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• MutWP4: CRUK Grand Challenge Mutographs of Cancer: Gastric Organoids (2019-08-07)

  The Mutographs project aims to advance our understanding of the causes of cancer through studies of mutational signatures. Led by Mike Stratton, together with Paul Brennan, Ludmil Alexandrov, Allan Balmain, David Phillips and Peter Campbell, this large-scale international research endeavour was awarded a Cancer Research UK Grand Challenge. Different patterns of somatic mutation are generated by the different environmental, lifestyle and genetic factors that cause cancer, many of them are still unknown. Within Mutographs, Kings College London will characterise the mutational signatures induced by putative human carcinogens in order to identify the origins of mutational signatures found in human cancers. To achieve this human organoid cell cultures will be exposed to a representative catalogue of known or suspected human carcinogens and mutagens and, using whole genome sequencing, the patterns of mutations induced by them will be determined. Somatic mutational signatures will be subsequently extracted by non-negative matrix factorisation methods and correlated with exposure data. Through an enhanced understanding of cancer aetiology, Mutographs unprecedented effort is anticipated to outline modifiable risk factors, lead to new approaches to prevent cancer, and provide opportunities to empower early detection, refine high-risk groups and contribute to further therapeutic development. . This dataset contains all the data available for this study on 2019-08-07.

  Dataset EGAD00001005234

• Single-cell RNA-sequencing of CD19 Chimeric Antigen Receptor (CAR) T-cells (CD19 CAR T-cells) from a Phase I clinical study in paediatric ALL: CARPALL

  Chimeric antigen receptor (CAR)-modified T-cells have become established as an effective treatment of haematological cancers. In the context of relapsed and refractory childhood pre-B cell acute lymphoblastic leukaemia (B ALL), CD19 targeting CAR T-cells often induce durable remissions. Previously, we generated a novel low-affinity CAR incorporating a CD19-specific single-chain variable fragment (scFV) called CAT, displaying a faster off-rate of interaction than the FMC63 CD19 binder used in prior clinical studies. Here, we systematically analysed CD19 CAR T-cells of ten children with relapsed or refractory B ALL enrolled in the CARPALL trial (NCT02443831). To characterize persisting CD19 CAR T-cells, we performed high throughput single-cell gene expression and T-cell receptor (TCR) sequencing of infusion products and serial blood and bone marrow samples up to five years post-infusion. We isolated CAR T-cells from peripheral blood or bone marrow by flow cytometry for CD3 and CAR expression, prior to single cell sequencing (Chromium 10X) platform.

  Dataset EGAD00001010018

• Exome sequencing of UK Birth Cohorts - Born in Bradford

  Birth cohort studies involve repeated surveys of large numbers of individuals from birth and throughout their lives. They collect information useful for a wide range of life course research domains, and biological samples which can be used to derive data from an increasing collection of omic technologies. This rich source of longitudinal data, when combined with genomic data, offers the scientific community valuable insights from population genetics to rare disease associations. Avon Longitudinal Study of Parents and Children (ALSPAC)recruited 14,775 babies of predominantly White ethnicity in the Avon county of south-west England between 1991 and 1992. Born in Bradford (BiB) is similarly focused on a particular local area, the city of Bradford in the north of England, and recruited 13,858 babies between 2007 and 2011, of whom ~41% self-report as white British and ~59% as other ethnicities, predominantly Pakistani. Millennium Cohort Study (MCS) is a national cohort that recruited 18,827 children born between 2000 and 2002, intentionally over-sampling areas with high child poverty, large ethnic minority populations, and smaller UK nations (Wales, Scotland and Northern Ireland) Available here is a subset of exome-sequenced parents and children from these studies (CRAMS and post-QC VCFs) as detailed in https://doi.org/10.12688/wellcomeopenres.22697 [doi.org]. Phenotypic data is also available by submitting an application to the corresponding cohort: https://borninbradford.nhs.uk/ [borninbradford.nhs.uk]

