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Basic Research

Analysis of prostate cancer association with four single-nucleotide polymorphisms from genome-wide studies and serum phyto-estrogen concentrations

Abstract

Background:

Both genetics and the environment are implicated as risk factors for prostate cancer (PCa). This population-based case–control study evaluated four single-nucleotide polymorphisms (SNPs) previously identified by genome-wide association studies to be associated with increased PCa susceptibility. Potential relationships between serum concentrations of phyto-estrogens and SNPs were also investigated.

Methods:

Four SNPs (rs10993994, rs2660753, rs1016343 and rs6983267) were genotyped in 247 PCa patients, 125 BPH patients and 274 control men recruited in Scotland. Serum concentrations of the phyto-estrogens enterolactone, equol, genistein and daidzein were measured by isotope dilution gas chromatography–mass spectrometry.

Results:

Increased PCa risk was associated with TT genotype of rs10993994 compared with CC and CT genotypes combined (odds ratio (OR)=1.87; 95% confidence interval (CI), 1.26–2.77). TT homozygotes who had low serum enterolactone concentrations (below median) were more likely to have PCa (OR=2.90; 95% CI, 1.28–6.57) than individuals with CC/CT genotype and high serum enterolactone concentrations (above median). PCa was not associated with the other three SNPs tested.

Conclusions:

PCa susceptibility was associated with TT genotype of SNP rs10993994 in this cohort of Scottish men and the increased risk of PCa was modified by serum enterolactone concentrations.

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Acknowledgements

This study was funded by Cancer Research UK and NHS Highland Endowment Fund.

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Correspondence to C K M Ho.

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The authors declare no conflict of interest.

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Supplementary Information accompanies the paper on the Prostate Cancer and Prostatic Diseases website

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Ho, C., Halley, L., Wei, J. et al. Analysis of prostate cancer association with four single-nucleotide polymorphisms from genome-wide studies and serum phyto-estrogen concentrations. Prostate Cancer Prostatic Dis 15, 365–368 (2012). https://doi.org/10.1038/pcan.2012.24

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