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

  1. 1Department of Social Medicine, University of Bristol, Bristol, UK
  2. 2Department of Social Medicine, MRC Centre for Causal Analyses in Translational Epidemiology, University of Bristol, Bristol, UK
  3. 3Nuffield Department of Surgery, John Radcliffe Hospital, Oxford, UK
  4. 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.

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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

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