  Dataset EGAD00001015370

• Sperm sequencing reveals extensive positive selection in the human germline -WGS

  Mutations that occur during human ageing in the cell lineages of sperm or eggs have the potential to be transmitted to offspring. In males, positive selection of driver mutations during spermatogenesis is known to increase the birth prevalence of certain developmental disorders and cancer predisposition syndromes. However, direct observation of the scope of this selection in sperm has been limited by the error rates of sequencing technologies. Using the duplex sequencing method known as NanoSeq, we sequenced bulk sperm samples from individuals aged 24 to 75 years. Our findings revealed a linear accumulation mutations per year and mutational signatures consistent with pedigree studies. Deep targeted and deep exome NanoSeq of sperm samples identified genes subject to significant positive selection in the male germline, which are linked to diverse cellular pathways including RAS/MAPK and BMP signaling. Strikingly, nearly all positively selected genes are associated with developmental or cancer predisposition disorders in children. We find that this effect drives an elevated risk of known likely disease-causing mutations in sperm across a wide age range. This implies that the disorders attributed to these genes likely exhibit elevated birth prevalence in human populations, particularly among older fathers. These findings shed light on the dynamics of germline mutations and highlight an increased disease risk for children born to fathers of advanced age.

  Dataset EGAD00001015592

• Sperm sequencing reveals extensive positive selection in the human germline -NanoSeq

  Mutations that occur during human ageing in the cell lineages of sperm or eggs have the potential to be transmitted to offspring. In males, positive selection of driver mutations during spermatogenesis is known to increase the birth prevalence of certain developmental disorders and cancer predisposition syndromes. However, direct observation of the scope of this selection in sperm has been limited by the error rates of sequencing technologies. Using the duplex sequencing method known as NanoSeq, we sequenced bulk sperm samples from individuals aged 24 to 75 years. Our findings revealed a linear accumulation mutations per year and mutational signatures consistent with pedigree studies. Deep targeted and deep exome NanoSeq of sperm samples identified genes subject to significant positive selection in the male germline, which are linked to diverse cellular pathways including RAS/MAPK and BMP signaling. Strikingly, nearly all positively selected genes are associated with developmental or cancer predisposition disorders in children. We find that this effect drives an elevated risk of known likely disease-causing mutations in sperm across a wide age range. This implies that the disorders attributed to these genes likely exhibit elevated birth prevalence in human populations, particularly among older fathers. These findings shed light on the dynamics of germline mutations and highlight an increased disease risk for children born to fathers of advanced age.

  Dataset EGAD00001015590

• Sperm sequencing reveals extensive positive selection in the human germline -TargetedNanoSeq

  Mutations that occur during human ageing in the cell lineages of sperm or eggs have the potential to be transmitted to offspring. In males, positive selection of driver mutations during spermatogenesis is known to increase the birth prevalence of certain developmental disorders and cancer predisposition syndromes. However, direct observation of the scope of this selection in sperm has been limited by the error rates of sequencing technologies. Using the duplex sequencing method known as NanoSeq, we sequenced bulk sperm samples from individuals aged 24 to 75 years. Our findings revealed a linear accumulation mutations per year and mutational signatures consistent with pedigree studies. Deep targeted and deep exome NanoSeq of sperm samples identified genes subject to significant positive selection in the male germline, which are linked to diverse cellular pathways including RAS/MAPK and BMP signaling. Strikingly, nearly all positively selected genes are associated with developmental or cancer predisposition disorders in children. We find that this effect drives an elevated risk of known likely disease-causing mutations in sperm across a wide age range. This implies that the disorders attributed to these genes likely exhibit elevated birth prevalence in human populations, particularly among older fathers. These findings shed light on the dynamics of germline mutations and highlight an increased disease risk for children born to fathers of advanced age.

