Glutathione S-transferase-mu (GSTM1) and -theta (GSTT1) genotypes in the etiology of prostate cancer

Citation
Tr. Rebbeck et al., Glutathione S-transferase-mu (GSTM1) and -theta (GSTT1) genotypes in the etiology of prostate cancer, CANC EPID B, 8(4), 1999, pp. 283-287
Citations number
21
Categorie Soggetti
Oncology,"Onconogenesis & Cancer Research
Journal title
CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
ISSN journal
10559965 → ACNP
Volume
8
Issue
4
Year of publication
1999
Part
1
Pages
283 - 287
Database
ISI
SICI code
1055-9965(199904)8:4<283:GS(A-(>2.0.ZU;2-S
Abstract
The glutathione S-transferases (GSTs) are involved in the metabolism of num erous potential prostate carcinogens. Common homozygous germ-line deletions exist in the genes that encode GST-mu (GSTM1) and GST-0 (GSTT1) and preclu de enzyme expression. To evaluate whether GSTM1 and/or GSTT1 contribute to prostate cancer (CaP) etiology, we studied 237 incident CaP cases and 239 a ge- and race-matched controls. The probability of having CaP was increased in men who had nondeleted (functional) genotypes at GSTT1 (odds ratio, 1.83 ; 95% confidence interval, 1.19-2.80) but not GSTM1 (odds ratio, 1.07; 95% confidence interval, 0.73-1.55). No interaction of these genes in CaP etiol ogy was observed. GST-0 is highly expressed in the prostate and can produce genotoxic effects upon exposure to specific carcinogens. These results sug gest that GSTT1 is associated with Cap risk.