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• TenK10K project

  This DAC handles access to data from the TenK10K project, which is comprised of matched whole-genome sequencing (WGS) and single-cell RNA-sequencing (scRNA-seq) datasets.

  Dac EGAC50000000931

• Res1_PC9_exp2_MC_01.04.22

  8 cell pellet samples for genomic DNA extraction. CRISPR PCR1 and PCR2 indexing - Please use standard Kosuke primers.

  Dataset EGAD00001012233

• Res1_PC9_exp1_MC_29.03.22

  8 cell pellet samples for genomic DNA extraction. CRISPR PCR1 and PCR2 indexing - Please use standard Kosuke primers.

  Dataset EGAD00001012232

• Whole Exome Sequencing Fastq PE Files

  Anal SCC cell line and parent tumour comparative whole exome sequencing

  Dataset EGAD00001007001

• KiCS cancer panel academic only data

  This data set contains KiCS cancer panel data for academic and for-profit use.

  Dataset EGAD00001009733

• H3Africa SIREN Phenotype

  Phenotype data for 3421 Samples from Nigeria and Ghana, sequenced with the Illumina NestSeq 500.

  Dataset EGAD00001011075

• A super-enhancer associated with CD47 links pro-inflammatory signaling to CD47 upregulation in breast cancer

  CD47 is a cell surface molecule that inhibits phagocytosis of cells that express it by binding to its receptor, SIRPα, on macrophages and other immune cells. CD47 is expressed at different levels in normal cells, however, in cancer cells, CD47 transcript and protein expression is aberrantly increased. Here we sought to uncover the regulators of CD47 transcription, including active enhancers that increase its aberrant expression in cancer cells, in order to reveal mechanisms by which different neoplastic cells generate this dominant 'don't eat me' signal. Enhancers are genomic regions, often referred to as "switches", that can turn on or off the transcription of target genes. Recently the discovery of super-enhancers (SEs) has given more insight into the regulatory architecture of key genes that are highly expressed in a specific cell type, during a particular developmental stage or in disease. By analyzing the CD47 regulatory genomic landscape, we discovered: i) A distinct super-enhancer (SE) is associated with CD47 upregulation in breast cancer cells ii) Disruption of CD47 SEs by using the BRD4 inhibitor JQ1 robustly reduces CD47 gene expression; and iii) The TNF-NFKB1 signaling pathway is directly involved in the regulation of CD47 by interacting with a distal downstream constituent enhancer located within a CD47-associated SE specific to breast cancer. Our results describe a novel mechanism that cancer cells have evolved to drive CD47 overexpression to escape immune surveillance.

  Study phs001264

• HuBMAP: A Spatially Resolved Molecular Atlas of Human Endothelium

  The human circulatory system plays a vital role in the proper functioning of every organ in the human body. Because vascular related diseases, such as atherosclerosis, do not occur homogeneously throughout the vascular tree, differences in the endothelium of various organs must exist. There is even evidence of heterogeneity of adjacent endothelial cells. We are studying normal endothelium throughout the body and across individuals of different ages to characterize these differences. The first step will be to procure normal tissue samples from a wide range of organs. From disaggregated samples of these tissues, we will perform single cell combinatorial indexing (sci-) to generate chromatin accessibility (sci-ATAC-seq) and transcriptome (sci-RNA-seq) data from millions of single cells across hundreds of samples.  Molecular heterogeneity might correlate with multiple facets of the anatomical distribution of endothelium, including vascular vs. lymphatic, arteries vs. veins, capillaries vs. larger vessels, differences between organs, organ zonation, cell-to-cell differences, etc. Based on heterogeneous markers defined from deep profiling of disaggregated cells, we will employ seqFISH to spatially relate the distinct endothelial subpopulations arising from the single nuclei data to histologic preparations. For example, this will allow us to identify subpopulations with particular markers as arterial, capillary, venous, or lymphatic. The end product will include multiparameter images in which the complete gene expression and chromatin accessibility profile can be interactively visualized for every cell.

  Study phs002267

• Plasma-Seq of patients with metastatic prostate cancer

  Study 1 In this study we analysed patients with metastatic prostate cancer to scan their tumor genomes noninvasively in plasma DNA. We wanted to make whole-genome analysis from plasma DNA amenable to clinical routine applications and developed an approach based on a benchtop high-throughput platform, i.e. Illuminas MiSeq instrument. We performed whole-genome sequencing from plasma at a shallow sequencing depth to establish a genome-wide copy number profile of the tumor at low costs within 2 days. The genome-wide profiling in the plasma of our patients revealed multiple copy number aberrations including those previously reported in prostate tumors, such as losses in 8p and gains in 8q. High-level copy number gains in the AR locus were observed in patients with CRPC but not with CSPC disease. We identified the TMPRSS2-ERG rearrangement associated 3-Mbp deletion on chromosome 21 and found corresponding fusion plasma fragments in these cases. In an index case multiregional sequencing of the primary tumor identified different copy number changes in each sector, suggesting multifocal disease. Our plasma analyses of this index case, performed 13 years after resection of the primary tumor, revealed novel chromosomal rearrangements, which were stable in serial plasma analyses over a 9 months period, which is consistent with the presence of one metastatic clone. Our approach provides specific genomic signatures within 2 days which may therefore serve as “liquid biopsy”.