  Dataset EGAD00001015591

• MutWP4: CRUK Grand Challenge Mutographs of Cancer: Pancreatic Organoids (2021-02-02)

  The Mutographs project aims to advance our understanding of the causes of cancer through studies of mutational signatures. Led by Mike Stratton, together with Paul Brennan, Ludmil Alexandrov, Allan Balmain, David Phillips and Peter Campbell, this large-scale international research endeavour was awarded a Cancer Research UK Grand Challenge. Different patterns of somatic mutation are generated by the different environmental, lifestyle and genetic factors that cause cancer, many of them are still unknown. Within Mutographs, Kings College London will characterise the mutational signatures induced by putative human carcinogens in order to identify the origins of mutational signatures found in human cancers. To achieve this human organoid cell cultures will be exposed to a representative catalogue of known or suspected human carcinogens and mutagens and, using whole genome sequencing, the patterns of mutations induced by them will be determined. Somatic mutational signatures will be subsequently extracted by non-negative matrix factorisation methods and correlated with exposure data. Through an enhanced understanding of cancer aetiology, Mutographs unprecedented effort is anticipated to outline modifiable risk factors, lead to new approaches to prevent cancer, and provide opportunities to empower early detection, refine high-risk groups and contribute to further therapeutic development. . This dataset contains all the data available for this study on 2021-02-02.

  Dataset EGAD00001006933

• Targeted Myeloid DNA-Panelsequencing, MLL

  Sequencing data from a targeted myeloid DNA-Panelsequnencing at the MLL Dx, Munich lab. Targeted sequencing was performed using the Nextera DNA Flex library preparation kit, starting with 100ng of genomic DNA (Illumina, San Diego, CA, USA). The target regions were enriched by a custom xGen Lockdown panel using a hybridization capture workflow (IDT Integrated DNA Technologies, Coralville, IA, USA). All libraries were sequenced with 100bp paired-end reads on a NovaSeq6000 (Illumina) with a mean coverage of 3206x. Somatic variant calling was performed with Pisces and a sensitivity cut off of 2%. Large deletions and medium-sized insertions, as they are for example found in CALR and FLT3, were called with Pindel. Variant annotation considered the publicly available data bases Cosmic (v91), ClinVar (2020-03), gnomAd (non-cancer, v2.1.1), dbNSFP (v3.5) and UMD TP53 (2017_R2). Variants that are described as somatic, protein truncating or affecting splice sites were considered as mutations while variants with no or discrepant data base information were considered as variant of uncertain significance.

  Dataset EGAD00001008485

• Integrated single-cell profiling dissects cell-state-specific enhancer landscapes of human tumor infiltrating T cells.

  Despite extensive studies on the chromatin landscape of exhausted T cells, the transcriptional wiring underlying functional and dysfunctional states of human tumor infiltrating lymphocytes (TILs) is incompletely understood. Here, we identify tissue-specific and general gene-regulatory landscapes in the wide breadth of CD8+ TIL functional states covering four cancer entities using single-cell chromatin profiling. We map enhancer-promoter interactions in human TILs by integrating single-cell chromatin accessibility with single-cell RNA-seq data from tumor entity-matching samples and prioritize key elements by super enhancer analysis. Our analysis reveals a human core chromatin trajectory to TIL dysfunction and identifies key enhancers, transcriptional regulators, and deregulated target genes involved in this process. Finally, we validate enhancer regulation at loci encoding PD1, TCF1, and TIM3 by targeting non-coding regulatory elements with potent CRISPR activators and repressors. In summary, our study advances the understanding of molecular regulation of TIL (dys-)function and provides a framework for modulating immunotherapeutic relevant TIL genes via their enhancers.

  Dataset EGAD00001008662

• Dataset for colorectal_cancer-RNA

  Rare cancer sequencing data of 97 runs in tumor/control pairs, which were uploaded to umbrella studies. The sequencing was always paired

  Dataset EGAD00001008855