Person: Palmer, Cameron Douglas
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Palmer
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Cameron Douglas
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Palmer, Cameron Douglas
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Publication New Susceptibility Loci Associated with Kidney Disease in Type 1 Diabetes(Public Library of Science, 2012) Sandholm, Niina; Salem, Rany M; McKnight, Amy Jayne; Brennan, Eoin P.; Forsblom, Carol; Isakova, Tamara; McKay, Gareth J.; Williams, Winfred; Sadlier, Denise M.; Mäkinen, Ville-Petteri; Swan, Elizabeth J.; Palmer, Cameron Douglas; Boright, Andrew P.; Ahlqvist, Emma; Deshmukh, Harshal A.; Keller, Benjamin J.; Huang, Huateng; Ahola, Aila J.; Fagerholm, Emma; Gordin, Daniel; Harjutsalo, Valma; He, Bing; Heikkilä, Outi; Hietala, Kustaa; Kytö, Janne; Lahermo, Päivi; Lehto, Markku; Lithovius, Raija; Österholm, Anne-May; Parkkonen, Maija; Pitkäniemi, Janne; Rosengård-Bärlund, Milla; Saraheimo, Markku; Sarti, Cinzia; Söderlund, Jenny; Soro-Paavonen, Aino; Syreeni, Anna; Thorn, Lena M.; Tikkanen, Heikki; Tolonen, Nina; Tryggvason, Karl; Tuomilehto, Jaakko; Wadén, Johan; Gill, Geoffrey V.; Prior, Sarah Virginie; Guiducci, Candace; Mirel, Daniel B.; Taylor, Andrew; Hosseini, S. Mohsen; Parving, Hans-Henrik; Rossing, Peter; Tarnow, Lise; Ladenvall, Claes; Alhenc-Gelas, François; Lefebvre, Pierre; Rigalleau, Vincent; Roussel, Ronan; Tregouet, David-Alexandre; Maestroni, Anna; Maestroni, Silvia; Falhammar, Henrik; Gu, Tianwei; Möllsten, Anna; Cimponeriu, Danut; Ioana, Mihai; Mota, Maria; Mota, Eugen; Serafinceanu, Cristian; Stavarachi, Monica; Hanson, Robert L.; Nelson, Robert G.; Kretzler, Matthias; Colhoun, Helen M.; Panduru, Nicolae Mircea; Gu, Harvest F.; Brismar, Kerstin; Zerbini, Gianpaolo; Hadjadj, Samy; Marre, Michel; Groop, Leif; Lajer, Maria; Bull, Shelley B.; Waggott, Daryl; Paterson, Andrew D.; Savage, David A.; Bain, Stephen C.; Martin, Finian; Hirschhorn, Joel; Godson, Catherine; Florez, Jose; Groop, Per-Henrik; Maxwell, Alexander P.Diabetic kidney disease, or diabetic nephropathy (DN), is a major complication of diabetes and the leading cause of end-stage renal disease (ESRD) that requires dialysis treatment or kidney transplantation. In addition to the decrease in the quality of life, DN accounts for a large proportion of the excess mortality associated with type 1 diabetes (T1D). Whereas the degree of glycemia plays a pivotal role in DN, a subset of individuals with poorly controlled T1D do not develop DN. Furthermore, strong familial aggregation supports genetic susceptibility to DN. However, the genes and the molecular mechanisms behind the disease remain poorly understood, and current therapeutic strategies rarely result in reversal of DN. In the GEnetics of Nephropathy: an International Effort (GENIE) consortium, we have undertaken a meta-analysis of genome-wide association studies (GWAS) of T1D DN comprising ∼2.4 million single nucleotide polymorphisms (SNPs) imputed in 6,691 individuals. After additional genotyping of 41 top ranked SNPs representing 24 independent signals in 5,873 individuals, combined meta-analysis revealed association of two SNPs with ESRD: rs7583877 in the AFF3 gene (P = 1.2×\(10^{−8}\)) and an intergenic SNP on chromosome 15q26 between the genes RGMA and MCTP2, rs12437854 (P = 2.0×\(10^{−9}\)). Functional data suggest that AFF3 influences renal tubule fibrosis via the transforming growth factor-beta (TGF-β1) pathway. The strongest association with DN as a primary