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• Somatic mutations and single cell transcriptomes reveal the root of malignant rhabdoid tumours

  Like many childhood cancers, malignant rhabdoid tumours (MRT) are thought to arise from aberrant foetal development. Although MRT predominantly exhibit a mesenchymal phenotype, it has been suggested that the foetal root of MRT lies in neural crest development. Here, we combine phylogenetic analyses of MRT, single cell mRNA assays, and functional experiments in patient-derived MRT organoids, to define the embryological origin of MRT and explore therapeutic avenues that may drive MRT differentiation. Phylogenetic analyses from the distribution of somatic mutations revealed that MRT were related to neural crest-derived, but not to mesodermal tissues, providing direct evidence of the neural crest origin of MRT in humans. In MRT organoids, reversal of the principal driver event underpinning MRT, SMARCB1 loss, induced differentiation along mesenchymal pathways. Together, these findings placed MRT cells on a developmental trajectory of neural crest to mesenchyme conversion, and defined the transcriptional changes underpinning MRT differentiation. Searching perturbation databases for agents that mimic these mRNA changes, we identified HDAC and mTOR inhibition as potential differentiation agents. Treatment of MRT organoids with this drug combination induced proliferation arrest with transcriptional changes akin to SMARCB1 re-expression. Our study defines the embryological root of MRT and proposes a differentiation treatment for this often fatal childhood cancer.

  Dataset EGAD00001006296

• Whole exome sequencing variant data for Mendelian disorders cohort

  This dataset contains whole exome sequencing variant data (VCF files) from individuals with suspected Mendelian disorders, including sickle cell disease, muscular dystrophy, haemophilia, and Fanconi anemia. Variant calling was performed using the Illumina DRAGEN pipeline, with downstream variant prioritisation conducted using the Zi-Mendelian bioinformatics pipeline. The dataset supports research into rare genetic diseases and genomic variation in African populations.

  Dataset EGAD50000002453

• CNV detection in targeted NGS panel data

  We present targeted NGS panel data from 170 samples that were processed using the TruSightTM Cancer (TSC) panel (Illumina, San Diego, CA, USA), which targets 94 genes and 284 SNPs associated with a predisposition towards cancer. The samples are enriched for CNVs in the genes of interest. All CNVs have previously been assessed with MLPA and can therefore be considered as confirmed.

  Dataset EGAD00001003400

• Exome sequencing data

  Exome sequencing fastq files from 6 mutation carriers and 5 non-carriers from 2 families. One µg DNA was used for library preparation using the TruSeq DNA LT Sample Prep Kit v2 according to the manufacturer’s instructions (Illumina). Hybridization was performed using Nimblegen SeqCap EZ Exome v3 (Roche) and Paired-end Sequencing (2x100 bp) on the Illumina HiSeq 2000 with TruSeq v3 chemistry (Illumina).

  Dataset EGAD00001003745

• 10x genomics RNAseq of an isogenic human iPSC model of SMA

  10x genomics single-cell RNAseq of an isogenic human iPSC model for SMA and control. The transcriptomic analysis was performed at 3 timepoints, day 4, day 20 and day 40. The analysis of this dataset was reported in the manuscript "An isogenic human iPSC model unravels neurodevelopmental abnormalities in SMA" from Grass et al.:

  Dataset EGAD00001011259

• atrial appendage RNA-seq in non-, paroxysmal and persistent atrial fibrillation

  Understanding the interconnectedness of structural remodelling processes atrial fibrillation (AF) in patients could identify targets for future therapies. These data include transcriptome sequencing of atrial tissues of patients without AF, with paroxysmal AF and persistent AF (total n=64). In AF patients, epicardial cell gene expression decreased, contrasting with an upregulation of epithelial to mesenchymal transition (EMT) and mesenchymal cell gene expression. Immunohistochemistry demonstrated thickening of the epicardium and an increased proportion of (myo)fibroblast-like cells in the myocardium, supporting enhanced EMT in AF. We furthermore report an upregulation of endothelial cell proliferation, angiogenesis and endothelial signalling. EMT and endothelial cell proliferation concurred with increased interstitial (myo)fibroblast-like cells and extracellular matrix gene expression including enhanced tenascin-c, thrombospondins, biglycan and versican. Morphological analysis discovered increased and redistributed glycosaminoglycans and collagens in the atria of AF patients. Signalling pathways, including cell-matrix interactions, PI3K-AKT and Notch signalling, that could regulate mesenchymal cell activation, were upregulated. These dynamic processes may provide targets to prevent or reverse structural remodelling.

  Study EGAS00001005295

• Study the differences at the trascriptome level between iNKT and T cells

  Chimeric antigen receptor anti-CD19 (CAR19)-T cell immunotherapy-induced clinical remissions in CD19+ B cell lymphomas are often short-lived. We tested whether CAR19-engineering of the CD1d-restricted invariant NKT (iNKT) cells would result in enhanced anti-lymphoma activity. CAR19-iNKT cells co-operatively activated by CD1d- and CAR19-CD19-dependent interactions are more effective than CAR19-T cells against CD1d-expressing lymphomas in vitro and in vivo. The swifter in vivo anti-lymphoma activity of CAR19-iNKT cells and their enhanced ability to eradicate brain lymphomas underpinned an improved tumor-free and overall survival. CD1d transcriptional de-repression by all-trans retinoic acid results in further enhanced cytotoxicity of CAR19-iNKT cells against CD19+ chronic lymphocytic leukemia cells. Thus, iNKT cells are a highly efficient platform for CAR-based immunotherapy of lymphomas and possibly other CD1d-expressing cancers.

  Study EGAS00001003176

• Expression quantitative trait loci influence DNA damage-induced apoptosis in cancer

  The analysis of e2QTL allows for the identification of context-specific eQTL effects (Kim-Hellmuth et al. (2017), PMID: 28814792). To evaluate how inter-individual genetic variability influences the regulation of DNA damage-induced apoptosis, we performed e2QTL analysis of CD8+ T cells from 461 healthy European participants stimulated with high doses of 5 different carcinogens. These include Methyl-methanesulfonate (MMS), tert-butyl-hydroperoxide (TBOOH), benzo(a)pyrene-7,8-diol-9,10-epoxide (BPDE), 4-hydroxycyclophosphamide (HC) and UVC radiation.

  Study EGAS50000000666

• Targeted_sequencing_of_genes_recurrently_mutated_in_AML___part2

  Genomic libraries will be generated from total genomic DNA derived from 4000 samples with Acute Myeloid Leukaemia. Libraries will be enriched for a selected panel of genes using a bespoke pulldown protocol. 64 Samples will be individually barcoded and subjected to up to one lanes of Illumina HiSeq. Paired reads will be mapped to build 37 of the human reference genome to facilitate the characterisation of known gene mutations in cancer as well as the validation of potentially novel variants identified by prior exome sequencing.

  Study EGAS00001000570

• Molecular analysis of FIT interval colorectal cancers

  To optimize a fecal immunochemical test-based screening program, the rate of missed colorectal cancers (CRCs), so-called FIT-interval CRCs, should be minimized. A specific molecular make-up of those CRCs could be an explanation for those interval CRCs. Knowledge of the molecular make-up of these missed lesions could facilitate more accurate detection of all precursor lesions. In this study we aimed to compare the molecular make-up of FIT-interval CRCs and screen-detected CRCs (SD-CRCs).

  Study EGAS00001004683