Rosenberger, Albert

[["dc.bibliographiccitation.firstpage","1709"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Cancer Causes & Control"],["dc.bibliographiccitation.lastpage","1720"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","McCormack, Valerie A."],["dc.contributor.author","Hung, Rayjean J."],["dc.contributor.author","Brenner, Darren R."],["dc.contributor.author","Bickeboeller, Heike"],["dc.contributor.author","Rosenberger, Albert"],["dc.contributor.author","Muscat, Joshua E."],["dc.contributor.author","Lazarus, Philip"],["dc.contributor.author","Tjonneland, Anne"],["dc.contributor.author","Friis, Soren"],["dc.contributor.author","Christiani, David C."],["dc.contributor.author","Chun, Eun-mi"],["dc.contributor.author","Le Marchand, Loic"],["dc.contributor.author","Rennert, Gad"],["dc.contributor.author","Rennert, Hedy S."],["dc.contributor.author","Andrew, Angeline S."],["dc.contributor.author","Orlow, Irene"],["dc.contributor.author","Park, Bernard J."],["dc.contributor.author","Boffetta, Paolo"],["dc.contributor.author","Duell, Eric J."],["dc.date.accessioned","2018-11-07T08:49:20Z"],["dc.date.available","2018-11-07T08:49:20Z"],["dc.date.issued","2011"],["dc.description.abstract","Purpose To investigate the hypothesis that non-steroidal anti-inflammatory drugs (NSAIDs) lower lung cancer risk. Methods We analysed pooled individual-level data from seven case-control and one cohort study in the International Lung Cancer Consortium (ILCCO). Relative risks for lung cancer associated with self-reported history of aspirin and other NSAID use were estimated within individual studies using logistic regression or proportional hazards models, adjusted for packyears of smoking, age, calendar period, ethnicity and education and were combined using random effects meta-analysis. Results A total of 4,309 lung cancer cases (mean age at diagnosis 65 years, 45% adenocarcinoma and 22% squamous-cell carcinoma) and 58,301 non-cases/controls were included. Amongst controls, 34% had used NSAIDs in the past (81% of them used aspirin). After adjustment for negative confounding by smoking, ever-NSAID use (affirmative answer to the study-specific question on NSAID use) was associated with a 26% reduction (95% confidence interval 8 to 41%) in lung cancer risk in men, but not in women (3% increase (-11% to 30%)). In men, the association was stronger in current and former smokers, and for squamous-cell carcinoma than for adenocarcinomas, but there was no trend with duration of use. No differences were found in the effects on lung cancer risk of aspirin and non-aspirin NSAIDs. Conclusions Evidence from ILCCO suggests that NSAID use in men confers a modest protection for lung cancer, especially amongst ever-smokers. Additional investigation is needed regarding the possible effects of age, duration, dose and type of NSAID and whether effect modification by smoking status or sex exists."],["dc.identifier.doi","10.1007/s10552-011-9847-z"],["dc.identifier.isi","000297799200010"],["dc.identifier.pmid","21987079"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21438"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1573-7225"],["dc.relation.issn","0957-5243"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Aspirin and NSAID use and lung cancer risk: a pooled analysis in the International Lung Cancer Consortium (ILCCO)"],["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","14"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","European Journal of Medical Research"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Rosenberger, Albert"],["dc.contributor.author","Muttray, Nils"],["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","Albanes, Demetrios"],["dc.contributor.author","Aldrich, Melinda C."],["dc.contributor.author","Tardon, Adonina"],["dc.contributor.author","Fernández-Tardón, Guillermo"],["dc.contributor.author","Rennert, Gad"],["dc.contributor.author","Field, John K."],["dc.contributor.author","Davies, Michael P. A."],["dc.contributor.author","Liloglou, Triantafillos"],["dc.contributor.author","Kiemeney, Lambertus