Bickeböller, Heike

[["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.firstpage","959"],["dc.bibliographiccitation.issue","13"],["dc.bibliographiccitation.journal","JNCI Journal of the National Cancer Institute"],["dc.bibliographiccitation.lastpage","971"],["dc.bibliographiccitation.volume","102"],["dc.contributor.author","Truong, T."],["dc.contributor.author","Hung, R. J."],["dc.contributor.author","Amos, Christopher I."],["dc.contributor.author","Wu, X."],["dc.contributor.author","Bickeböller, H."],["dc.contributor.author","Rosenberger, A."],["dc.contributor.author","Sauter, W."],["dc.contributor.author","Illig, T."],["dc.contributor.author","Wichmann, H.- E."],["dc.contributor.author","Risch, A."],["dc.contributor.author","Dienemann, H."],["dc.contributor.author","Kaaks, R."],["dc.contributor.author","Yang, P."],["dc.contributor.author","Jiang, R."],["dc.contributor.author","Wiencke, J. K."],["dc.contributor.author","Wrensch, M."],["dc.contributor.author","Hansen, Helen"],["dc.contributor.author","Kelsey, K. T."],["dc.contributor.author","Matsuo, K."],["dc.contributor.author","Tajima, K."],["dc.contributor.author","Schwartz, A. G."],["dc.contributor.author","Wenzlaff, A."],["dc.contributor.author","Seow, A."],["dc.contributor.author","Ying, C."],["dc.contributor.author","Staratschek-Jox, A."],["dc.contributor.author","Nurnberg, P."],["dc.contributor.author","Stoelben, E."],["dc.contributor.author","Wolf, J."],["dc.contributor.author","Lazarus, P."],["dc.contributor.author","Muscat, J. E."],["dc.contributor.author","Gallagher, C. J."],["dc.contributor.author","Zienolddiny, S."],["dc.contributor.author","Haugen, A."],["dc.contributor.author","van der Heijden, H. F. M."],["dc.contributor.author","Kiemeney, L. A."],["dc.contributor.author","Isla, D."],["dc.contributor.author","Mayordomo, J. I."],["dc.contributor.author","Rafnar, T."],["dc.contributor.author","Stefansson, K."],["dc.contributor.author","Zhang, Z.-F."],["dc.contributor.author","Chang, S.-C."],["dc.contributor.author","Kim, J. H."],["dc.contributor.author","Hong, Y.-C."],["dc.contributor.author","Duell, E. J."],["dc.contributor.author","Andrew, Angeline S."],["dc.contributor.author","Lejbkowicz, F."],["dc.contributor.author","Rennert, G."],["dc.contributor.author","Muller, H."],["dc.contributor.author","Brenner, H."],["dc.contributor.author","Le Marchand, L."],["dc.contributor.author","Benhamou, S."],["dc.contributor.author","Bouchardy, C."],["dc.contributor.author","Teare, M. D."],["dc.contributor.author","Xue, X."],["dc.contributor.author","McLaughlin, J."],["dc.contributor.author","Liu, G."],["dc.contributor.author","McKay, J. D."],["dc.contributor.author","Brennan, P."],["dc.contributor.author","Spitz, M. R."],["dc.date.accessioned","2019-07-09T11:52:53Z"],["dc.date.available","2019-07-09T11:52:53Z"],["dc.date.issued","2010"],["dc.description.abstract","Background Genome-wide association studies have identified three chromosomal regions at 15q25, 5p15, and 6p21 as being associated with the risk of lung cancer. To confirm these associations in independent studies and investigate heterogeneity of these associations within specific subgroups, we conducted a coordinated genotyping study within the International Lung Cancer Consortium based on independent studies that were not included in previous genome-wide association studies. Methods Genotype data for single-nucleotide polymorphisms at chromosomes 15q25 (rs16969968, rs8034191), 5p15 (rs2736100, rs402710), and 6p21 (rs2256543, rs4324798) from 21 case–control studies for 11 645 lung cancer case patients and 14 954 control subjects, of whom 85% were white and 15% were Asian, were pooled. Associations between the variants and the risk of lung cancer were estimated by logistic regression models. All statistical tests were two-sided. Results Associations between 15q25 and the risk of lung cancer were replicated in white ever-smokers (rs16969968: odds ratio [OR] = 1.26, 95% confidence interval [CI] = 1.21 to 1.32, Ptrend = 2 × 10226), and this association was stronger for those diagnosed at younger ages. There was no association in never-smokers or in Asians between either of the 15q25 variants and the risk of lung cancer. For the chromosome 5p15 region, we confirmed statistically significant associations in whites for both rs2736100 (OR = 1.15, 95% CI = 1.10 to 1.20, Ptrend = 1 × 10210) and rs402710 (OR = 1.14, 95% CI = 1.09 to 1.19, Ptrend = 5 × 1028) and identified similar associations in Asians (rs2736100: OR = 1.23, 95% CI = 1.12 to 1.35, Ptrend = 2 × 1025; rs402710: OR = 1.15, 95% CI = 1.04 to 1.27, Ptrend = .007). The associations between the 5p15 variants and lung cancer differed by histology; odds ratios for rs2736100 were highest in adenocarcinoma and for rs402710 were highest in adenocarcinoma and squamous cell carcinomas. This pattern was observed in both ethnic groups. Neither of the two variants on chromosome 6p21 was associated with the risk of lung cancer. Conclusions In this international genetic association study of lung cancer, previous associations found in white populations were replicated and new associations were identified in Asian populations. Future genetic studies of lung cancer should include detailed stratification by histology."],["dc.identifier.doi","10.1093/jnci/djq178"],["dc.identifier.fs","575235"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6100"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60298"],["dc.notes.intern","Merged from goescholar"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Replication of Lung Cancer Susceptibility Loci at Chromosomes 15q25, 5p15, and 6p21: A Pooled Analysis From the International Lung Cancer Consortium"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]