A genome-wide association study of early menopause and the combined impact of identified variants

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Perry, John R. B.
Corre, Tanguy
Esko, Tõnu
Fischer, Krista
Franceschini, Nora
He, Chunyan
Kutalik, Zoltan
Mangino, Massimo
Rose, Lynda M.
Vernon Smith, Albert
Stolk, Lisette
Sulem, Patrick
Weedon, Michael N.
Zhuang, Wei V.
Arnold, Alice
Ashworth, Alan
Bergmann, Sven
Burri, Andrea
Couper, David J.
Goodarzi, Mark O.
Gudnason, Vilmundur
Harris, Tamara
Launer, Lenore
Laven, Joop S. E.
McKnight, Barbara
Masciullo, Corrado
Milani, Lili
Orr, Nicholas
Psaty, Bruce M.
Rivadeneira, Fernando
Sala, Cinzia
Salumets, Andres
Schoemaker, Minouk
Traglia, Michela
Waeber, Gérard
Chanock, Stephen J.
Demerath, Ellen W.
Garcia, Melissa
Lunetta, Kathryn L.
Metspalu, Andres
Montgomery, Grant W.
Murabito, Joanne M.
Newman, Anne B.
Ong, Ken K.
Spector, Tim D.
Stefansson, Kari
Swerdlow, Anthony J.
Thorsteinsdottir, Unnur
Uitterlinden, André G.
Visser, Jenny A.
Vollenweider, Peter
Toniolo, Daniela
Murray, Anna
Note: Order does not necessarily reflect citation order of authors.
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https://doi.org/10.1093/hmg/dds551Metadata
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Perry, John R. B., Tanguy Corre, Tõnu Esko, Daniel I. Chasman, Krista Fischer, Nora Franceschini, Chunyan He, et al. 2013. A genome-wide association study of early menopause and the combined impact of identified variants. Human Molecular Genetics 22(7): 1465-1472.Abstract
Early menopause (EM) affects up to 10% of the female population, reducing reproductive lifespan considerably. Currently, it constitutes the leading cause of infertility in the western world, affecting mainly those women who postpone their first pregnancy beyond the age of 30 years. The genetic aetiology of EM is largely unknown in the majority of cases. We have undertaken a meta-analysis of genome-wide association studies (GWASs) in 3493 EM cases and 13 598 controls from 10 independent studies. No novel genetic variants were discovered, but the 17 variants previously associated with normal age at natural menopause as a quantitative trait (QT) were also associated with EM and primary ovarian insufficiency (POI). Thus, EM has a genetic aetiology which overlaps variation in normal age at menopause and is at least partly explained by the additive effects of the same polygenic variants. The combined effect of the common variants captured by the single nucleotide polymorphism arrays was estimated to account for ∼30% of the variance in EM. The association between the combined 17 variants and the risk of EM was greater than the best validated non-genetic risk factor, smoking.Other Sources
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3596848/pdf/Terms of Use
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