Bickeböller, Heike

[["dc.bibliographiccitation.artnumber","e31816"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Fehringer, Gordon"],["dc.contributor.author","Liu, Geoffrey"],["dc.contributor.author","Briollais, Laurent"],["dc.contributor.author","Brennan, P. C."],["dc.contributor.author","Amos, Christopher I."],["dc.contributor.author","Spitz, Margaret R."],["dc.contributor.author","Bickeboeller, Heike"],["dc.contributor.author","Wichmann, Heinz-Erich"],["dc.contributor.author","Risch, Angela"],["dc.contributor.author","Hung, Rayjean J."],["dc.date.accessioned","2018-11-07T09:13:21Z"],["dc.date.available","2018-11-07T09:13:21Z"],["dc.date.issued","2012"],["dc.description.abstract","Pathway analysis has been proposed as a complement to single SNP analyses in GWAS. This study compared pathway analysis methods using two lung cancer GWAS data sets based on four studies: one a combined data set from Central Europe and Toronto (CETO); the other a combined data set from Germany and MD Anderson (GRMD). We searched the literature for pathway analysis methods that were widely used, representative of other methods, and had available software for performing analysis. We selected the programs EASE, which uses a modified Fishers Exact calculation to test for pathway associations, GenGen (a version of Gene Set Enrichment Analysis (GSEA)), which uses a Kolmogorov-Smirnov-like running sum statistic as the test statistic, and SLAT, which uses a p-value combination approach. We also included a modified version of the SUMSTAT method (mSUMSTAT), which tests for association by averaging chi(2) statistics from genotype association tests. There were nearly 18000 genes available for analysis, following mapping of more than 300,000 SNPs from each data set. These were mapped to 421 GO level 4 gene sets for pathway analysis. Among the methods designed to be robust to biases related to gene size and pathway SNP correlation (GenGen, mSUMSTAT and SLAT), the mSUMSTAT approach identified the most significant pathways (8 in CETO and 1 in GRMD). This included a highly plausible association for the acetylcholine receptor activity pathway in both CETO (FDR <= 0.001) and GRMD (FDR = 0.009), although two strong association signals at a single gene cluster (CHRNA3-CHRNA5-CHRNB4) drive this result, complicating its interpretation. Few other replicated associations were found using any of these methods. Difficulty in replicating associations hindered our comparison, but results suggest mSUMSTAT has advantages over the other approaches, and may be a useful pathway analysis tool to use alongside other methods such as the commonly used GSEA (GenGen) approach."],["dc.identifier.doi","10.1371/journal.pone.0031816"],["dc.identifier.isi","000302873700103"],["dc.identifier.pmid","22363742"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7891"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27153"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Comparison of Pathway Analysis Approaches Using Lung Cancer GWAS Data Sets"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Genetic Epidemiology"],["dc.bibliographiccitation.volume","39"],["dc.contributor.author","Friedrichs, Stefanie"],["dc.contributor.author","Amos, Christopher I."],["dc.contributor.author","Brennan, P. C."],["dc.contributor.author","Christiani, David"],["dc.contributor.author","Hung, Rayjean J."],["dc.contributor.author","Risch, Angela"],["dc.contributor.author","Brueske, Irene"],["dc.contributor.author","Caporaso, Neil E."],["dc.contributor.author","Landi, Maria Teresa"],["dc.contributor.author","Rafnar, Thorunn"],["dc.contributor.author","Bickeboeller, Heike"],["dc.date.accessioned","2018-11-07T09:49:47Z"],["dc.date.available","2018-11-07T09:49:47Z"],["dc.date.issued","2015"],["dc.format.extent","549"],["dc.identifier.isi","000363340500056"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35571"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.conference","Annual Meeting of the International-Genetic-Epidemiology-Society (IGES)"],["dc.relation.eventlocation","Baltimore, MD"],["dc.relation.issn","1098-2272"],["dc.relation.issn","0741-0395"],["dc.title","Kernel-based Pathway Meta-Analysis in ILCCO / TRICL Genome-wide Association Studies"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","44634"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Pan, Yongchu"],["dc.contributor.author","Liu, Hongliang"],["dc.contributor.author","Wang, Y."],["dc.contributor.author","Kang, Xiaozheng"],["dc.contributor.author","Liu, Zhensheng"],["dc.contributor.author","Owzar, Kouros"],["dc.contributor.author","Han, Younghun"],["dc.contributor.author","Su, L. I."],["dc.contributor.author","Wei, Yongyue"],["dc.contributor.author","Hung, Rayjean J."],["dc.contributor.author","Brhane, Yonathan"],["dc.contributor.author","McLaughlin, John R."],["dc.contributor.author","Brennan, P. C."],["dc.contributor.author","Bickeboeller, Heike"],["dc.contributor.author","Rosenberger, Albert"],["dc.contributor.author","Houlston, Richard S."],["dc.contributor.author","Caporaso, Neil E."],["dc.contributor.author","Landi, Maria Teresa"],["dc.contributor.author","Heinrich, Joachim"],["dc.contributor.author","Risch, Angela"],["dc.contributor.author","Wu, X."],["dc.contributor.author","Ye, Yuanqing"],["dc.contributor.author","Christiani, David C."],["dc.contributor.author","Amos, Christopher I."],["dc.contributor.author","Wei, Qingyi"],["dc.date.accessioned","2018-11-07T10:26:10Z"],["dc.date.available","2018-11-07T10:26:10Z"],["dc.date.issued","2017"],["dc.description.abstract","mRNA splicing is an important mechanism to regulate mRNA expression. Abnormal regulation of this process may lead to lung cancer. Here, we investigated the associations of 11,966 single-nucleotide polymorphisms (SNPs) in 206 mRNA splicing-related genes with lung cancer risk by using the summary data from six published genome-wide association studies (GWASs) of Transdisciplinary Research in Cancer of the Lung (TRICL) (12,160 cases and 16,838 controls) and another two lung cancer GWASs of Harvard University (984 cases and 970 controls) and deCODE (1,319 cases and 26,380 controls). We found that a total of 12 significant SNPs with false discovery rate (FDR) <= 0.05 were mapped to one novel gene PRPF6 and two previously reported genes (DHX16 and LSM2) that were also confirmed in this study. The six novel SNPs in PRPF6 were in high linkage disequilibrium and associated with PRPF6 mRNA expression in lymphoblastoid cells from 373 Europeans in the 1000 Genomes Project. Taken together, our studies shed new light on the role of mRNA splicing genes in the development of lung cancer."],["dc.identifier.doi","10.1038/srep44634"],["dc.identifier.isi","000397001600001"],["dc.identifier.pmid","28304396"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14434"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42982"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","2045-2322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Associations between genetic variants in mRNA splicing-related genes and risk of lung cancer: a pathway-based analysis from published GWASs"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5356"],["dc.bibliographiccitation.issue","18"],["dc.bibliographiccitation.journal","Human Molecular Genetics"],["dc.bibliographiccitation.lastpage","5366"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Zhang, C."],["dc.contributor.author","Doherty, Jennifer Anne"],["dc.contributor.author","Burgess, Stephen"],["dc.contributor.author","Hung, Rayjean J."],["dc.contributor.author","Lindstroem, Sara"],["dc.contributor.author","Kraft, Peter"],["dc.contributor.author","Gong, Jian"],["dc.contributor.author","Amos, Christopher I."],["dc.contributor.author","Sellers, Thomas A."],["dc.contributor.author","Monteiro, Alvaro N. A."],["dc.contributor.author","Chenevix-Trench, Georgia"],["dc.contributor.author","Bickeböller, Heike"],["dc.contributor.author","Risch, Angela"],["dc.contributor.author","Brennan, P. C."],["dc.contributor.author","McKay, James