Original Article
Prostate Cancer and Prostatic Diseases (2009) 12, 296–300; doi:10.1038/pcan.2009.18; published online 2 June 2009
PTGS2–899G>C and prostate cancer risk: a population-based nested case–control study (ProtecT) and a systematic review with meta-analysis
A Murad1, S J Lewis1,2, G Davey Smith1,2, S M Collin1, L Chen1, F C Hamdy3, D E Neal4, J Donovan1 and R M Martin1,2
- 1Department of Social Medicine, University of Bristol, Bristol, UK
- 2Department of Social Medicine, MRC Centre for Causal Analyses in Translational Epidemiology, University of Bristol, Bristol, UK
- 3Nuffield Department of Surgery, John Radcliffe Hospital, Oxford, UK
- 4Department of Oncology, Addenbrooke's Hospital, University of Cambridge, Cambridge, UK
Correspondence: Professor RM Martin, Department of Social Medicine, University of Bristol, Canynge Hall, Whatley Road, Bristol BS8 2PS, UK. E-mail: Richard.Martin@bristol.ac.uk
Received 1 April 2009; Revised 21 April 2009; Accepted 21 April 2009; Published online 2 June 2009.
Abstract
Prostaglandin endoperoxidase synthase 2 is a key regulator of inflammation and may play a role in prostate carcinogenesis. The polymorphism, –899G>C (rs20417), alters a transcription factor-binding site and is associated with a reduced risk of colorectal adenoma. We tested the hypothesis that rs20417 may influence prostate cancer risk, using a large case–control study (ncases=1608, ncontrols=3058). We found no evidence that rs20417 alters prostate cancer risk (odds ratio (ORCC & GC v GG=1.05, 95% confidence interval (CI)=0.91–1.20). A meta-analysis of three studies also found little evidence that rs20417 alters risk (pooled ORCC & GC v GG=1.04, 95% CI=0.93–1.17), making it unlikely that rs20417 contributes in any major way to prostate cancer aetiology.
Keywords:
PTGS2, polymorphism, case–control, epidemiology
