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","879"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Archives of General Psychiatry"],["dc.bibliographiccitation.lastpage","888"],["dc.bibliographiccitation.volume","67"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Grube, Sabrina"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Malzahn, Dörte"],["dc.contributor.author","Krampe, Henning"],["dc.contributor.author","Ribbe, Katja"],["dc.contributor.author","Friedrichs, Heidi"],["dc.contributor.author","Radyushkin, Konstantin"],["dc.contributor.author","El-Kordi, Ahmed"],["dc.contributor.author","Benseler, Fritz"],["dc.contributor.author","Hannke, Kathrin"],["dc.contributor.author","Sperling, Swetlana"],["dc.contributor.author","Schwerdtfeger, Dayana"],["dc.contributor.author","Thanhäuser, Ivonne"],["dc.contributor.author","Gerchen, Martin Fungisai"],["dc.contributor.author","Ghorbani, Mohammed"],["dc.contributor.author","Gutwinski, Stefan"],["dc.contributor.author","Hilmes, Constanze"],["dc.contributor.author","Leppert, Richard"],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Sowislo, Julia"],["dc.contributor.author","Stawicki, Sabina"],["dc.contributor.author","Stödtke, Maren"],["dc.contributor.author","Szuszies, Christoph"],["dc.contributor.author","Reim, Kerstin"],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Eckstein, Fritz"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Bickeböller, Heike"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:57Z"],["dc.date.available","2017-09-07T11:46:57Z"],["dc.date.issued","2010"],["dc.description.abstract","Context: Schizophrenia is the collective term for a heterogeneous group of mental disorders with a still obscure biological basis. In particular, the specific contribution of risk or candidate gene variants to the complex schizophrenic phenotype is largely unknown. Objective: To prepare the ground for a novel “phenomics” approach, a unique schizophrenia patient database was established by GRAS (Göttingen Research Association for Schizophrenia), designed to allow association of genetic information with quantifiable phenotypes. Because synaptic dysfunction plays a key role in schizophrenia, the complexin 2 gene (CPLX2) was examined in the first phenotype-based genetic association study (PGAS) of GRAS. Design: Subsequent to a classic case-control approach, we analyzed the contribution of CPLX2 polymorphisms to discrete cognitive domains within the schizophrenic population. To gain mechanistic insight into how certain CPLX2 variants influence gene expression and function, peripheral blood mononuclear cells of patients, Cplxnull mutantmice, and transfected cells were investigated.Setting: Coordinating research center (Max Planck Institute of Experimental Medicine) and 23 collaboratingpsychiatric centers all over Germany.Participants: One thousand seventy-one patients with schizophrenia (DSM-IV) examined by an invariant investigator team, resulting in the GRAS database with more than 3000 phenotypic data points per patient, and 1079 healthy control subjects of comparable ethnicity.Main Outcome Measure: Cognitive performance including executive functioning, reasoning, and verbal learning/memory. Results: Six single-nucleotide polymorphisms, distributed over the whole CPLX2 gene, were found to be highly associated with current cognition of schizophrenic subjects but only marginally with premorbid intelligence. Correspondingly, in Cplx2-null mutant mice, prominent cognitive loss of function was obtained only in combination with a minor brain lesion applied during puberty, modeling a clinically relevant environmental risk (“second hit”) for schizophrenia. In the human CPLX2 gene, 1 of the identified 6 cognition-relevant single-nucleotide polymorphisms, rs3822674 in the 3´ untranslated region, was detected to influence microRNA-498 binding and gene expression. The same marker was associated with differential expression of CPLX2 in peripheral blood mononuclear cells. Conclusions: The PGAS allows identification of markerassociated clinical/biological traits. Current cognitive performance in schizophrenic patients is modified by CPLX2 variants modulating