D."],["dc.contributor.author","Houlston, Richard S."],["dc.contributor.author","Landi, Maria Teresa"],["dc.contributor.author","Timofeeva, Maria N."],["dc.contributor.author","Wang, Y."],["dc.contributor.author","Heinrich, Joachim"],["dc.contributor.author","Kote-Jarai, Zsofia"],["dc.contributor.author","Eeles, Rosalind A."],["dc.contributor.author","Muir, Ken"],["dc.contributor.author","Wiklund, Fredrik"],["dc.contributor.author","Gronberg, Henrik"],["dc.contributor.author","Berndt, Sonja I."],["dc.contributor.author","Chanock, Stephen J."],["dc.contributor.author","Schumacher, Frederick R."],["dc.contributor.author","Haiman, Christopher A."],["dc.contributor.author","Henderson, Brian E."],["dc.contributor.author","Al Olama, Ali Amin"],["dc.contributor.author","Andrulis, Irene L."],["dc.contributor.author","Hopper, John L."],["dc.contributor.author","Chang-Claude, Jenny"],["dc.contributor.author","John, Esther M."],["dc.contributor.author","Malone, Kathleen E."],["dc.contributor.author","Gammon, Marilie D."],["dc.contributor.author","Ursin, Giske"],["dc.contributor.author","Whittemore, Alice S."],["dc.contributor.author","Hunter, David J."],["dc.contributor.author","Gruber, Stephen B."],["dc.contributor.author","Knight, Julia A."],["dc.contributor.author","Hou, Lifang"],["dc.contributor.author","Le Marchand, Loic"],["dc.contributor.author","Newcomb, Polly A."],["dc.contributor.author","Hudson, Thomas J."],["dc.contributor.author","Chan, Andrew T."],["dc.contributor.author","Li, L. I."],["dc.contributor.author","Woods, Michael O."],["dc.contributor.author","Ahsan, Habibul"],["dc.contributor.author","Pierce, Brandon L."],["dc.date.accessioned","2018-11-07T09:51:38Z"],["dc.date.available","2018-11-07T09:51:38Z"],["dc.date.issued","2015"],["dc.description.abstract","Epidemiological studies have reported inconsistent associations between telomere length (TL) and risk for various cancers. These inconsistencies are likely attributable, in part, to biases that arise due to post-diagnostic and post-treatment TL measurement. To avoid such biases, we used a Mendelian randomization approach and estimated associations between nine TL-associated SNPs and risk for five common cancer types (breast, lung, colorectal, ovarian and prostate cancer, including subtypes) using data on 51 725 cases and 62 035 controls. We then used an inverse-variance weighted average of the SNP-specific associations to estimate the association between a genetic score representing long TL and cancer risk. The long TL genetic score was significantly associated with increased risk of lung adenocarcinoma (P = 6.3 x 10(-15)), even after exclusion of a SNP residing in a known lung cancer susceptibility region (TERT-CLPTM1L) P = 6.6 x 10(-6)). Under Mendelian randomization assumptions, the association estimate [odds ratio (OR) = 2.78] is interpreted as the OR for lung adenocarcinoma corresponding to a 1000 bp increase in TL. The weighted TL SNP score was not associated with other cancer types or subtypes. Our finding that genetic determinants of long TL increase lung adenocarcinoma risk avoids issues with reverse causality and residual confounding that arise in observational studies of TL and disease risk. Under Mendelian randomization assumptions, our finding suggests that longer TL increases lung adenocarcinoma risk. However, caution regarding this causal interpretation is warranted in light of the potential issue of pleiotropy, and a more general interpretation is that SNPs influencing telomere biology are also implicated in lung adenocarcinoma risk."],["dc.identifier.doi","10.1093/hmg/ddv252"],["dc.identifier.isi","000361317200024"],["dc.identifier.pmid","26138067"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12147"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35955"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1460-2083"],["dc.relation.issn","0964-6906"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Genetic determinants of telomere length and risk