A."],["dc.contributor.author","Lazarus, Philip"],["dc.contributor.author","Wendel, Bernadette"],["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","Duell, Eric J."],["dc.contributor.author","Arnold, Susanne M."],["dc.contributor.author","Goodman, Gary E."],["dc.contributor.author","Chen, Chu"],["dc.contributor.author","Doherty, Jennifer A."],["dc.contributor.author","Taylor, Fiona"],["dc.contributor.author","Cox, Angela"],["dc.contributor.author","Woll, Penella J."],["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 T."],["dc.contributor.author","Shete, Sanjay S."],["dc.contributor.author","Amos, Christopher I."],["dc.contributor.author","Bickeböller, Heike"],["dc.contributor.authorgroup","The INTEGRAL-ILCCO Consortium"],["dc.date.accessioned","2022-04-01T10:03:08Z"],["dc.date.accessioned","2022-08-18T12:40:47Z"],["dc.date.available","2022-04-01T10:03:08Z"],["dc.date.available","2022-08-18T12:40:47Z"],["dc.date.issued","2022-01-31"],["dc.date.updated","2022-07-29T12:18:28Z"],["dc.description.abstract","Background\r\nAberrant Wnt signalling, regulating cell development and stemness, influences the development of many cancer types. The Aryl hydrocarbon receptor (AhR) mediates tumorigenesis of environmental pollutants. Complex interaction patterns of genes assigned to AhR/Wnt-signalling were recently associated with lung cancer susceptibility.\r\n\r\nAim\r\nTo assess the association and predictive ability of AhR/Wnt-genes with lung cancer in cases and controls of European descent.\r\n\r\nMethods\r\nOdds ratios (OR) were estimated for genomic variants assigned to the Wnt agonist and the antagonistic genes DKK2, DKK3, DKK4, FRZB, SFRP4 and Axin2. Logistic regression models with variable selection were trained, validated and tested to predict lung cancer, at which other previously identified SNPs that have been robustly associated with lung cancer risk could also enter the model. Furthermore, decision trees were created to investigate variant × variant interaction. All analyses were performed for overall lung cancer and for subgroups.\r\n\r\nResults\r\nNo genome-wide significant association of AhR/Wnt-genes with overall lung cancer was observed, but within the subgroups of ever smokers (e.g., maker rs2722278 SFRP4; OR  = 1.20; 95% CI 1.13–1.27; p  = 5.6 × 10–10) and never smokers (e.g., maker rs1133683 Axin2; OR  = 1.27; 95% CI 1.19–1.35; p  = 1.0 × 10–12). Although predictability is poor, AhR/Wnt-variants are unexpectedly overrepresented in optimized prediction scores for overall lung cancer and for small cell lung cancer. Remarkably, the score for never-smokers contained solely two AhR/Wnt-variants. The optimal decision tree for never smokers consists of 7 AhR/Wnt-variants and only two lung cancer variants.\r\n\r\nConclusions\r\nThe role of variants belonging to Wnt/AhR-pathways in lung cancer susceptibility may be underrated in main-effects association analysis. Complex interaction patterns in individuals of European descent have moderate predictive capacity for lung cancer or subgroups thereof, especially in never smokers."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.citation","European Journal of Medical Research. 2022 Jan 31;27(1):14"],["dc.identifier.doi","10.1186/s40001-022-00638-7"],["dc.identifier.pii","638"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/106090"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112985"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.publisher","BioMed Central"],["dc.relation.eissn","2047-783X"],["dc.rights","CC BY 4.0"],["dc.rights.holder","The Author(s)"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject","Susceptibility"],["dc.subject","Association"],["dc.subject","Gene–gene integration"],["dc.subject","Prediction"],["dc.subject","Polygenic risk score"],["dc.subject","Decision trees"],["dc.subject","Never smoker"],["dc.subject","Small cell lung cancer"],["dc.title","Gene–gene interaction of AhRwith and within the Wntcascade affects susceptibility to lung cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["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"]]