Rosenberger, Albert

[["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","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","4980"],["dc.bibliographiccitation.issue","22"],["dc.bibliographiccitation.journal","Human Molecular Genetics"],["dc.bibliographiccitation.lastpage","4995"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Timofeeva, Maria N."],["dc.contributor.author","Hung, Rayjean J."],["dc.contributor.author","Rafnar, Thorunn"],["dc.contributor.author","Christiani, David C."],["dc.contributor.author","Field, John K."],["dc.contributor.author","Bickeboeller, Heike"],["dc.contributor.author","Risch, Angela"],["dc.contributor.author","McKay, James D."],["dc.contributor.author","Wang, Y."],["dc.contributor.author","Dai, Juncheng"],["dc.contributor.author","Gaborieau, Valerie"],["dc.contributor.author","McLaughlin, John R."],["dc.contributor.author","Brenner, Darren"],["dc.contributor.author","Narod, Steven A."],["dc.contributor.author","Caporaso, Neil E."],["dc.contributor.author","Albanes, Demetrius"],["dc.contributor.author","Thun, Michael"],["dc.contributor.author","Eisen, Timothy"],["dc.contributor.author","Wichmann, Heinz-Erich"],["dc.contributor.author","Rosenberger, Albert"],["dc.contributor.author","Han, Younghun"],["dc.contributor.author","Chen, Wei"],["dc.contributor.author","Zhu, D."],["dc.contributor.author","Spitz, Margaret R."],["dc.contributor.author","Wu, X."],["dc.contributor.author","Pande, Mala"],["dc.contributor.author","Zhao, Yang"],["dc.contributor.author","Zaridze, David"],["dc.contributor.author","Szeszenia-Dabrowska, Neonilia"],["dc.contributor.author","Lissowska, Jolanta"],["dc.contributor.author","Rudnai, Peter"],["dc.contributor.author","Fabianova, Eleonora"],["dc.contributor.author","Mates, Dana"],["dc.contributor.author","Bencko, Vladimir"],["dc.contributor.author","Foretova, Lenka"],["dc.contributor.author","Janout, Vladimir"],["dc.contributor.author","Krokan, Hans E."],["dc.contributor.author","Gabrielsen, Maiken Elvestad"],["dc.contributor.author","Skorpen, Frank"],["dc.contributor.author","Vatten, Lars"],["dc.contributor.author","Njolstad, Inger"],["dc.contributor.author","Chen, Chu"],["dc.contributor.author","Goodman, Gary"],["dc.contributor.author","Lathrop, Mark"],["dc.contributor.author","Benhamou, Simone"],["dc.contributor.author","Vooder, Tonu"],["dc.contributor.author","Vaelk, Kristjan"],["dc.contributor.author","Nelis, Mari"],["dc.contributor.author","Metspalu, Andres"],["dc.contributor.author","Raji, Olaide Y."],["dc.contributor.author","Chen, Ying"],["dc.contributor.author","Gosney, John"],["dc.contributor.author","Liloglou, Triantafillos"],["dc.contributor.author","Muley, Thomas"],["dc.contributor.author","Dienemann, Hendrik"],["dc.contributor.author","Thorleifsson, Gudmar"],["dc.contributor.author","Shen, Hongbing"],["dc.contributor.author","Stefansson, Kari"],["dc.contributor.author","Brennan, P. C."],["dc.contributor.author","Amos, Christopher I."],["dc.contributor.author","Houlston, Richard S."],["dc.contributor.author","Landi, Maria Teresa"],["dc.date.accessioned","2018-11-07T09:03:28Z"],["dc.date.available","2018-11-07T09:03:28Z"],["dc.date.issued","2012"],["dc.description.abstract","Recent genome-wide association studies (GWASs) have identified common genetic variants at 5p15.33, 6p216p22 and 15q25.1 associated with lung cancer risk. Several other genetic regions including variants of CHEK2 (22q12), TP53BP1 (15q15) and RAD52 (12p13) have been demonstrated to influence lung cancer risk in candidate- or pathway-based analyses. To identify novel risk variants for lung cancer, we performed a meta-analysis of 16 GWASs, totaling 14 900 cases and 29 485 controls of European descent. Our data provided increased support for previously identified risk loci at 5p15 (P 7.2 10(16)), 6p21 (P 2.3 10(14)) and 15q25 (P 2.2 10(63)). Furthermore, we demonstrated histology-specific effects for 5p15, 6p21 and 12p13 loci but not for the 15q25 region. Subgroup