of common cancers: a Mendelian randomization study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0177875"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","PloS one"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Carreras-Torres, Robert"],["dc.contributor.author","Johansson, Mattias"],["dc.contributor.author","Haycock, Philip C."],["dc.contributor.author","Wade, Kaitlin H."],["dc.contributor.author","Relton, Caroline L."],["dc.contributor.author","Martin, Richard M."],["dc.contributor.author","Davey Smith, George"],["dc.contributor.author","Albanes, Demetrius"],["dc.contributor.author","Aldrich, Melinda C."],["dc.contributor.author","Andrew, Angeline"],["dc.contributor.author","Arnold, Susanne M."],["dc.contributor.author","Bickeböller, Heike"],["dc.contributor.author","Bojesen, Stig E."],["dc.contributor.author","Brunnström, Hans"],["dc.contributor.author","Manjer, Jonas"],["dc.contributor.author","Brüske, Irene"],["dc.contributor.author","Caporaso, Neil E."],["dc.contributor.author","Chen, Chu"],["dc.contributor.author","Christiani, David C."],["dc.contributor.author","Christian, W. Jay"],["dc.contributor.author","Doherty, Jennifer A."],["dc.contributor.author","Duell, Eric J."],["dc.contributor.author","Field, John K."],["dc.contributor.author","Davies, Michael P. A."],["dc.contributor.author","Marcus, Michael W."],["dc.contributor.author","Goodman, Gary E."],["dc.contributor.author","Grankvist, Kjell"],["dc.contributor.author","Haugen, Aage"],["dc.contributor.author","Hong, Yun-Chul"],["dc.contributor.author","Kiemeney, Lambertus A."],["dc.contributor.author","van der Heijden, Erik H. F. M."],["dc.contributor.author","Kraft, Peter"],["dc.contributor.author","Johansson, Mikael B."],["dc.contributor.author","Lam, Stephen"],["dc.contributor.author","Landi, Maria Teresa"],["dc.contributor.author","Lazarus, Philip"],["dc.contributor.author","Le Marchand, Loïc"],["dc.contributor.author","Liu, Geoffrey"],["dc.contributor.author","Melander, Olle"],["dc.contributor.author","Park, Sungshim L."],["dc.contributor.author","Rennert, Gad"],["dc.contributor.author","Risch, Angela"],["dc.contributor.author","Haura, Eric B."],["dc.contributor.author","Scelo, Ghislaine"],["dc.contributor.author","Zaridze, David"],["dc.contributor.author","Mukeriya, Anush"],["dc.contributor.author","Savić, Milan"],["dc.contributor.author","Lissowska, Jolanta"],["dc.contributor.author","Swiatkowska, Beata"],["dc.contributor.author","Janout, Vladimir"],["dc.contributor.author","Holcatova, Ivana"],["dc.contributor.author","Mates, Dana"],["dc.contributor.author","Schabath, Matthew B."],["dc.contributor.author","Shen, Hongbing"],["dc.contributor.author","Tardon, Adonina"],["dc.contributor.author","Teare, M. Dawn"],["dc.contributor.author","Woll, Penella"],["dc.contributor.author","Tsao, Ming-Sound"],["dc.contributor.author","Wu, Xifeng"],["dc.contributor.author","Yuan, Jian-Min"],["dc.contributor.author","Hung, Rayjean J."],["dc.contributor.author","Amos, Christopher I."],["dc.contributor.author","McKay, James"],["dc.contributor.author","Brennan, Paul"],["dc.date.accessioned","2019-07-09T11:43:32Z"],["dc.date.available","2019-07-09T11:43:32Z"],["dc.date.issued","2017"],["dc.description.abstract","BACKGROUND: Assessing the relationship between lung cancer and metabolic conditions is challenging because of the confounding effect of tobacco. Mendelian randomization (MR), or the use of genetic instrumental variables to assess causality, may help to identify the metabolic drivers of lung cancer. METHODS AND FINDINGS: We identified genetic instruments for potential metabolic risk factors and evaluated these in relation to risk using 29,266 lung cancer cases (including 11,273 adenocarcinomas, 7,426 squamous cell and 2,664 small cell cases) and 56,450 controls. The MR risk analysis suggested a causal effect of body mass index (BMI) on lung cancer risk for two of the three major histological subtypes, with evidence of a risk increase for squamous cell carcinoma (odds ratio (OR) [95% confidence