of expressed human genes, and with common complex human diseases, including obesity, atherosclerosis, type 2 diabetes, Crohn's disease, and asthma. Additionally, few studies have examined the tissue specificity of eQTLs. A subset of banked tissue samples will also be analyzed for other molecular phenotypes, such as DNA methylation, DNaseI hypersensitivity sites, and proteomics. The GTEx project will thus serve as a resource database and tissue bank for many future studies, especially for understanding the functional basis of inherited susceptibility to disease. All GTEx releases since Version 5 follow the NIH Genomic Data Sharing (GDS) Policy whereby there are no restrictions on use or publication after release. Additional information about the GTEx Data Release and Publication policy can be found on the GTEx Data Portal at www.gtexportal.org.

  Study phs000424