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• USARC 10X Genomics Single Cell DNA Sequencing Data

  We investigated the impact of ploidy heterogeneity on copy number inference at a single cell level using fluorescence-activated cell sorted (FACS) nuclei from an undifferentiated soft tissue sarcoma. FACS revealed the presence of three aberrant subpopulations, including a haploid, a near diploid and a whole genome doubled population. Once sorted, single cell nuclei underwent whole genome sequencing using the chromium CNV single cell DNA library kit (10X Genomics). We sequenced single normal nuclei (2n) and single aberrant / tumour nuclei (1n, 2n and 2n+).

  Dataset EGAD00001008668

• Neurodevelopment_Nantes_hospital

  The neurodevelopmental team in the genetics unit of Nantes hospital focus on the identification on new genes causing neurodevelopmental disorders through whole-genome and transcriptomics sequencing.

  Dac EGAC50000000542

• Genomic architecture and evolution of clear cell renal cell carcinomas defined by multiregion sequencing

  We applied multi-region exome sequencing to 10 clear cell renal carcinomas to resolve the genetic architecture, intra tumour heterogeneity and evolutionary histories of these tumours.

  Study EGAS00001000667

• RNA-seq data from DMD patients and healthy controls

  This dataset comprises RNA-seq expression profiles from 57 subjects, of which 39 are DMD patients and 18 healthy controls. The data are described in the following article: Signorelli, Ebrahimpoor et al. (in review). Peripheral blood transcriptome profiling enables monitoring disease progression in dystrophic mice and patients.

  Dataset EGAD00001006826

• Analyses of RNAseq data from NEN patient derived tumor organoids (PDTOs) and matched parental tumors

  The dataset includes RNA-seq expression R data, RNA-seq gene counts matrix, and RNA-seq gene FPKM matrix from 21 NEN tumors or metastases and matched PDTOs. The sequencing was done with either a Nextseq 2000 or a NovaSeq 6000 instrument.

  Dataset EGAD00001009994

• FASTQ files

  Raw FASTQ files obtained from in situ Hi-C of 16 normal B cells (3 naive B cells, 3 germinal center B cells, 3 plasma cells, and 3 memory B cells, together with a merge file for each subpopulation), 7 chronic lymphocytic leukemias (2 unmutated IGHV and 5 mutated IGHV), and 5 mantle cell lymphomas (2 conventional and 3 leukemic non-nodal).

  Dataset EGAD00001006485

• Dynamic human admixture histories over the past ~1,300 years at the northern Himalayan frontier

  Whole-genome sequencing data from ten present-day individuals from Himachal Pradesh, India. DNA from these ten present-day individuals was converted to double-stranded libraries and sequenced on Illumina NovaSeq 6000 in 150 bp paired-end mode. The dataset consists of raw fastq and bam (hg19) files.

  Dataset EGAD50000001925

• Primary breast cancers and paired brain metastases

  Targeted next-generation-sequencing of 494 cancer-associated genes was done in a series of 14 frozen pairs of matched primary breast cancers and brain metastases (28 samples). DNA libraries of all coding exons were prepared using the Haloplex Target Enrichment System. Sequencing was done using the 2*150bp paired-end technology on the Illumina NextSeq500 platform.

  Dataset EGAD00001004309

• Biallelic HMBS Inactivation Defines a Homogenous Clinico-Molecular Subtype of Hepatocellular Carcinoma

  Acute intermittent porphyria (AIP), caused by heterozygous germline mutations of the heme synthesis pathway enzyme HMBS (hydroxymethylbilane synthase), confers high risk of hepatocellular carcinoma (HCC) development. Yet, the role of HMBS in liver tumorigenesis remains unclear. Here we explore HMBS alterations in a large series of 758 HCC. We identify recurrent bi-allelic HMBS inactivation, both in AIP patients acquiring a second somatic HMBS mutation and in sporadic HCC with two somatic hits. HMBS alterations are enriched in truncative mutations, in particular in splice regions, leading to abnormal transcript structures. Bi-allelic HMBS inactivation results in a massive accumulation of its toxic substrate porphobilinogen and synergizes with CTNNB1 activating mutations, leading to the development of well differentiated tumors with a transcriptomic signature of Wnt/ß-catenin pathway activation and a DNA methylation signature related to ageing. HMBS-inactivated HCC mostly affect females, in absence of fibrosis and classical HCC risk factors. These data identify HMBS as a tumor suppressor gene whose bi-allelic inactivation defines a homogenous clinical and molecular HCC subtype.

  Study EGAS00001005986

• Patient-Specific Factors Influence Somatic Variation Patterns in Von Hippel-Lindau Disease Renal Tumors

  Patients affected with von Hippel-Lindau disease are at risk of developing multiple independent clear cell renal carcinomas. This study performed whole genome sequencing on 40 tumors from 6 VHL patients to compare somatic variation patterns within and between patients. Although tumors from the same patient showed many differences, within-patient patterns were discernible. Single-nucleotide substitution type rates were significantly different between patients and showed biases in trinucleotide mutation context. We also observed biases in chromosome copy number aberrations. These results show that genetic background and/or environment can influence the types of mutations that occur.

  Study phs001107