phenotype was seen for an intronic SNP in the ERBB4 gene (rs7588550, P = 2.1×\(10^{−7}\)), a gene with type 2 diabetes DN differential expression and in the same intron as a variant with cis-eQTL expression of ERBB4. All these detected associations represent new signals in the pathogenesis of DN.Publication Genome-Wide Association Studies of Asthma in Population-Based Cohorts Confirm Known and Suggested Loci and Identify an Additional Association near HLA(Public Library of Science, 2012) Ramasamy, Adaikalavan; Kuokkanen, Mikko; Vedantam, Sailaja; Gajdos, Zofia; Couto Alves, Alexessander; Lyon, Helen N.; Ferreira, Manuel A. R.; Strachan, David P.; Zhao, Jing Hua; Abramson, Michael J.; Brown, Matthew A.; Coin, Lachlan; Dharmage, Shyamali C.; Duffy, David L.; Haahtela, Tari; Heath, Andrew C.; Janson, Christer; Kähönen, Mika; Khaw, Kay-Tee; Laitinen, Jaana; Le Souef, Peter; Lehtimäki, Terho; Madden, Pamela A. F.; Marks, Guy B.; Martin, Nicholas G.; Matheson, Melanie C.; Palmer, Cameron Douglas; Palotie, Aarno; Pouta, Anneli; Robertson, Colin F.; Viikari, Jorma; Widen, Elisabeth; Wjst, Matthias; Jarvis, Deborah L.; Montgomery, Grant W.; Thompson, Philip J.; Wareham, Nick; Eriksson, Johan; Jousilahti, Pekka; Laitinen, Tarja; Pekkanen, Juha; Raitakari, Olli T.; O'Connor, George T.; Salomaa, Veikko; Jarvelin, Marjo-Riitta; Hirschhorn, JoelRationale: Asthma has substantial morbidity and mortality and a strong genetic component, but identification of genetic risk factors is limited by availability of suitable studies. Objectives: To test if population-based cohorts with self-reported physician-diagnosed asthma and genome-wide association (GWA) data could be used to validate known associations with asthma and identify novel associations. Methods: The APCAT (Analysis in Population-based Cohorts of Asthma Traits) consortium consists of 1,716 individuals with asthma and 16,888 healthy controls from six European-descent population-based cohorts. We examined associations in APCAT of thirteen variants previously reported as genome-wide significant (P<5x\(10^{−8}\)) and three variants reported as suggestive (P<5×\(10^{−7}\)). We also searched for novel associations in APCAT (Stage 1) and followed-up the most promising variants in 4,035 asthmatics and 11,251 healthy controls (Stage 2). Finally, we conducted the first genome-wide screen for interactions with smoking or hay fever. Main Results: We observed association in the same direction for all thirteen previously reported variants and nominally replicated ten of them. One variant that was previously suggestive, rs11071559 in RORA, now reaches genome-wide significance when combined with our data (P = 2.4×\(10^{−9}\)). We also identified two genome-wide significant associations: rs13408661 near IL1RL1/IL18R1 (\(P_{Stage1+Stage2}\) = 1.1x\(10^{−9}\)), which is correlated with a variant recently shown to be associated with asthma (rs3771180), and rs9268516 in the HLA region (\(P_{Stage1+Stage2}\) = 1.1x\(10^{−8}\)), which appears to be independent of previously reported associations in this locus. Finally, we found no strong evidence for gene-environment interactions with smoking or hay fever status. Conclusions: Population-based cohorts with simple asthma phenotypes represent a valuable and largely untapped resource for genetic studies of asthma.Publication The Metabochip, a Custom Genotyping Array for Genetic Studies of Metabolic, Cardiovascular, and Anthropometric Traits(Public Library of Science, 2012) Voight, Benjamin F.; Ding, Jun; Sidore, Carlo; Chines, Peter