| Literature DB >> 26363033 |
Darren R Brenner1, Christopher I Amos2, Yonathan Brhane3, Maria N Timofeeva4, Neil Caporaso5, Yufei Wang6, David C Christiani7, Heike Bickeböller8, Ping Yang9, Demetrius Albanes5, Victoria L Stevens10, Susan Gapstur10, James McKay11, Paolo Boffetta12, David Zaridze13, Neonilia Szeszenia-Dabrowska14, Jolanta Lissowska15, Peter Rudnai16, Eleonora Fabianova17, Dana Mates18, Vladimir Bencko19, Lenka Foretova20, Vladimir Janout21, Hans E Krokan22, Frank Skorpen23, Maiken E Gabrielsen23, Lars Vatten24, Inger Njølstad25, Chu Chen26, Gary Goodman26, Mark Lathrop27, Tõnu Vooder28, Kristjan Välk29, Mari Nelis30, Andres Metspalu30, Peter Broderick6, Timothy Eisen31, Xifeng Wu32, Di Zhang32, Wei Chen33, Margaret R Spitz34, Yongyue Wei7, Li Su7, Dong Xie9, Jun She9, Keitaro Matsuo35, Fumihiko Matsuda36, Hidemi Ito37, Angela Risch38, Joachim Heinrich39, Albert Rosenberger8, Thomas Muley40, Hendrik Dienemann41, John K Field42, Olaide Raji42, Ying Chen42, John Gosney42, Triantafillos Liloglou42, Michael P A Davies42, Michael Marcus42, John McLaughlin3, Irene Orlow43, Younghun Han2, Yafang Li2, Xuchen Zong3, Mattias Johansson11, Geoffrey Liu44, Shelley S Tworoger45, Loic Le Marchand46, Brian E Henderson47, Lynne R Wilkens46, Juncheng Dai48, Hongbing Shen48, Richard S Houlston6, Maria T Landi5, Paul Brennan11, Rayjean J Hung49.
Abstract
Large-scale genome-wide association studies (GWAS) have likely uncovered all common variants at the GWAS significance level. Additional variants within the suggestive range (0.0001> P > 5×10(-8)) are, however, still of interest for identifying causal associations. This analysis aimed to apply novel variant prioritization approaches to identify additional lung cancer variants that may not reach the GWAS level. Effects were combined across studies with a total of 33456 controls and 6756 adenocarcinoma (AC; 13 studies), 5061 squamous cell carcinoma (SCC; 12 studies) and 2216 small cell lung cancer cases (9 studies). Based on prior information such as variant physical properties and functional significance, we applied stratified false discovery rates, hierarchical modeling and Bayesian false discovery probabilities for variant prioritization. We conducted a fine mapping analysis as validation of our methods by examining top-ranking novel variants in six independent populations with a total of 3128 cases and 2966 controls. Three novel loci in the suggestive range were identified based on our Bayesian framework analyses: KCNIP4 at 4p15.2 (rs6448050, P = 4.6×10(-7)) and MTMR2 at 11q21 (rs10501831, P = 3.1×10(-6)) with SCC, as well as GAREM at 18q12.1 (rs11662168, P = 3.4×10(-7)) with AC. Use of our prioritization methods validated two of the top three loci associated with SCC (P = 1.05×10(-4) for KCNIP4, represented by rs9799795) and AC (P = 2.16×10(-4) for GAREM, represented by rs3786309) in the independent fine mapping populations. This study highlights the utility of using prior functional data for sequence variants in prioritization analyses to search for robust signals in the suggestive range.Entities:
Mesh:
Year: 2015 PMID: 26363033 PMCID: PMC4635669 DOI: 10.1093/carcin/bgv128
Source DB: PubMed Journal: Carcinogenesis ISSN: 0143-3334 Impact factor: 4.944