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• MPNST - 10X single nucleus RNAseq

  Understanding the spatial and temporal dynamics of tumour evolution is crucial for determining the drivers of cancer progression. Here, we comprehensively profile a primary malignant peripheral nerve sheath tumour (MPNST) and its recurrence with a multi-omic and spatial approach at single-cell resolution. Leveraging the extensive heterogeneity in copy number aberrations (CNAs) as a native barcoding system, we fully resolve the evolutionary tree of this tumour revealing multi-furcations suggestive of ongoing chromosomal instability. We show gene dosage effects contribute to phenotypic diversity and are predominantly linear with the exception of FOS in a specific subclone. Using laser capture microdissection, we performed spatial lineage tracing in a human tumour, elucidating the relationship between local expansions and interactions between tumour cells and the microenvironment.

  Study EGAS50000001787

• AYA glioma NGS

  Gliomas are a major cause of cancer-related death in adolescents and young adults (AYA, ages 15-39 years). Different molecular alterations drive gliomas in children and adults leading to distinct biology and clinical consequences. At the convergence of these age groups - the AYA population – little is known about the implications of pediatric vs adult-type alterations. To address this, we analyzed a population-based cohort of 1456 clinically and molecularly characterized gliomas aged 0-39 years. Potentially targetable pediatric-type alterations were found in 31% of AYA gliomas and conferred superior outcomes compared to adult-type alterations. This submission includes the generated NGS data for children, adolescent, and young adults with gliomas. Data includes targeted panel of glioma genes and low-pass WGS (1x coverage).

  Study EGAS50000000383

• Combination therapies for personalized cancer medicine

  It is the ambition of the team formed by members of the Netherlands Cancer Institute (NKI) and the Cancer Genome Project at the Wellcome Trust Sanger Institute (WTSI) to unravel the genomic and phenotypic complexity of human cancers in order to identify optimal drug combinations for personalized cancer therapy. Our integrated approach will entail (i) deep sequencing of human tumours and cognate mouse tumours; (ii) drug screens in a 1000+ fully characterized tumour cell line panel; (iii) high-throughput in vitro and in vivo shRNA and cDNA drug resistance and enhancement screens; (iv) computational analysis of the acquired data, leading to significant response predictions; (v) rigorous validation of these predictions in genetically engineered mouse models and patient-derived xenografts. This integrated effort is expected to yield a number of combination therapies and companion-diagnostics biomarkers that will be further explored in our existing clinical trial networks.

  Dataset EGAD00001000869

• H3Africa - Respiratory Microbiota of African Children

  Shotgun metagenomic sequencing of nasopharyngeal (NP) samples, from children enrolled in a PCV13-vaccinated South African birth cohort was used to explore strain-level pneumococcal colonization patterns and transmission dynamics, and associated antimicrobial-resistance determinants. NP swabs were collected at two-week intervals from birth through the first year of life from 137 infants. Pneumococcal isolates were serotyped and tested for phenotypic antimicrobial resistance. 196 NP samples from a subset of 23 infants were then selected based on changes in serotype or antimicrobial resistance. DNA was extracted directly from the enriched NP samples and shotgun metagenomic sequencing performed. Reads were assembled and aligned against reference pneumococcal genomes. in silico pneumococcal capsular, multilocus sequence typing, and resistome analyses were performed.

  Study EGAS00001004401

• Comprehensive genetic analysis of uveal melanoma heterogeneity during metastatic progression

  Uveal melanoma (UM) is the most common primary intraocular malignancy in adults. Despite improvement of diagnosis and treatment of the primary tumor, there is no effective treatment of metastatic disease and approximately half of patients will die within one year or less following metastases detection. Tumor heterogeneity has been proposed as a key factor of drug resistance. However, it has been scarcely studied in UM. The present project aims searching for specific drivers of the metastatic progression, describing the genomic and transcriptomic landscape of metastatic UM, exploring tumor heterogeneity and investigating its role in drug resistance. Thus whole exome sequencing and transcriptomics have been performed on constitutional, primary tumor and metastatic samples from 28 UM patients.