S.; Burtt, Noël P.; Fuchsberger, Christian; Li, Yanming; Erdmann, Jeanette; Frayling, Timothy M.; Heid, Iris M.; Jackson, Anne U.; Johnson, Toby; Kilpeläinen, Tuomas O.; Lindgren, Cecilia M.; Morris, Andrew P.; Prokopenko, Inga; Randall, Joshua C.; Soranzo, Nicole; Speliotes, Elizabeth K.; Teslovich, Tanya M.; Wheeler, Eleanor; Maguire, Jared; Potter, Simon; Rayner, N. William; Robertson, Neil; Stirrups, Kathleen; Winckler, Wendy; Sanna, Serena; Mulas, Antonella; Nagaraja, Ramaiah; Cucca, Francesco; Barroso, Inês; Deloukas, Panos; Loos, Ruth J. F.; Kathiresan, Sekar; Munroe, Patricia B.; Pfeufer, Arne; Samani, Nilesh J.; Schunkert, Heribert; McCarthy, Mark I.; Abecasis, Gonçalo R.; Boehnke, Michael; Kang, Hyun Min; Palmer, Cameron Douglas; Saxena, Richa; Parkin, Melissa; Newton-Cheh, Christopher; Hirschhorn, Joel; Altshuler, DavidGenome-wide association studies have identified hundreds of loci for type 2 diabetes, coronary artery disease and myocardial infarction, as well as for related traits such as body mass index, glucose and insulin levels, lipid levels, and blood pressure. These studies also have pointed to thousands of loci with promising but not yet compelling association evidence. To establish association at additional loci and to characterize the genome-wide significant loci by fine-mapping, we designed the “Metabochip,” a custom genotyping array that assays nearly 200,000 SNP markers. Here, we describe the Metabochip and its component SNP sets, evaluate its performance in capturing variation across the allele-frequency spectrum, describe solutions to methodological challenges commonly encountered in its analysis, and evaluate its performance as a platform for genotype imputation. The metabochip achieves dramatic cost efficiencies compared to designing single-trait follow-up reagents, and provides the opportunity to compare results across a range of related traits. The metabochip and similar custom genotyping arrays offer a powerful and cost-effective approach to follow-up large-scale genotyping and sequencing studies and advance our understanding of the genetic basis of complex human diseases and traits.Publication Evidence of Widespread Selection on Standing Variation in Europe at Height-Associated SNPs(Nature Publishing Group, 2012) Turchin, Michael C.; Chiang, Charleston W. K.; Palmer, Cameron Douglas; Sankararaman, Sriram; Reich, David; Hirschhorn, Joel; GIANT ConsortiumStrong signatures of positive selection at newly arising genetic variants are well-documented in humans, but this form of selection may not be widespread in recent human evolution. Because many human traits are highly polygenic and partly determined by common, ancient genetic variation, an alternative model for rapid genetic adaptation has been proposed: weak selection acting on many pre-existing (standing) genetic variants, or polygenic adaptation. By studying height, a classic polygenic trait, we demonstrate the first human signature of widespread selection on standing variation. We show that frequencies of alleles associated with increased height, both at known loci and genome-wide, are systematically elevated in Northern Europeans compared with Southern Europeans \((p<4.3×10^{−4})\). This pattern mirrors intra-European height differences and is not confounded by ancestry or other ascertainment biases. The systematic frequency differences are consistent with the presence of widespread weak selection (selection coefficients \(~10^{−3}–10^{−5}\) per allele) rather than genetic drift alone \((p<10^{−15})\).