interval (CI)] = 1.20 [1.01-1.43] and for small cell lung cancer (OR [95%CI] = 1.52 [1.15-2.00]) for each standard deviation (SD) increase in BMI [4.6 kg/m2]), but not for adenocarcinoma (OR [95%CI] = 0.93 [0.79-1.08]) (Pheterogeneity = 4.3x10-3). Additional analysis using a genetic instrument for BMI showed that each SD increase in BMI increased cigarette consumption by 1.27 cigarettes per day (P = 2.1x10-3), providing novel evidence that a genetic susceptibility to obesity influences smoking patterns. There was also evidence that low-density lipoprotein cholesterol was inversely associated with lung cancer overall risk (OR [95%CI] = 0.90 [0.84-0.97] per SD of 38 mg/dl), while fasting insulin was positively associated (OR [95%CI] = 1.63 [1.25-2.13] per SD of 44.4 pmol/l). Sensitivity analyses including a weighted-median approach and MR-Egger test did not detect other pleiotropic effects biasing the main results. CONCLUSIONS: Our results are consistent with a causal role of fasting insulin and low-density lipoprotein cholesterol in lung cancer etiology, as well as for BMI in squamous cell and small cell carcinoma. The latter relation may be mediated by a previously unrecognized effect of obesity on smoking behavior."],["dc.identifier.doi","10.1371/journal.pone.0177875"],["dc.identifier.pmid","28594918"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14558"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58904"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Obesity, metabolic factors and risk of different histological types of lung cancer: A Mendelian randomization study."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Genetic Epidemiology"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Sohns, Melanie"],["dc.contributor.author","Viktorova, Elena"],["dc.contributor.author","Fehringer, Gord"],["dc.contributor.author","Gaborieau, Valerie"],["dc.contributor.author","Han, Younghun"],["dc.contributor.author","Chang-Claude, Jenny"],["dc.contributor.author","Heinrich, Joachim"],["dc.contributor.author","Risch, Angela"],["dc.contributor.author","Amos, Christopher I."],["dc.contributor.author","Brennan, P. C."],["dc.contributor.author","Hung, Rayjean J."],["dc.contributor.author","Bickeboeller, Heike"],["dc.date.accessioned","2018-11-07T09:04:08Z"],["dc.date.available","2018-11-07T09:04:08Z"],["dc.date.issued","2012"],["dc.format.extent","756"],["dc.identifier.isi","000309913200133"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25044"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.conference","Annual Meeting of the International-Genetic-Epidemiology-Society (IGES)"],["dc.relation.eventlocation","Stevenson, WA"],["dc.relation.issn","0741-0395"],["dc.title","Application of the Empirical Hierarchical Bayes Approach for Gene-Environment Interaction to TRICL Lung Cancer GWAS"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","937"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","International Archives of Occupational and Environmental Health"],["dc.bibliographiccitation.lastpage","950"],["dc.bibliographiccitation.volume","91"],["dc.contributor.author","Rosenberger, Albert"],["dc.contributor.author","Hung, Rayjean J."],["dc.contributor.author","Christiani, David C."],["dc.contributor.author","Caporaso, Neil E."],["dc.contributor.author","Liu, Geoffrey"],["dc.contributor.author","Bojesen, Stig E."],["dc.contributor.author","Le Marchand, Loic"],["dc.contributor.author","Haiman, Ch. A."],["dc.contributor.author","Albanes, Demetrios"],["dc.contributor.author","Aldrich, Melinda C."],["dc.contributor.author","Tardon, Adonina"],["dc.contributor.author","Fernández-Tardón, G."],["dc.contributor.author","Rennert, Gad"],["dc.contributor.author","Field, John K."],["dc.contributor.author","Kiemeney, B."],["dc.contributor.author","Lazarus, Philip"],["dc.contributor.author","Haugen, Aage"],["dc.contributor.author","Zienolddiny, Shanbeh"],["dc.contributor.author","Lam, Stephen"],["dc.contributor.author","Schabath, Matthew B."],["dc.contributor.author","Andrew, Angeline S."],["dc.contributor.author","Brunnsstöm, Hans"],["dc.contributor.author","Goodman, Gary E."],["dc.contributor.author","Doherty, Jennifer A."],["dc.contributor.author","Chen, Chu"],["dc.contributor.author","Teare, M. Dawn"],["dc.contributor.author","Wichmann, H.