  Study EGAS00001002761

• Aberrant ERBB4-SRC Signaling as a Hallmark of Group 4 Medulloblastoma Revealed by Integrative Phosphoproteomic Profiling

  The four main medulloblastoma subgroups are characterized by distinct biology, clinicopathological features and clinical outcomes. While the WNT and SHH subgroups are characterized by clearly defined aberrant signaling of developmental pathways, the underlying biology of Group 3 and 4 remains poorly understood. Here, we delineate distinct post-translational regulation orchestrating active oncogenic signaling networks in Groups 3 and 4. Specifically, aberrant ERBB4-SRC signaling constitutes a novel hallmark feature of Group 4, with great promise as a novel oncogenic mechanism and potential vulnerability for therapeutic intervention in the most common subgroup. Altogether, this novel integrative proteogenomic landscape demonstrates the added value of proteomics and phosphoproteomics analysis to discover and exploit unexpected oncogenic mechanisms in medulloblastoma and beyond.

  Study EGAS00001002757

• Targeted deep sequencing on Pediatric MDS

  Targeted NGS using custom panels with SAMD9, SAMD9L genes and 22 single nucleotide polymorphisms (SNP) on chromosome 7q (allele frequency >35% in all ethnic sub-populations in gnomAD) (Ampliseq #IAD10417) was performed in 667/669 cases. Additionally, 559 cases were sequenced using 28 pediatric MDS genes (GATA2, RUNX1, HOXA9, CEBPA, GATA1, KRAS, NRAS, CBL, PTPN11, ASXL1, EZH2, SETBP1, FLT3, KIT, JAK2, JAK3, CSF3R, MPL, SH2, BCOR, BCORL1; RAD21, STAG2, CTCF, TP53, PTEN, CALR, VPS45; Ampliseq #IAD51150). Libraries for targeted NGS were prepared using NEBNext Ultra II DNA library prep kit (New England BioLabs, cat#E7645S/L) per manufacturer’s instruction and samples were sequenced on an Illumina Miseq 2000 with 2 x 150 bp reads. The BAM files are uploaded here.

  Study EGAS00001005431

• Myocardial Infarction Genetics Exome Sequencing Consortium: Malmo Diet and Cancer Study

  The Malmo Diet and Cancer Study (MDCS) is a community-based prospective epidemiologic cohort of 28,449 subjects who were recruited for baseline examination between 1991 and 1996. From this cohort, 6103 subjects were randomly selected to participate in a cardiovascular cohort (MDCSCC), which seeks to investigate risk factors for cardiovascular disease. This study is a subset of those samples. All exome sequencing was performed at the Broad Institute of Harvard and MIT; samples sequence capture was performed using Illumina's ICE Capture reagent and sequencing was performed on an Illumina HiSeq 2000 or 2500.

  Study phs001101

• High-Throughput RNA Isoform Sequencing using Programmable cDNA Concatenation

  MAS-ISO-seq is a novel technique for programmably concatenating cDNAs into single molecules for optimal long-read sequencing. In practice, this boosts throughput >15 fold to nearly 40 million cDNA reads per run on the PacBio Sequel IIe sequencer. We have validated this method via application to synthetic RNA isoforms and single-cell sequencing of tumor-infiltrating T cells. Results demonstrated a >30 fold boosted discovery of differentially spliced genes and robust cell clustering, as well as canonical PTPRC splicing patterns across T cell subpopulations and the concerted expression of the associated hnRNPLL splicing factor.

  Study phs003200

• NCI CCSG CCDI Supplement Additional Genomic Submission

  The implementation of targeted therapies for acute myeloid leukaemia (AML) has been challenging because of the complex mutational patterns within and across patients as well as a dearth of pharmacologic agents for most mutational events. This supplement data from the Beat AML program provides Adolescent and Young Adult (AYA) and pediatric tumor specimens not previously released. These data include exome and RNA level characterization as well as analyses of ex vivo drug sensitivity. Collectively, this data can be leveraged to address clinical, genomic, transcriptomic and functional analyses of the biology of leukemia in pediatric and AYA populations.

  Study phs002599