  Study EGAS00001000451

• Long-read trio sequencing of unsolved patients with intellectual disability

  Long-read sequencing (LRS) has the potential to comprehensively identify all medically-relevant genome variation, including variation commonly missed by short read sequencing (SRS) approaches. To determine this potential, we performed LRS up to 40x coverage using the Pacific Biosciences Sequel instrument for 5 patient-parent trios with intellectual disability, whose aetiology remained unresolved after SRS exomes and genomes. A first systematic assessment of LRS coverage showed that ~35Mb of the genome was only accessible by LRS and not SRS. Structural variant (SV) calling yielded on average 28,292 SV calls per individual, totalling 12.9 MB of sequence. Trio-based analyses showed concordance for up to 95% of these SV calls across the genome, and 80% of the LRS SV calls were not identified by SRS. De novo mutation analysis did not identify any de novo SVs, confirming these are rare events. Because of high sequence coverage, we were also able to call single nucleotide substitutions. On average, we identified 3 million substitutions per genome, with a Mendelian inheritance concordance of up to 97%. Of these, approximately 100,000 were located in the ~35Mb of the genome that was only captured by LRS. Moreover, these variants affected the coding sequence of 64 genes, including 32 known to cause Mendelian disorders. Although no clinical diagnoses were made in these 5 patients, our data show the potential added value of LRS compared to SRS for identifying medically relevant genome variation.

  Study EGAS00001004319

• Identification of the mutational consequences of precancerous liver disease (including alcohol abuse) on the genomes of human adult stem cells.

  Stem cells are believed to be the cells-of-origin cancer. Nevertheless, their genome remains remarkably stable during life. To increase insight into how these cells can drive tumorigenesis, we set out to determine the genomic integrity of human adult stem cells from patients with liver disease associated with increased cancer risk. To this end, we characterized genome-wide mutation profiles of single ASCs from livers of patients with alcoholic liver disease, non-alcoholic liver disease and primary sclerosing cholangitis. The patients included in our study received a liver transplant due to their liver disease. Strikingly, we found that ASCs in these livers maintain a stable genome and have comparable mutation rates as healthy human liver ASCs. We did observe more nonsense and nonsynonymous mutations in COSMIC cancer genes that are hit by dominant mutations in tumors in comparison to healthy ASCs (n.s.), including two ASCs in alcoholic liver disease patients with a nonsense mutation in PTPRK. Next, we sequenced 5 biopsies of an alcoholic tumour to identify the mutational patterns in the tumour-initiating ASC. We found that the mutational patterns are, again, similar to healthy liver, but the mutational load is slightly higher. This suggests that the increased cancer risk in the liver disease patients is not caused by an increased mutational load, but rather that the precancerous liver environment promotes outgrowth of cells that would normally be selected against.

  Study EGAS00001002983

• ParityImmune

  Blood transcriptome from women participating in the Norwegian Women and Cancer study (NOWAC)

  Dataset EGAD00010001412

• wtcccan-exome

  WTCCC3 Anorexia Nervosa Infinium-HumanCoreExome

  Dataset EGAD00010001043

• SNParray copy number dataset

  4 oesophageal cancer derived organoid lines and 2 ovarian cancer derived organoid lines

  Dataset EGAD00010002002

• OSC Global Screening Array Genotypes

  DNA was extracted from saliva samples and genotyping was performed on Illumina Infinium Global Screening Array.

  Dataset EGAD00010002374

• RNA-seq, WGS and WES of Hepatocellular carcinomas, enriched in fibrolamellar carcinomas

  Dataset EGAD00001005308

• PBMC all cell metadata

  Cell annotation for single cells of PBMC collected from 113 patients, including UMAP coordinates and annotation.

  Dataset EGAD50000000145

• DAC for TFHL single-cell analysis project at Department of Hematology, University of Tsukuba

  DAC for study of tumor heterogeneity and immune-evasive microenvironment in T follicular helper cell lymphomas

  Dac EGAC50000000201

• BROCA cancer panel sequencing for 15 samples

  BROCA panel sequencing using the BROCA-HR v8 and BROCA-GO v1 versions of the gene panel

  Dataset EGAD50000000035

• bfast CohortD clinical data

  Clinical data for BFAST Cohort D, including time-to-event, tumor response, and baseline prognostics data.

  Dataset EGAD50000000149

• H3K27me3 Cut&Tag on beta cells

  H3K27me3 Cut&Tag datasets in human pancreatic islets and the EndoC-bH1 cell line

  Dataset EGAD50000000463

• Spatially resolved TME alterations in GCPM

  Whole exome sequencing of 66 gastric samples and whole transcriptome sequencing of 191 gastric samples.

  Dataset EGAD50000000715

• H3Africa KDRN Phenotype

  The phenotypic data for 6431 samples of the KDRN Study from Ghana and Nigeria.

  Dataset EGAD00001009333

• DAC for "High-Resolution Spatial Transcriptomics Uncover Epidermal-Dermal Divergences in Merkel Cell Carcinoma: Spatial Context Reshapes the Gene Expression Landscape" with Jürgen C. Becker(j.becker@dkfz-heidelberg.de) and Nalini Srinivas(n.srinivas@dkfz-heidelberg.de )

  Dac EGAC00001003599

• Tumor Normal WES dataset

  This dataset contains tumor-normal WES data in BAM files aqcuired from patients with renal cancer tumors and treated with Sunitinib

  Dataset EGAD50000001174