-Erich"],["dc.contributor.author","Manz, Judith"],["dc.contributor.author","Risch, Angela"],["dc.contributor.author","Muley, Thomas R."],["dc.contributor.author","Johansson, Mikael"],["dc.contributor.author","Brennan, Paul"],["dc.contributor.author","Landi, Maria Teresa"],["dc.contributor.author","Amos, Christopher I."],["dc.contributor.author","Pesch, Beate"],["dc.contributor.author","Johnen, Georg"],["dc.contributor.author","Brüning, Thomas"],["dc.contributor.author","Bickeböller, Heike"],["dc.contributor.author","Gomolka, Maria"],["dc.date.accessioned","2020-12-10T14:10:35Z"],["dc.date.available","2020-12-10T14:10:35Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1007/s00420-018-1334-3"],["dc.identifier.eissn","1432-1246"],["dc.identifier.issn","0340-0131"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70809"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Genetic modifiers of radon-induced lung cancer risk: a genome-wide interaction study in former uranium miners"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","935"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Cancer Epidemiology, Biomarkers & Prevention"],["dc.bibliographiccitation.lastpage","942"],["dc.bibliographiccitation.volume","28"],["dc.contributor.author","Zhu, Ying"],["dc.contributor.author","Wei, Yongyue"],["dc.contributor.author","Zhang, Ruyang"],["dc.contributor.author","Dong, Xuesi"],["dc.contributor.author","Shen, Sipeng"],["dc.contributor.author","Zhao, Yang"],["dc.contributor.author","Bai, Jianling"],["dc.contributor.author","Albanes, Demetrius"],["dc.contributor.author","Caporaso, Neil E."],["dc.contributor.author","Landi, Maria Teresa"],["dc.contributor.author","Zhu, Bin"],["dc.contributor.author","Chanock, Stephen J."],["dc.contributor.author","Gu, Fangyi"],["dc.contributor.author","Lam, Stephen"],["dc.contributor.author","Tsao, Ming-Sound"],["dc.contributor.author","Shepherd, Frances A."],["dc.contributor.author","Tardon, Adonina"],["dc.contributor.author","Fernández-Somoano, Ana"],["dc.contributor.author","Fernandez-Tardon, Guillermo"],["dc.contributor.author","Chen, Chu"],["dc.contributor.author","Barnett, Matthew J."],["dc.contributor.author","Doherty, Jennifer"],["dc.contributor.author","Bojesen, Stig E."],["dc.contributor.author","Johansson, Mattias"],["dc.contributor.author","Brennan, Paul"],["dc.contributor.author","McKay, James D."],["dc.contributor.author","Carreras-Torres, Robert"],["dc.contributor.author","Muley, Thomas"],["dc.contributor.author","Risch, Angela"],["dc.contributor.author","Wichmann, Heunz-Erich"],["dc.contributor.author","Bickeboeller, Heike"],["dc.contributor.author","Rosenberger, Albert"],["dc.contributor.author","Rennert, Gad"],["dc.contributor.author","Saliba, Walid"],["dc.contributor.author","Arnold, Susanne M."],["dc.contributor.author","Field, John K."],["dc.contributor.author","Davies, Michael P.A."],["dc.contributor.author","Marcus, Michael W."],["dc.contributor.author","Wu, Xifeng"],["dc.contributor.author","Ye, Yuanqing"],["dc.contributor.author","Le Marchand, Loic"],["dc.contributor.author","Wilkens, Lynne R."],["dc.contributor.author","Melander, Olle"],["dc.contributor.author","Manjer, Jonas"],["dc.contributor.author","Brunnström, Hans"],["dc.contributor.author","Hung, Rayjean J."],["dc.contributor.author","Liu, Geoffrey"],["dc.contributor.author","Brhane, Yonathan"],["dc.contributor.author","Kachuri, Linda"],["dc.contributor.author","Andrew, Angeline S."],["dc.contributor.author","Duell, Eric J."],["dc.contributor.author","Kiemeney, Lambertus A."],["dc.contributor.author","van der Heijden, Erik