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• BLUEPRINT Gene expression analysis during human B-cell differentiation using the Affymetrix Human Genome U219 Array

  We performed gene expression analysis using the Affymetrix Human Genome U219 Array of 9 subpopulations covering the complete B-cell maturation program: hematopoietic progenitor cells (HPC); pre-B-I cells (preB1C); pre-B-II cells (preB2C); naive B cells from peripheral blood (naiBC); naive B cells from tonsil (t-naiBC); germinal center B cells (gcBC); plasma cells from tonsil (t-PC); memory B cells from peripheral blood (memBC) and plasma cells from bone marrow (bm-PC). All the samples were isolated from healthy donors and, with the exception of bm-PC (only 1 replicate), we used 3 to 11 biological replicates of each subtype.

  Study EGAS00001001197

• Carbamazepine-induced hypersensitivity reactions in Europeans

  An antiepileptic drug carbamazepine is well tolerated by the majority of patients, but can cause severe and potentialy fatal hypersensitivity reactions in a small number of individuals. The aim of this study was to identify genetic predictors of hypersensitivity reactions to carbamazepine. We undertook a genome-wide association study (GWAS) in 22 patients of European ancestry with carbamazepine-induced hypersensitivity syndrome (HSS) and compared our data with genotypes from a healthy population within the WTCCC. We performed imputation of classical HLA alleles according to a recently described method (Science. 2010 Dec 10;330(6010):1551-7. Epub 2010 Nov 4). GWAS statistical analysis was performed using logistic regression with an additive model of inheritance.

  Study EGAS00000000037

• Metformin for Oral Cancer Prevention

  The M4OC-PREVENT clinical trial addressed whether metformin has utility in the prevention of oral cancer. It is a phase IIa clinical trial of metformin ER 2,000 mg per day given for 12-14 weeks to individuals with oral premalignant lesions, either oral leukoplakia or erythroplakia (which are precursors to oral cancer). The goal was to determine if metformin decreases the size of oral leukoplakia (clinical response). Additionally, effects on biomarkers of cancer risk and metformin effect were ascertained. The clinical trial was performed at the University of California San Diego Moores Cancer Center, the University of Minnesota, and the British Columbia Cancer Agency, with monitoring and oversight provided by the University of Arizona.

  Study phs002437

• Germline

  This study is part of the 'First 1,000 Days of Life and Beyond' study at the Inova Translational Medicine Institute. Whole-genome sequencing data from 1,291 parent-offspring trios was used to study the properties of clustered de novo mutations. The maternal clusters were found to be enriched in regions with accelerated maternal mutation rate and show distinct mutational signatures. For additional details, please refer to: "Germline de novo mutation clusters arise during oocyte aging in genomic regions with increased double-strand break incidence". Jakob M. Goldmann, Vladimir B. Seplyarskiy, Wendy S.W. Wong, Thierry Vilboux, Pieter B. Neerincx, Dale L. Bodian, Benjamin D. Solomon, Joris A. Veltman, John F. Deeken, Christian Gilissen, John E. Niederhuber. Nature Genetics.

  Study phs001522

• Selenium Chemoprevention: Benefits and Harms

  Selenium is a trace element that may have anti-carcinogenetic effect, but heterogenous treatment effects have been observed. This genome-wide association study investigates if genetic variation modifies the effect of selenium chemoprevention in the Selenium and Celecoxib Trial, a randomized, double-blind, placebo-controlled trial conducted at the University of Arizona Cancer Center. The objective of the clinical trial was to determine whether daily intake of 200 µg/d of selenium as a supplement could reduce the risk for developing metachronous colorectal adenomas. The study participants were recruited between 2001 and 2011. Genome-wide association study was performed for 1,323 study participants who provided blood sample at the time of study entry.

  Study phs002283

• National Cancer Institute (NCI) Head and Neck Cancer Study

  Head and neck cancers have well-documented associations with tobacco and alcohol exposure, but the disease develops in only a small fraction of users, which implies an important role for genetic susceptibility. Therefore, head and neck cancers are an excellent model for studying genetic susceptibility to environmental carcinogens. The primary goal of this study is to perform a comprehensive two-stage, high-density, genome-wide single-nucleotide polymorphism (SNP) analysis of head and neck cancer cases and corresponding frequency matched controls to identify novel genetic risk factors for head and neck cancer. In the study, we genotyped 2242 head and neck cancer cases and 1198 controls using Illumina HumanOmniExpress-12v1 BeadChip.

  Study phs001173

• Gene-Environment Interactions in COCCaINE Use Disorder: Collaborative Case-Control Initiative in Cocaine Addiction

  Drug addiction is a phenotype that has high heritability estimates. In recent years, association studies of candidate genes and some genome-wide association studies (GWAS) have identified a large number of SNPs associated with substance use, abuse or dependence, particularly in phenotypes related to alcohol and nicotine use. Regarding snorted or smoked cocaine dependency, only one GWAS has been conducted so far. In addition, genetic association studies that specifically evaluated smoked cocaine dependence (e.g. crack) are rare, because of characteristics related to the route of administration and duration of the effect of the drug. Thus, the main aim of this GWAS was to identify genetic variations that modulate the risk for the cocaine dependence.

  Study phs001810

• International Consortium for Blood Pressure (ICBP)

  The ICBP consortium is an international effort to investigate blood-pressure genetics. The consortium was formed by two parent consortia, the CHARGE-BP consortium (Cohorts for Heart and Aging Research in Genomic Epidemiology - blood pressure) and the GBPGEN consortium (Global Blood Pressure Genetics Consortium). In 2011 we performed genome-wide association analyses based on genome-wide SNPs imputed to HapMap for systolic and diastolic blood pressure (SBP and DBP) and mean arterial pressure and pulse pressure (MAP and PP). In 2016 we performed an analysis based on the Cardio-MetaboChip for SBP and DBP. All these datasets are available here, however, full association statistics including effect size directions, only under controlled access by dbGaP.

  Study phs000585

• The Genomic Analysis of Medulloblastoma

  Medulloblastoma is a heterogenous disease made up of at least four distinct subtypes of disease which appear to exploit and disrupt naturally occurring developmental pathways of cellular growth and hindbrain development. To better understand the driver mutations of this disease, we performed whole genome sequencing of 37 medulloblastomas and the corresponding normal DNA of the 37 affected children treated at St. Jude Children's Research Hospital. We have found several novel mutations which appear subtype specific. These mutations were checked for frequency in a separate tumor cohort of 56 children with medulloblastoma, also treated on the St. Jude Medulloblastoma 2003 trial, and were tested in several animal models of medulloblastoma for proof of oncogenic potential.

  Study phs000409

• Mucosal Melanoma Targeted Exome Sequencing Study (UCSF)

  Mucosal melanoma is a deadly disease that carries the worst prognosis amongst subtypes of melanoma. Like all melanomas, mucosal melanomas are frequently driven by activating mutations in the MAPK and/or PI3K pathways; however, unlike melanomas that arise on sun-exposed skin, mucosal melanomas harbor few point mutations. Instead, most somatic alterations involve structural alterations, which appear early during tumor progression. Molecular studies in mucosal melanoma generally only profile point mutations without interrogating copy number alterations, and pathogenic mutations are only found in 30% of cases. We sequenced 38 mucosal melanomas, and in addition to profiling point mutations, we looked for copy number alterations that amplify oncogenes or delete tumor suppressors.

  Study phs001594