Association of GSTM1, GSTT1, and GSTP1 Gene Polymorphisms with the Risk of Prostate Cancer: A Meta-analysis

• Published in: Cancer epidemiology, biomarkers & prevention Vol. 14; no. 1; pp. 176 - 181
• Main Authors: NTAIS, Christos, POLYCARPOU, Anastasia, IOANNIDIS, John P. A
• Format: Journal Article
• Language: English
• Published: Philadelphia, PA American Association for Cancer Research 01.01.2005
• Subjects: Alleles; Biological and medical sciences; Chi-Square Distribution; Genotype; glutathione; Glutathione S-Transferase pi; Glutathione Transferase - genetics; GST; Humans; Isoenzymes - genetics; Male; Medical sciences; meta-analysis; Nephrology. Urinary tract diseases; Odds Ratio; polymorphism; Polymorphism, Genetic; prostate cancer; Prostatic Neoplasms - genetics; Risk Assessment; Risk Factors; transferase; Tumors; Tumors of the urinary system; Urinary tract. Prostate gland; Human; Urinary system disease; Genetic variability; Prostate disease; Enzyme; Isozyme; Transferases; Genotype; Malignant tumor; Epidemiology; Urology; Metaanalysis; Gene; Glutathione transferase; Risk factor; Genetics; Male genital diseases; Prostate cancer; Public health; Polymorphism
• ISSN: 1055-9965; 1538-7755
• DOI: 10.1158/1055-9965.176.14.1

The glutathione S -transferase ( GST ) gene superfamily encodes for enzymes involved in conjugation of electrophilic compounds to glutathione. Several polymorphisms in the GST genes have been implicated as risk factors for prostate cancer. We did a meta-analysis of 11 studies with GSTM1 genotyping (2,063 prostate cancer cases and 2,625 controls), 10 studies with GSTT1 genotyping (1,965 cases and 2,554 controls), and 12 studies with GSTP1 genotyping (2,528 cases and 3,076 controls). The random effects odds ratio was 1.08 [95% confidence interval (95% CI), 0.93-1.25, no significant between-study heterogeneity] for the GSTM1 null versus nondeleted genotype and 0.90 (95% CI, 0.73-1.12; P = 0.03 for heterogeneity) for the GSTT1 null versus nondeleted genotype. Overall, the random effects odds ratio was 1.05 (95% CI, 0.90-1.21; P < 0.01 for heterogeneity) for the GSTP1-Val versus GSTP1-Ile allele. For all three polymorphisms, there was a trend for the presence of an association in the earliest published studies, but this did not seem to be validated in subsequent research. For GSTT1 , larger studies gave different results than smaller ones. The meta-analysis shows that these three polymorphisms are unlikely to be major determinants of susceptibility to prostate cancer on a wide population basis.