HFM"],["dc.contributor.author","Haugen, Aage"],["dc.contributor.author","Zienolddiny, Shanbeh"],["dc.contributor.author","Skaug, Vidar"],["dc.contributor.author","Grankvist, Kjell"],["dc.contributor.author","Johansson, Mikael"],["dc.contributor.author","Woll, Penella J."],["dc.contributor.author","Cox, Angela"],["dc.contributor.author","Taylor, Fiona"],["dc.contributor.author","Teare, Dawn M."],["dc.contributor.author","Lazarus, Philip"],["dc.contributor.author","Schabath, Matthew B."],["dc.contributor.author","Aldrich, Melinda C."],["dc.contributor.author","Houlston, Richard S."],["dc.contributor.author","McLaughlin, John"],["dc.contributor.author","Stevens, Victoria L."],["dc.contributor.author","Shen, Hongbing"],["dc.contributor.author","Hu, Zhibin"],["dc.contributor.author","Dai, Juncheng"],["dc.contributor.author","Amos, Christopher I."],["dc.contributor.author","Han, Younghun"],["dc.contributor.author","Zhu, Dakai"],["dc.contributor.author","Goodman, Gary E."],["dc.contributor.author","Chen, Feng"],["dc.contributor.author","Christiani, David C."],["dc.date.accessioned","2020-12-10T18:37:45Z"],["dc.date.available","2020-12-10T18:37:45Z"],["dc.date.issued","2019"],["dc.description.abstract","Platelets are a critical element in coagulation and inflammation, and activated platelets are linked to cancer risk through diverse mechanisms. However, a causal relationship between platelets and risk of lung cancer remains unclear."],["dc.identifier.doi","10.1158/1055-9965.EPI-18-0356"],["dc.identifier.eissn","1538-7755"],["dc.identifier.issn","1055-9965"],["dc.identifier.pmid","30700444"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77082"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation.eissn","1538-7755"],["dc.relation.issn","1055-9965"],["dc.relation.issn","1538-7755"],["dc.title","Elevated Platelet Count Appears to Be Causally Associated with Increased Risk of Lung Cancer: A Mendelian Randomization Analysis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","6742763"],["dc.bibliographiccitation.journal","Computational and mathematical methods in medicine"],["dc.bibliographiccitation.lastpage","17"],["dc.bibliographiccitation.volume","2017"],["dc.contributor.author","Friedrichs, Stefanie"],["dc.contributor.author","Manitz, Juliane"],["dc.contributor.author","Burger, Patricia"],["dc.contributor.author","Amos, Christopher I."],["dc.contributor.author","Risch, Angela"],["dc.contributor.author","Chang-Claude, Jenny"],["dc.contributor.author","Wichmann, Heinz-Erich"],["dc.contributor.author","Kneib, Thomas"],["dc.contributor.author","Bickeböller, Heike"],["dc.contributor.author","Hofner, Benjamin"],["dc.date.accessioned","2018-03-13T14:55:43Z"],["dc.date.available","2018-03-13T14:55:43Z"],["dc.date.issued","2017"],["dc.description.abstract","The analysis of genome-wide association studies (GWAS) benefits from the investigation of biologically meaningful gene sets, such as gene-interaction networks (pathways). We propose an extension to a successful kernel-based pathway analysis approach by integrating kernel functions into a powerful algorithmic framework for variable selection, to enable investigation of multiple pathways simultaneously. We employ genetic similarity kernels from the logistic kernel machine test (LKMT) as base-learners in a boosting algorithm. A model to explain case-control status is created iteratively by selecting pathways that improve its prediction ability. We evaluated our method in simulation studies adopting 50 pathways for different sample sizes and genetic effect strengths. Additionally, we included an exemplary application of kernel boosting to a rheumatoid arthritis and a lung cancer dataset. Simulations indicate that kernel boosting outperforms the LKMT in certain genetic scenarios. Applications to GWAS data on rheumatoid arthritis and lung cancer resulted in sparse models which were based on pathways interpretable in a clinical sense. Kernel boosting is highly flexible in terms of considered variables and overcomes the problem of multiple testing. Additionally, it enables the prediction of clinical outcomes. Thus, kernel boosting