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• Mutation of FOXL2 in granulosa cell tumors of the ovary

  We generated paired-end RNA-Seq data using the Illumina Genome Analyzer II platform for four adult granulosa cell tumours (GCTs) of the ovary (1 primary, 3 recurrent). We screened this data for the presence of GCT specific sequence variants and detected a non-synonymous mutation in the FOXL2 gene that was found to be recurrent in 97% of 89 additional GCTs. To measure genomic stability of the four index cases, we generated Affmetrix SNP 6.0 data and analysed these data for copy number changes. Raw sequence reads as well as Affymetrix CEL files are available to applicants.

  Study EGAS00000000040

• Whole_Exome_Sequencing_for_Characterization_of_Disease_Causing_Mutations_in_two_Pakistani_Families_Suffering_from_Autosomal_Recessive_Ocular_Disorders_

  We propose to use whole exome Agilent solutionprobes and paired end Illumina sequencing to sequence 4 individualsfrom two families suffering from novel autosomal recessive disease[microphthalmia, MOP (OMIM %251600) and non-syndromic persistenthyperplastic primary vitreous, PHPV (OMIM %611311)]. Selectedcandidate variants will subsequently be genotyped in the remainingfamily members in Pakistan with the aim of identifying the rarehomozygous recessive mutations responsible for the disease phenotype. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/

  Study EGAS00001000026

• Primary plasma cell leukemia (pPCL) samples were sequenced using the Nimblegen MedExome hybridization capture to detect translocations, copy number changes, and mutations in 20 pPCL samples and patient matched controls.

  Primary plasma cell leukemia (pPCL) is a rare malignancy related to multiple myeloma. Here we have assembled 20 patient samples and performed whole exome sequencing to determine the differences between multiple myeloma and pPCL. CD138+ cells were purified from bone marrow aspirates from patients with pPCL. Control cells were obtained from CD34+ stem cell harvests or CD3+ T cells. DNA was extracted and processed using the HyperPlus library prep kit (KAPA Biosystems) and sequenced using 75 bp paired end reads on an Illumina NextSeq500.

  Study EGAS00001003104

• 300BCG study ATAC-seq data: human population variation of trained immunity

  ATAC-seq dataset for the paper: Title Multi-omics analysis of human population variation in immune function and in vivo response to BCG vaccination Abstract Immune responses are tightly regulated, yet highly variable between individuals. To investigate human population variation of trained immunity, we immunized healthy individuals with Bacillus Calmette-Guérin (BCG). This live attenuated vaccine induces not only an adaptive immune response against tu-berculosis, but also triggers innate immune activation and memory. We established personal immune profiles and chromatin accessibility maps over a time course of BCG vaccination in 323 individuals. This large resource uncovered genetic and epigenetic predictors of baseline immunity and BCG vaccine response. We found that BCG vaccination enhances the innate immune response only in individuals with dormant immune states at baseline, suggesting that exogeneous induction of trained immunity is not a universal booster of innate immunity, but specifically elevates weak innate immune responses. This study advances our understanding of BCG’s heterologous immune-stimulatory effects and trained immunity in humans. Moreover, our results highlight the value of epigenetic cell states as an “endo-phenotype” that connects immune function with genotype and the environment.

  Dataset EGAD50000000123

• Gut 16S rRNA/FINRISK 2002

  Gut microbiome 16S rRNA raw data for N=7174 FINRISK 2002 participants. FINRISK fecal samples were mailed to the Knight laboratory at the University of California (San Diego, CA), for microbiota sequencing using the standard Earth Microbiome Project protocols (https://earthmicrobiome.org/protocols-and-standards/). DNA was extracted using a magnetic bead-based DNA extraction protocol. Amplicon sequence data for the V4 region of the 16S rRNA gene was generated using 515F (Parada) and 806R (Apprill) primers. For a total of 25μl reaction volume, 13 µl PCR-grade water was combined with 10 µl PCR master mix (Platinum Hot Start PCR Master Mix, 2x, ThermoFisher), 0.5 µl forward primer (10 µM), 0.5 µl reverse primer (10 µM), and 1 µl template DNA. Amplification was performed in triplicate reactions, and triplicate PCR reactions were pooled afterwards. Expected products were visualized on agarose gels (300–350 bp) and quantified with Quant-iT PicoGreen dsDNA kit (Invitrogen). Equal amounts (240 ng) of amplicon were combined for each sample and cleaned (MoBio UltraClean PCR Clean-Up Kit). Cleaned amplicon pools were sequenced with 515F and 806R primers.