analysis also identified a novel disease locus for squamous cell carcinoma at 9p21 (CDKN2A/p16(INK4A)/p14(ARF)/CDKN2B/p15(INK4B)/ANRIL; rs1333040, P 3.0 10(7)) which was replicated in a series of 5415 Han Chinese (P 0.03; combined analysis, P 2.3 10(8)). This large analysis provides additional evidence for the role of inherited genetic susceptibility to lung cancer and insight into biological differences in the development of the different histological types of lung cancer."],["dc.identifier.doi","10.1093/hmg/dds334"],["dc.identifier.isi","000310369000016"],["dc.identifier.pmid","22899653"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10648"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24907"],["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-NC 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/2.5"],["dc.title","Influence of common genetic variation on lung cancer risk: meta-analysis of 14 900 cases and 29 485 controls"],["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","34234"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Yuan, Hua"],["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","McLaughlin, John R."],["dc.contributor.author","Brhane, Yonathan"],["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","Gumus, Zeynep H."],["dc.contributor.author","Klein, Robert J."],["dc.contributor.author","Amos, Christopher I."],["dc.contributor.author","Wei, Qingyi"],["dc.date.accessioned","2018-11-07T10:07:09Z"],["dc.date.available","2018-11-07T10:07:09Z"],["dc.date.issued","2016"],["dc.description.abstract","Lung cancer etiology is multifactorial, and growing evidence has indicated that long non-coding RNAs (lncRNAs) are important players in lung carcinogenesis. We performed a large-scale meta-analysis of 690,564 SNPs in 15,531 autosomal lncRNAs by using datasets from six previously published genome-wide association studies (GWASs) from the Transdisciplinary Research in Cancer of the Lung (TRICL) consortium in populations of European ancestry. Previously unreported significant SNPs (P value < 1 x 10(-7)) were further validated in two additional independent lung cancer GWAS datasets from Harvard University and deCODE. In the final meta-analysis of all eight GWAS datasets with 17,153 cases and 239,337 controls, a novel risk SNP rs114020893 in the lncRNA NEXN-AS1 region at 1p31.1 remained statistically significant (odds ratio = 1.17; 95% confidence interval = 1.11-1.24; P = 8.31 x 10(-9)). In further in silico analysis, rs114020893 was predicted to change the secondary structure of the lncRNA. Our finding indicates that SNP rs114020893 of NEXN-AS1 at 1p31.1 may contribute to lung cancer susceptibility."],["dc.identifier.doi","10.1038/srep34234"],["dc.identifier.isi","000384833100001"],["dc.identifier.pmid","27713484"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13809"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39229"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["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","A Novel Genetic Variant in Long Non-coding RNA Gene NEXN-AS1 is Associated with Risk of Lung Cancer"],["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","e0173339"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Rosenberger, Albert"],["dc.contributor.author","Sohns, Melanie"],["dc.contributor.author","Friedrichs, Stefanie"],["dc.contributor.author","Hung, Rayjean J."],["dc.contributor.author","Fehringer, Gord"],["dc.contributor.author","McLaughlin, John R."],["dc.contributor.author","Amos, Christopher I."],["dc.contributor.author","Brennan, P. C."],["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","Christiani, David C."],["dc.contributor.author","Wei, Yongyue"],["dc.contributor.author","Bickeboeller, Heike"],["dc.date.accessioned","2018-11-07T10:26:17Z"],["dc.date.available","2018-11-07T10:26:17Z"],["dc.date.issued","2017"],["dc.description.abstract","Introduction Gene-set analysis (GSA) is an approach using the results