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• Exome-wide analysis identifies three low-frequency missense variants associated with pancreatic cancer risk in Chinese populations

  Germline coding variants have not been systematically investigated for pancreatic ductal adenocarcinoma (PDAC). Here, we report an exome-wide investigation using the Illumina Human Exome Beadchip with 943 PDAC cases and 3,908 controls in the Chinese population, followed by two independent replicate samples including 2,142 cases and 4,697 controls. We identify three low-frequency missense variants associated with the PDAC risk: rs34309238 in PKN1 (OR = 1.77, 95% CI: 1.48-2.12, P = 5.35 X 10-10), rs2242241 in DOK2 (OR = 1.85, 95% CI: 1.50-2.27, P = 4.34 X 10-9) and rs183117027 in APOB (OR = 2.34, 95% CI: 1.72-3.16, P = 4.21 X 10-8).

  Study EGAS00001003040

• Molecular profiling of longitudinally observed small colorectal polyps: a cohort study

  Knowledge of the natural history of colorectal adenomas is limited because these lesions are removed upon detection. The few studies in which small adenomas have been left in situ for a limited period of time have shown that most lesions remain stable or even completely vanish. Lesions that have grown in size more often turn out to be advanced adenomas when resected. Specific DNA copy number changes (cancer associated events or CAEs) are associated with progression of adenomas to cancer. The aim of the study was to evaluate whether growth of small colorectal polyps left in situ is associated with specific molecular features.

  Study EGAS00001003284

• Genome Wide Association Study:GR@ACE Stage I

  The Genome Research program at Fundacio ACE (GR@ACE, Barcelona, Spain), represents a new effort to study Alzheimer's Disease susceptibility. The GR@ACE study comprises 7,409 unrelated individuals. 4,120 AD cases were diagnosed at Fundació ACE Memory Clinic (Barcelona, Spain). 3,289 Controls were obtained from three collections (Fundació ACE, Barcelona; DNA National Biobank, Salamanca and HU Valme, Seville). Genotyping was carried out using the 815K Axiom Spain Biobank array (Affymetrix.) in the Spanish national center for genotyping (CEGEN, Santiago de Compostela, Spain). After genotyping, an extensive quality control was conducted, including re-sampling, gender match, stratification, relatedness, heterozygosity, differential missingness and HWD analyses.

  Study EGAS00001003424

• Exome-sequencing of two UFM individuals and their Fragile X family members.

  Fragile X syndrome (FXS) is a monogenic neurodevelopmental disease often caused by a CGG triplet expansion in the 5’UTR of the FMR1 gene, which results in DNA methylation of the FMR1 promoter and its transcriptional silencing. Exceptional healthy individuals named "unmethylated full mutation (UFM)" have been identified in the families of FX patients. They carry an expanded CGG repeat, but show normal FMR1 epigenetic configuration and expression. In this study we performed exome-sequencing of two UFM individuals and their family members to identify possible genetic mutations responsible for the escape of silencing in the unmethylated full mutation (UFM) phenotype.

  Study EGAS00001001737

• Native_American_Ancient_DNA_sequencing

  The morphology of the first humans in the Americas (Paleoamericans) differs from that of Native Americans, and has raised the question of whether or not there are also differences in origin or genetics. A few populations who survived until relatively recently have been suggested to retain Paleoamerican morphology. One of these populations is from La Jolla. Here, we have generated genome sequence data from four La Jolla individuals in order to investigate these questions 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 EGAS00001001802

• LifeLines-DEEP population multi-omix cohort from the noth of the Netherlands.

  The LifeLines-DEEP cohort is a sub-cohort of the LifeLines cohort (167,729 participants) that employs a broad range of investigative procedures to assess the biomedical, socio-demographic, behavioral, physical and psychological factors that contribute to health and disease in the general Dutch population, (Scholtens 2015). A subset of approximately 1,500 participants also took part in LifeLines-DEEP. For these participants, additional biological materials were collected, including analysis of the gut microbiome composition. The phenotyping and processing of LifeLines-DEEP has been described in Tigchelaar (2015).

  Study EGAS00001001704

• Investigating_low_frequency_variants_in_CAD_MI_cases__controls_and_pedigrees_using_whole_exome_sequencing_and_custom_pulldowns

  The Cardiogenics re-sequencing study will consist of three parts: Eight pools of 25 individuals will be sequenced using a Nimblegen hybrid-capture solution specific to miRNA sequences, 80 pools of 25 individuals will be sequenced using a custom Agilent SureSelect array covering genes associated with coronary artery disease (CAD) and myocardial infarction (MI), 10 individuals from families with a history of CAD/MI will be exome sequenced using the Sanger exome array. The experiment will use the early onset patients from the German MI cohort and the UK BHF CAD/MI cohort both of which have strong family history. For controls we will consider individuals from the UKBS and KORA cohorts.

  Study EGAS00001000043

• Investigating_low_frequency_variants_in_CAD_MI_cases__controls_and_pedigrees_using_whole_exome_sequencing_and_custom_pulldowns

  The Cardiogenics re-sequencing study will consist of three parts: Eight pools of 25 individuals will be sequenced using a Nimblegen hybrid-capture solution specific to miRNA sequences, 80 pools of 25 individuals will be sequenced using a custom Agilent SureSelect array covering genes associated with coronary artery disease (CAD) and myocardial infarction (MI), 10 individuals from families with a history of CAD/MI will be exome sequenced using the Sanger exome array. The experiment will use the early onset patients from the German MI cohort and the UK BHF CAD/MI cohort both of which have strong family history. For controls we will consider individuals from the UKBS and KORA cohorts.

  Study EGAS00001000050

• Somatic_mutation_and_clonal_evolution_in_premalignant_lung_disease___WGS

  Cancer is a genetic disease caused by an accumulations of mutations, however many of these mutations have been identified in pathologically normal tissue. We aim to use laser-capture microscopy (LCM) to sample individual clones from the lung tissue of individuals with a variety of lung diseases (COPD, UIP, IPF, Emphysema, pulmonary hypertension). This will allow us to identify whether cancer-associated mutations appear in this normal tissue, assess the mutational burden present, and identify the mutational processes causing these mutations. Smoking is a large risk factor for developing many of these lung diseases so we are particularly keen to determining whether there is evidence of a smoking signature in these patients.

  Study EGAS00001002747

• MutWP5__CRUK_Mutographs_of_Cancer__Lung__PD38234__Targeted_

  Sequencing of LCM-derived microbiopsies from explanted lung from pulmonary fibrosis patient. Goal to assess the mutational burden, spectrum, and clonal dynamics within the tissue. Deep sampling throughout multiple regions of the lung will determine whether there are differences in smoking-related mutation burden in different portions of the lung. Targeted sequencing will be conducted on samples to identify drivers of interest and clonality of the samples, well-performing samples will be sent for subsequent whole-genome sequencing. Results from this portion of the study will be compared to other individuals with smoking-related diseases (COPD, pulmonary fibrosis, lung cancer), and normal, non-smoking lungs.

  Study EGAS00001003325