  Dataset EGAD50000000287

• Genomic gain of EBV's LMP-1 in NKTCL

  The study found a high recurrence of genomic gain of LMP1 locus within EBV-associated NKTCL. The pilot data set and extended dataset of 77 WGS NKTCLs found 18/77 tumoral genomes to harbour genomic gain of LMP-1 locus within the EBV viral genomes within NKTCL tumoral sequencing data. The study also found 1/10 NKTCL cell lines to be positive for LMP-1 locus gain within EBV genomes too. This dataset includes solely the confirmatory WGS data of LMP-1 gain from NKYS cell lines using Oxford Nanopore long-read sequencing technology.

  Study EGAS50000000260

• Novel Factors for Unexplained Phenotypes of Subclinical Carotid Atherosclerosis

  The overall goal for this study was to determine the genetic factors associated with extreme phenotypes of subclinical atherosclerosis (protective and deleterious). Study participants were selected from the Northern Manhattan Study (NOMAS), a population based cohort study investigating stroke and stroke risk factors in Northern Manhattan. Cases and controls were individuals at the extreme ends of the distribution for carotid intima-media thickness and carotid plaque, with cases defined as individuals with subclinical atherosclerosis that could not be explained by traditional vascular risk factors (USAth) and controls defined as individuals with unexplained protection against atherosclerosis (UPAth).

  Study phs001560

• Transcriptomic Profiling of Patient Derived Alternative Lengthening of Telomeres (ALT) and Non-MYCN-Amplified Neuroblastoma Cell Lines

  Patient derived neuroblastoma cell lines are excellent tools to study biology of the disease. While many previous studies sequenced neuroblastoma cell lines, there are very few ALT and non-MYCN-amplified neuroblastoma cell lines that were sequenced previously. Here, we present raw RNA sequencing data for 3 ALT (CHLA-90, SK-N-FI, COG-N-515) and 8 non-MYCN-amplified telomerase positive (CHLA-171, Felix, COG-N-579h, COG-N-615, COG-N-618h, COG-N-619h, COG-N-708h, COG-N-709) neuroblastoma cell lines. Additionally, gene expression data are provided as a supplement files.

  Study phs002421

• Pooled Genome-Wide Analysis of Kidney Cancer Risk (KIDRISK)

  Incidence rates of renal cell carcinoma (RCC) are rising and the latest estimates show that it accounts for over 300,000 cases and 120,000 deaths worldwide each year. Mechanisms underlying RCC occurrence are not fully understood and a large part of the disease heritability remains unexplained. The study aimed at augmenting the size of available RCC genome-wide association studies to increase the statistical power to detect genetic variants associated with the disease. The study includes genome-wide genotyping data from RCC cases (n=2,781) and controls (n=2,526) recruited in Western Europe, Central and Eastern Europe, and Australia.

  Study phs001271

• Subtyping Sub-Saharan Esophageal Squamous Cell Carcinoma by Comprehensive Molecular Analysis

  Esophageal squamous cell carcinoma (ESCC) occurs as much as 20x more frequently in sub-Saharan Africa than Western countries. Through the UNC-Malawi project collaboration we obtained whole-exome matched tumor/normal and RNA sequencing of 59 ESCC from Malawi between 2011-2012. DNA analysis revealed similar mutations as other cohorts, while RNA analysis revealed three distinct subtypes. Mutational signature analysis revealed a pattern of mutation not previously reported in other cohorts or more broadly. Taken together this suggests the high prevalence of ESCC in the region is secondary to an as yet identified mutagen.

  Study phs001448