of single-marker genome-wide association studies when investigating pathways as a whole with respect to the genetic basis of a disease. Methods We performed a meta-analysis of seven GSAs for lung cancer, applying the method METAGSA. Overall, the information taken from 11,365 cases and 22,505 controls from within the TRICL/ILCCO consortia was used to investigate a total of 234 pathways from the Kyoto Encyclopedia of Genes and Genomes (KEGG) database. Results META-GSA reveals the systemic lupus erythematosus KEGG pathway hsa05322, driven by the gene region 6p21-22, as also implicated in lung cancer (p = 0.0306). This gene region is known to be associated with squamous cell lung carcinoma. The most important genes driving the significance of this pathway belong to the genomic areas HIST1-H4L,- 1BN, -2BN, -H2AK, -H4K and C2/C4A/C4B. Within these areas, the markers most significantly associated with LC are rs13194781 (located within HIST12BN) and rs1270942 (located between C2 and C4A). Conclusions We have discovered a pathway currently marked as specific to systemic lupus erythematosus as being significantly implicated in lung cancer. The gene region 6p21-22 in this pathway appears to be more extensively associated with lung cancer than previously assumed. Given wide-stretched linkage disequilibrium to the area APOM/BAG6/MSH5, there is currently simply not enough information or evidence to conclude whether the potential pleiotropy of lung cancer and systemic lupus erythematosus is spurious, biological, or mediated. Further research into this pathway and gene region will be necessary."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2017"],["dc.identifier.doi","10.1371/journal.pone.0173339"],["dc.identifier.isi","000396073700053"],["dc.identifier.pmid","28273134"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14395"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43006"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights.access","openAccess"],["dc.title","Gene-set meta-analysis of lung cancer identifies pathway related to systemic lupus erythematosus"],["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","825"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Feng, Yun"],["dc.contributor.author","Wang, Y."],["dc.contributor.author","Liu, Hongliang"],["dc.contributor.author","Liu, Zhensheng"],["dc.contributor.author","Mills, Coleman"],["dc.contributor.author","Han, Younghun"],["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","Brueske, Irene"],["dc.contributor.author","Risch, Angela"],["dc.contributor.author","Ye, Yuanqing"],["dc.contributor.author","Wu, X."],["dc.contributor.author","Christiani, David C."],["dc.contributor.author","Amos, Christopher I."],["dc.contributor.author","Wei, Qingyi"],["dc.date.accessioned","2018-11-07T10:25:00Z"],["dc.date.available","2018-11-07T10:25:00Z"],["dc.date.issued","2017"],["dc.description.abstract","The T-cell protein tyrosine phosphatase (TCPTP) pathway consists of signaling events mediated by TCPTP. Mutations and genetic variants of some genes in the TCPTP pathway are associated with lung cancer risk and survival. In the present study, we first investigated associations of 5,162 single nucleotide polymorphisms (SNPs) in 43 genes of this TCPTP pathway with lung cancer risk by using summary data of six published genome-wide association studies (GWAS) of 12,160 cases and 16,838 controls. We identified 11 independent SNPs in eight genes after correction for multiple comparisons by a false discovery rate <0.20. Then, we performed in silico functional analyses for these 11 SNPs by eQTL analysis, two of which, PTPN2 SNPs rs2847297 and rs2847282, were chosen as tagSNPs. We further included two additional GWAS datasets of Harvard University (984 cases and 970 controls) and deCODE (1,319 cases and 26,380 controls), and the overall effects of these two SNPs among all eight GWAS studies remained significant (OR = 0.95, 95% CI = 0.92-0.98, and P = 