Genome-wide association and replication studies identify four variants associated with prostate cancer susceptibility

Julius Gudmundsson*, Patrick Sulem, Daniel F. Gudbjartsson, Thorarinn Blondal, Arnaldur Gylfason, Bjarni A. Agnarsson, Kristrun R. Benediktsdottir, Droplaug N. Magnusdottir, Gudbjorg Orlygsdottir, Margret Jakobsdottir, Simon N. Stacey, Asgeir Sigurdsson, Tiina Wahlfors, Teuvo Tammela, Joan P. Breyer, Kate M. McReynolds, Kevin M. Bradley, Berta Saez, Javier Godino, Sebastian NavarreteFernando Fuertes, Laura Murillo, Eduardo Polo, Katja K. Aben, Inge M. Van Oort, Brian K. Suarez, Brian T. Helfand, Donghui Kan, Carlo Zanon, Michael L. Frigge, Kristleifur Kristjansson, Jeffrey R. Gulcher, Gudmundur V. Einarsson, Eirikur Jonsson, William J. Catalona, Jose I. Mayordomo, Lambertus A. Kiemeney, Jeffrey R. Smith, Johanna Schleutker, Rosa B. Barkardottir, Augustine Kong, Unnur Thorsteinsdottir, Thorunn Rafnar, Kari Stefansson

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

299 Scopus citations

Abstract

We report a prostate cancer genome-wide association follow-on study. We discovered four variants associated with susceptibility to prostate cancer in several European populations: rs10934853[A] (OR = 1.12, P = 2.9 × 1010) on 3q21.3; two moderately correlated (r2 = 0.07) variants, rs16902094[G] (OR = 1.21, P = 6.2 × 1015) and rs445114[T] (OR = 1.14, P = 4.7 × 1010), on 8q24.21; and rs8102476[C] (OR = 1.12, P = 1.6 × 1011) on 19q13.2. We also refined a previous association signal on 11q13 with the SNP rs11228565[A] (OR = 1.23, P = 6.7 × 1012). In a multivariate analysis using 22 prostate cancer risk variants typed in the Icelandic population, we estimated that carriers in the top 1.3% of the risk distribution are at a 2.5 times greater risk of developing the disease than members of the general population.

Original languageEnglish (US)
Pages (from-to)1122-1126
Number of pages5
JournalNature Genetics
Volume41
Issue number10
DOIs
StatePublished - Oct 2009

Funding

We thank the individuals who participated in the study and whose contribution made this work possible. This project was funded in part by contract number 202059 (PROMARK) from the Seventh Framework Program of the European Union to deCODE Genetics (T.R. and L.A.K.), in part by FP7-MC-IAPP Grant agreement no. 218071 (CancerGene) to deCODE Genetics, in part by a V Foundation award and US Department of Veterans Affairs grants to J.R.S., and in part by Academy of Finland, Sigrid Juselius Foundation, Finnish Cancer Organisations and the Competitive Research Funding of the Pirkanmaa Hospital District, Tampere University Hospital, to J.S.

ASJC Scopus subject areas

  • Genetics

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