constitutes a new, powerful tool in the analysis of GWAS data and towards the understanding of biological processes involved in disease susceptibility."],["dc.identifier.doi","10.1155/2017/6742763"],["dc.identifier.pmid","28785300"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14774"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13019"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.relation.eissn","1748-6718"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Pathway-Based Kernel Boosting for the Analysis of Genome-Wide Association Studies"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1663"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Molecular Carcinogenesis"],["dc.bibliographiccitation.lastpage","1672"],["dc.bibliographiccitation.volume","56"],["dc.contributor.author","Yin, Jieyun"],["dc.contributor.author","Liu, Hongliang"],["dc.contributor.author","Liu, Zhensheng"],["dc.contributor.author","Owzar, Kouros"],["dc.contributor.author","Han, Younghun"],["dc.contributor.author","Su, L. I."],["dc.contributor.author","Wei, Yongyue"],["dc.contributor.author","Hung, Rayjean J."],["dc.contributor.author","Brhane, Yonathan"],["dc.contributor.author","McLaughlin, John R."],["dc.contributor.author","Brennan, P. C."],["dc.contributor.author","Bickeboeller, Heike"],["dc.contributor.author","Rosenberger, Albert"],["dc.contributor.author","Houlston, Richard S."],["dc.contributor.author","Caporaso, Neil E."],["dc.contributor.author","Landi, Maria Teresa"],["dc.contributor.author","Heinrich, Joachim"],["dc.contributor.author","Risch, Angela"],["dc.contributor.author","Christiani, David C."],["dc.contributor.author","Amos, Christopher I."],["dc.contributor.author","Wei, Qingyi"],["dc.date.accessioned","2018-11-07T10:22:59Z"],["dc.date.available","2018-11-07T10:22:59Z"],["dc.date.issued","2017"],["dc.description.abstract","The fatty acids (FAs) metabolism is suggested to play a pivotal role in the development of lung cancer, and we explored that by conducting a pathway-based analysis. We performed a meta-analysis of published datasets of six genome wide association studies (GWASs) from the Transdisciplinary Research in Cancer of the Lung (TRICL) consortium, which included 12 160 cases with lung cancer and 16 838 cancer-free controls. A total of 30 722 single-nucleotide polymorphisms (SNPs) from 317 genes relevant to FA metabolic pathways were identified. An additional dataset fromthe Harvard Lung Cancer Study with 984 cases and 970 healthy controls was also added to the final meta-analysis. In the initial meta-analysis, 26 of 28 SNPs that passed false discovery rate multiple tests were mapped to the CYP4F3 gene. Among the 26 top ranked hits was a proxy SNP, CYP4F3 rs4646904 (P=8.65x10(-6), FDR = 0.018), which is suggested to change splicing pattern/efficiency and to be associated with gene expression levels. However, after adding data of rs4646904 from the Harvard GWAS, the significance in the combined analysis was reduced to P=3.52x10(-3) [odds ratio (OR) = 1.07, 95% confidence interval (95% CI) = 1.03-1.12]. Interestingly, the small Harvard dataset also pointed to the same direction of the association in subgroups of smokers (OR = 1.07) and contributed to a combined OR of 1.13 (95% CI = 1.06-1.20, P=6.70x10(-5)). The results suggest that a potentially functional SNP in CYP4F3 (rs4646904) may contribute to the etiology of lung cancer, especially in smokers. Additional mechanistic studies are warranted to unravel the potential biological significance of the finding."],["dc.identifier.doi","10.1002/mc.22622"],["dc.identifier.isi","000403698200012"],["dc.identifier.pmid","28150878"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42374"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Wiley"],["dc.relation.issn","1098-2744"],["dc.relation.issn","0899-1987"],["dc.title","Pathway-analysis of published genome-wide association studies of lung cancer: A potential role for the CYP4F3 locus"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]