Journal article

Genome-wide association study identifies new prostate cancer susceptibility loci

Fredrick R Schumacher, Sonja I Berndt, Afshan Siddiq, Kevin B Jacobs, Zhaoming Wang, Sara Lindstrom, Victoria L Stevens, Constance Chen, Alison M Mondul, Ruth C Travis, Daniel O Stram, Rosalind A Eeles, Douglas F Easton, Graham Giles, John L Hopper, David E Neal, Freddie C Hamdy, Jenny L Donovan, Kenneth Muir, Ali Amin Al Olama Show all

HUMAN MOLECULAR GENETICS | OXFORD UNIV PRESS | Published : 2011

Abstract

Prostate cancer (PrCa) is the most common non-skin cancer diagnosed among males in developed countries and the second leading cause of cancer mortality, yet little is known regarding its etiology and factors that influence clinical outcome. Genome-wide association studies (GWAS) of PrCa have identified at least 30 distinct loci associated with small differences in risk. We conducted a GWAS in 2782 advanced PrCa cases (Gleason grade ≥ 8 or tumor stage C/D) and 4458 controls with 571 243 single nucleotide polymorphisms (SNPs). Based on in silico replication of 4679 SNPs (Stage 1, P < 0.02) in two published GWAS with 7358 PrCa cases and 6732 controls, we identified a new susceptibility locus as..

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Grants

Awarded by U.S. National Institutes of Health, National Cancer Institute


Awarded by Cancer Research UK


Awarded by National Health and Medical Research Council, Australia


Awarded by Health Technology Assessment Programme


Awarded by Medical Research Council of England


Awarded by USA Dept of Defense


Awarded by Swedish Research Council


Awarded by Swedish Cancer Foundation


Awarded by National Cancer Institute


Awarded by Medical Research Council


Awarded by National Institute for Health Research


Awarded by NATIONAL CANCER INSTITUTE


Funding Acknowledgements

The BPC3 was supported by the U.S. National Institutes of Health, National Cancer Institute (cooperative agreements U01-CA98233 to D.J.H., U01-CA98710 to M.J.T., U01-CA98216 to E.R., and U01-CA98758 to B.E.H., and Intramural Research Program of NIH/National Cancer Institute, Division of Cancer Epidemiology and Genetics). This work was supported by Cancer Research UK Grants C5047/A7357, C1287/A10118, C5047/A3354, C5047/A10692, C16913/A6135, and C16913/A6835. We would also like to thank the following for funding support: The Institute of Cancer Research and The Everyman Campaign, The Prostate Cancer Research Foundation, Prostate Research Campaign UK, The National Cancer Research Network UK, The National Cancer Research Institute (NCRI) UK. We acknowledge NHS funding to the NIHR Biomedical Research Centre at The Institute of Cancer Research and The Royal Marsden NHS Foundation Trust. We also acknowledge grant support from The National Health and Medical Research Council, Australia (209057, 251533, 450104, 390130), VicHealth, The Cancer Council Victoria, Cancer Council Queensland, The Whitten Foundation, and Tattersall's. The ProtecT study is ongoing and is funded by the Health Technology Assessment Programme (projects 96/20/06, 96/20/99). The ProtecT trial and its linked ProMPT and CAP (Comparison Arm for ProtecT) studies are supported by Department of Health, England; Cancer Research UK grant number C522/A8649, Medical Research Council of England grant number G0500966, ID 75466 and The NCRI, UK. The epidemiological data for ProtecT were generated though funding from the Southwest National Health Service Research and Development. DNA extraction in ProtecT was supported by USA Dept of Defense award W81XWH-04-1-0280, Yorkshire Cancer Research and Cancer Research UK. The bio-repository from ProtecT is supported by the NCRI (ProMPT) study and the Cambridge BMRC grant from NIHR. Financial support for CAPS was provided through a grant from the Swedish Research Council (grant no K2010-70X-20430-04-3 and 70867901), the Swedish Cancer Foundation (grant no 09-0677), the Hedlund Foundation, Soderberg Foundation, Enqvist Foundation, ALF funds from the Stockholm County Council. W.B.I. was supported by National Cancer Institute grants CA112517 and CA133009.