0.004 for rs2847297; OR = 0.95, 95% CI = 0.92-0.99, and P = 0.009 for rs2847282). In conclusion, the PTPN2 rs2847297 and rs2847282 may be potential susceptible loci for lung cancer risk."],["dc.identifier.doi","10.1038/s41598-017-00850-0"],["dc.identifier.isi","000398824300042"],["dc.identifier.pmid","28400551"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14776"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42767"],["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","Genetic variants of PTPN2 are associated with lung cancer risk: a re-analysis of eight GWASs in the TRICL-ILCCO consortium"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0140179"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Rosenberger, Albert"],["dc.contributor.author","Friedrichs, Stefanie"],["dc.contributor.author","Amos, Christopher I."],["dc.contributor.author","Brennan, P. C."],["dc.contributor.author","Fehringer, Gordon"],["dc.contributor.author","Heinrich, Joachim"],["dc.contributor.author","Hung, Rayjean J."],["dc.contributor.author","Muley, Thomas"],["dc.contributor.author","Mueller-Nurasyid, Martina"],["dc.contributor.author","Risch, Angela"],["dc.contributor.author","Bickeboeller, Heike"],["dc.date.accessioned","2018-11-07T09:50:02Z"],["dc.date.available","2018-11-07T09:50:02Z"],["dc.date.issued","2015"],["dc.description.abstract","Introduction Gene-set analysis (GSA) methods are used as complementary approaches to genome-wide association studies (GWASs). The single marker association estimates of a prede-fined set of genes are either contrasted with those of all remaining genes or with a null non-associated background. To pool the p-values from several GSAs, it is important to take into account the concordance of the observed patterns resulting from single marker association point estimates across any given gene set. Here we propose an enhanced version of Fisher's inverse chi(2)-method META-GSA, however weighting each study to account for imperfect correlation between association patterns. Simulation and Power We investigated the performance of META-GSA by simulating GWASs with 500 cases and 500 controls at 100 diallelic markers in 20 different scenarios, simulating different relative risks between 1 and 1.5 in gene sets of 10 genes. Wilcoxon's rank sum test was applied as GSA for each study. We found that META-GSA has greater power to discover truly associated gene sets than simple pooling of the p-values, by e.g. 59% versus 37%, when the true relative risk for 5 of 10 genes was assume to be 1.5. Under the null hypothesis of no difference in the true association pattern between the gene set of interest and the set of remaining genes, the results of both approaches are almost uncorrelated. We recommend not relying on p-values alone when combining the results of independent GSAs. Application We applied META-GSA to pool the results of four case-control GWASs of lung cancer risk (Central European Study and Toronto/Lunenfeld-Tanenbaum Research Institute Study; German Lung Cancer Study and MD Anderson Cancer Center Study), which had already been analyzed separately with four different GSA methods (EASE; SLAT, mSUMSTAT and GenGen). This application revealed the pathway GO0015291 \"transmembrane transporter activity\" as significantly enriched with associated genes (GSA-method: EASE, p = 0.0315 corrected for multiple testing). Similar results were found for GO0015464 \"acetylcholine receptor activity\" but only when not corrected for multiple testing (all GSA-methods applied; p approximate to 0.02)."],["dc.description.sponsorship","Open-Access Publikationsfonds 2015"],["dc.identifier.doi","10.1371/journal.pone.0140179"],["dc.identifier.isi","000363799900005"],["dc.identifier.pmid","26501144"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12563"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35627"],["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 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","META-GSA: Combining Findings from Gene-Set Analyses across Several Genome-Wide Association Studies"],["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","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Ferreiro-Iglesias, Aida"],["dc.contributor.author","Lesseur, Corina"],["dc.contributor.author","McKay, James"],["dc.contributor.author","Hung, Rayjean J."],["dc.contributor.author","Han, Younghun"],["dc.contributor.author","Zong, Xuchen"],["dc.contributor.author","Christiani, David"],["dc.contributor.author","Johansson, Mattias"],["dc.contributor.author","Xiao, Xiangjun"],["dc.contributor.author","Li, Yafang"],["dc.contributor.author","Qian, David C."],["dc.contributor.author","Ji, Xuemei"],["dc.contributor.author","Liu, Geoffrey"],["dc.contributor.author","Caporaso, Neil"],["dc.contributor.author","Scelo, Ghislaine"],["dc.contributor.author","Zaridze, David"],["dc.contributor.author","Mukeriya, Anush"],["dc.contributor.author","Kontic, Milica"],["dc.contributor.author","Ognjanovic, Simona"],["dc.contributor.author","Lissowska, Jolanta"],["dc.contributor.author","Szołkowska, Małgorzata"],["dc.contributor.author","Swiatkowska, Beata"],["dc.contributor.author","Janout, Vladimir"],["dc.contributor.author","Holcatova, Ivana"],["dc.contributor.author","Bolca, Ciprian"],["dc.contributor.author","Savic, Milan"],["dc.contributor.author","Ognjanovic, Miodrag"],["dc.contributor.author","Bojesen, Stig Egil"],["dc.contributor.author","Wu, Xifeng"],["dc.contributor.author","Albanes, Demetrios"],["dc.contributor.author","Aldrich, Melinda C."],["dc.contributor.author","Tardon, Adonina"],["dc.contributor.author","Fernandez-Somoano, Ana"],["dc.contributor.author","Fernandez-Tardon, Guillermo"],["dc.contributor.author","Le Marchand, Loic"],["dc.contributor.author","Rennert, Gadi"],["dc.contributor.author","Chen, Chu"],["dc.contributor.author","Doherty, Jennifer"],["dc.contributor.author","Goodman, Gary"],["dc.contributor.author","Bickeböller, Heike"],["dc.contributor.author","Wichmann, H-Erich"],["dc.contributor.author","Risch, Angela"],["dc.contributor.author","Rosenberger, Albert"],["dc.contributor.author","Shen, Hongbing"],["dc.contributor.author","Dai, Juncheng"],["dc.contributor.author","Field, John K."],["dc.contributor.author","Davies, Michael"],["dc.contributor.author","Woll, Penella"],["dc.contributor.author","Teare, M. Dawn"],["dc.contributor.author","Kiemeney, Lambertus A."],["dc.contributor.author","van der Heijden, Erik H. F. M."],["dc.contributor.author","Yuan, Jian-Min"],["dc.contributor.author","Hong, Yun-Chul"],["dc.contributor.author","Haugen, Aage"],["dc.contributor.author","Zienolddiny, Shanbeh"],["dc.contributor.author","Lam, Stephen"],["dc.contributor.author","Tsao, Ming-Sound"],["dc.contributor.author","Johansson, Mikael"],["dc.contributor.author","Grankvist, Kjell"],["dc.contributor.author","Schabath, Matthew B."],["dc.contributor.author","Andrew, Angeline"],["dc.contributor.author","Duell, Eric"],["dc.contributor.author","Melander, Olle"],["dc.contributor.author","Brunnström, Hans"],["dc.contributor.author","Lazarus, Philip"],["dc.contributor.author","Arnold, Susanne"],["dc.contributor.author","Slone, Stacey"],["dc.contributor.author","Byun, Jinyoung"],["dc.contributor.author","Kamal, Ahsan"],["dc.contributor.author","Zhu, Dakai"],["dc.contributor.author","Landi, Maria Teresa"],["dc.contributor.author","Amos, Christopher I."],["dc.contributor.author","Brennan, Paul"],["dc.date.accessioned","2020-12-10T18:09:48Z"],["dc.date.available","2020-12-10T18:09:48Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1038/s41467-018-05890-2"],["dc.identifier.eissn","2041-1723"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15606"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73761"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Fine mapping of MHC region in lung cancer highlights independent susceptibility loci by ethnicity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]