posttranscriptional gene expression"],["dc.identifier.doi","10.1001/archgenpsychiatry.2010.107"],["dc.identifier.fs","577608"],["dc.identifier.gro","3150567"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6097"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7343"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.notes.status","final"],["dc.rights.access","closedAccess"],["dc.subject","Schizophrenia"],["dc.subject.ddc","610"],["dc.title","Modification of cognitive performance in schizophrenia by complexin 2 gene polymorphisms"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["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"]]

[["dc.bibliographiccitation.firstpage","156"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","European Neuropsychopharmacology : The Journal of the European College of Neuropsychopharmacology"],["dc.bibliographiccitation.lastpage","170"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Budde, Monika"],["dc.contributor.author","Friedrichs, Stefanie"],["dc.contributor.author","Alliey-Rodriguez, Ney"],["dc.contributor.author","Ament, Seth"],["dc.contributor.author","Badner, Judith A."],["dc.contributor.author","Berrettini, Wade H."],["dc.contributor.author","Bloss, Cinnamon S."],["dc.contributor.author","Byerley, William"],["dc.contributor.author","Cichon, Sven"],["dc.contributor.author","Comes, Ashley L."],["dc.contributor.author","Coryell, William"],["dc.contributor.author","Craig, David W."],["dc.contributor.author","Degenhardt, Franziska"],["dc.contributor.author","Edenberg, Howard J."],["dc.contributor.author","Foroud, Tatiana"],["dc.contributor.author","Forstner, Andreas J."],["dc.contributor.author","Frank, Josef"],["dc.contributor.author","Gershon, Elliot S."],["dc.contributor.author","Goes, Fernando S."],["dc.contributor.author","Greenwood, Tiffany A."],["dc.contributor.author","Guo, Yiran"],["dc.contributor.author","Hipolito, Maria"],["dc.contributor.author","Hood, Leroy"],["dc.contributor.author","Keating, Brendan J."],["dc.contributor.author","Koller, Daniel L."],["dc.contributor.author","Lawson, William B."],["dc.contributor.author","Liu, Chunyu"],["dc.contributor.author","Mahon, Pamela B."],["dc.contributor.author","McInnis, Melvin G."],["dc.contributor.author","McMahon, Francis J."],["dc.contributor.author","Meier, Sandra M."],["dc.contributor.author","Mühleisen, Thomas W."],["dc.contributor.author","Murray, Sarah S."],["dc.contributor.author","Nievergelt, Caroline M."],["dc.contributor.author","Nurnberger, John I."],["dc.contributor.author","Nwulia, Evaristus A."],["dc.contributor.author","Potash, James B."],["dc.contributor.author","Quarless, Danjuma"],["dc.contributor.author","Rice, John"],["dc.contributor.author","Roach, Jared C."],["dc.contributor.author","Scheftner, William A."],["dc.contributor.author","Schork, Nicholas J."],["dc.contributor.author","Shekhtman, Tatyana"],["dc.contributor.author","Shilling, Paul D."],["dc.contributor.author","Smith, Erin N."],["dc.contributor.author","Streit, Fabian"],["dc.contributor.author","Strohmaier, Jana"],["dc.contributor.author","Szelinger, Szabolcs"],["dc.contributor.author","Treutlein, Jens"],["dc.contributor.author","Witt, Stephanie H."],["dc.contributor.author","Zandi, Peter P."],["dc.contributor.author","Zhang, Peng"],["dc.contributor.author","Zöllner, Sebastian"],["dc.contributor.author","Bickeböller, Heike"],["dc.contributor.author","Falkai, Peter G."],["dc.contributor.author","Kelsoe, John R."],["dc.contributor.author","Nöthen, Markus M."],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Malzahn, Dörthe"],["dc.date.accessioned","2019-07-09T11:50:26Z"],["dc.date.available","2019-07-09T11:50:26Z"],["dc.date.issued","2019-"],["dc.description.abstract","Genome-wide association studies of case-control status have advanced the understanding of the genetic basis of psychiatric disorders. Further progress may be gained by increasing sample size but also by new analysis strategies that advance the exploitation of existing data, especially for clinically important quantitative phenotypes. The functionally-informed efficient region-based test strategy (FIERS) introduced herein uses prior knowledge on biological