Abstract | UNLABELLED: OBJECTIVE: To evaluate whether GSTM1 and/or GSTT1 contribute to prostate cancer (CaP) etiology, we studied 110 incident CaP cases and 122 controls. RESULTS: The probability of having CaP was increased in men who had homozygous deleted (non-functional) genotypes at GSTT1 (OR=2.17; 95% CI=1-3.79) but not GSTM1 (OR=0.89; 95% CI=0.66-1.88). Hence, individuals lacking the GSTT1 gene are at approximately twofold higher risk of developing prostate cancer in comparison with individuals with at least one active allele in the GSTT1 locus. CONCLUSION: These results suggest that GSTT1 is associated with CaP risk. The effect of smoking associated with the GSTT10/0 genotype was not found to affect the risk of prostate cancer.
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Authors | Yousra Souiden, Manel Mahdouani, Kamel Chaieb, Rafick Elkamel, Kacem Mahdouani |
Journal | Cancer epidemiology
(Cancer Epidemiol)
Vol. 34
Issue 5
Pg. 598-603
(Oct 2010)
ISSN: 1877-783X [Electronic] Netherlands |
PMID | 20599479
(Publication Type: Journal Article)
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Copyright | Copyright © 2010 Elsevier Ltd. All rights reserved. |
Chemical References |
- glutathione S-transferase T1
- Glutathione Transferase
- glutathione S-transferase M1
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Topics |
- Adult
- Age Factors
- Aged
- Aged, 80 and over
- Case-Control Studies
- Genetic Predisposition to Disease
- Glutathione Transferase
(genetics, metabolism)
- Humans
- Male
- Middle Aged
- Prostatic Neoplasms
(enzymology, epidemiology, genetics)
- Smoking
(epidemiology, genetics, metabolism)
- Tunisia
(epidemiology)
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