Journal
PROSTATE
Volume 66, Issue 2, Pages 146-156Publisher
WILEY
DOI: 10.1002/pros.20305
Keywords
genetic polymorphisms; glutathione S-transferase; prostate cancer; gene-environment interactions; population-attributable risk percent
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Funding
- NCI NIH HHS [R01-CA556678, R01-CA082664, N01-CN-05230] Funding Source: Medline
- NIEHS NIH HHS [R01-ES10548] Funding Source: Medline
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BACKGROUND. The glutathione S-transferase (GST) enzymes detoxify several carcinogens. Genetic polymorphisms in GSTM1, T1, and P1 (Ile105Val) have been associated with prostate cancer, however, results have been inconsistent across studies. METHODS. Data from a population-based case-control study in King County, Washington, were used to further evaluate the relationships between these GST polymorphisms and prostate cancer. Incident cases (n = 590) were 40-64 years old, diagnosed from 1993 through 1996, and identified via the SEER cancer registry. Controls (n = 538) were identified via random digit dialing, and frequency age-matched to cases. Logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI). RESULTS. Risk of prostate cancer was moderately increased among Caucasians with the GSTM1-null genotype (OR = 1.54; 95% Cl 1.19-2.01). There were no associations for either GSTT1 or P1 (Ile105Val). The association between the GSTM1-null genotype and prostate cancer was not different according to cancer aggressiveness defined by stage at diagnosis and Gleason score. Among GSTM1-null Caucasians, the relative risk of prostate cancer increased linearly with increasing pack-years of smoking (P-value for trend = 0.007), with the highest ORs observed for smokers of > 30 pack-years. CONCLUSIONS. Findings suggest that the GSTM1-null genotype defines a subgroup of men at higher risk of prostate cancer, particularly if they are heavy smokers.
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