function and dependence of genotypes within a powerful statistical framework with improved sensitivity and specificity for detecting consistent genetic effects across studies. As proof of concept, FIERS was used for the first genome-wide single nucleotide polymorphism (SNP)-based investigation on bipolar disorder (BD) that focuses on an important aspect of disease course, the functional outcome. FIERS identified a significantly associated locus on chromosome 15 (hg38: chr15:48965004 - 49464789 bp) with consistent effect strength between two independent studies (GAIN/TGen: European Americans, BOMA: Germans; n = 1592 BD patients in total). Protective and risk haplotypes were found on the most strongly associated SNPs. They contain a CTCF binding site (rs586758); CTCF sites are known to regulate sets of genes within a chromatin domain. The rs586758 - rs2086256 - rs1904317 haplotype is located in the promoter flanking region of the COPS2 gene, close to microRNA4716, and the EID1, SHC4, DTWD1 genes as plausible biological candidates. While implication with BD is novel, COPS2, EID1, and SHC4 are known to be relevant for neuronal differentiation and function and DTWD1 for psychopharmacological side effects. The test strategy FIERS that enabled this discovery is equally applicable for tag SNPs and sequence data."],["dc.identifier.doi","10.1016/j.euroneuro.2018.10.005"],["dc.identifier.pmid","30503783"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15939"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59772"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1873-7862"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.subject.ddc","610"],["dc.title","Efficient region-based test strategy uncovers genetic risk factors for functional outcome in bipolar disorder"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S1"],["dc.bibliographiccitation.issue","Suppl 9"],["dc.bibliographiccitation.journal","BMC Proceedings"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Ghosh, Saurabh"],["dc.contributor.author","Bickeböller, Heike"],["dc.contributor.author","Bailey, Julia"],["dc.contributor.author","Bailey-Wilson, Joan E."],["dc.contributor.author","Cantor, Rita"],["dc.contributor.author","Culverhouse, Robert"],["dc.contributor.author","Daw, Warwick"],["dc.contributor.author","DeStefano, Anita L."],["dc.contributor.author","Engelman, Corinne D."],["dc.contributor.author","Hinrichs, Anthony"],["dc.contributor.author","Houwing-Duistermaat, Jeanine"],["dc.contributor.author","König, Inke R."],["dc.contributor.author","Kent, Jack"],["dc.contributor.author","Laird, Nan"],["dc.contributor.author","Pankratz, Nathan"],["dc.contributor.author","Paterson, Andrew"],["dc.contributor.author","Pugh, Elizabeth"],["dc.contributor.author","Suarez, Brian"],["dc.contributor.author","Sun, Yan"],["dc.contributor.author","Thomas, Alun"],["dc.contributor.author","Tintle, Nathan"],["dc.contributor.author","Zhu, Xiaofeng"],["dc.contributor.author","Ziegler, Andreas"],["dc.contributor.author","MacCluer, Jean W."],["dc.contributor.author","Almasy, Laura"],["dc.date.accessioned","2012-01-17T08:51:25Z"],["dc.date.accessioned","2021-10-27T13:10:54Z"],["dc.date.available","2012-01-17T08:51:25Z"],["dc.date.available","2021-10-27T13:10:54Z"],["dc.date.issued","2011"],["dc.description.abstract","Genetic Analysis Workshop 17 (GAW17) provided a platform for evaluating existing statistical genetic methods and for developing novel methods to analyze rare variants that modulate complex traits. In this article, we present an overview of the 1000 Genomes Project exome data and simulated phenotype data that were distributed to GAW17 participants for analyses, the different issues addressed by the participants, and the process of preparation of manuscripts resulting from the discussions during the workshop."],["dc.identifier.doi","10.1186/1753-6561-5-S9-S1"],["dc.identifier.fs","585073"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7060"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/91542"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Identifying rare variants from exome scans: the GAW17 experience"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]