Laboratory of Molecular Biology, Hospital of Ibn Eljazzar of Kairouan, Avenue Ibn Eljazzar, Kairouan 3140, Tunisia.
Cancer Epidemiol. 2010 Oct;34(5):598-603. doi: 10.1016/j.canep.2010.06.002. Epub 2010 Jul 4.
Several genes involved in the metabolism of carcinogenesis have been found to be polymorphic in the human population, and specific alleles are associated with increase risk of cancer of various sites. This study is focused on the polymorphic enzymes glutathione-S-transferase M1 (GSTM1) and T1 (GSTT1) that involved in the detoxification of many xenobiotics involved in the etiology of prostate cancer.
To evaluate whether GSTM1 and/or GSTT1 contribute to prostate cancer (CaP) etiology, we studied 110 incident CaP cases and 122 controls.
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.
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.
在人类群体中，已经发现有几个参与致癌作用代谢的基因呈多态性，而特定的等位基因与各种部位癌症的风险增加有关。本研究集中在多态酶谷胱甘肽-S-转移酶 M1（GSTM1）和 T1（GSTT1）上，它们参与许多参与前列腺癌病因的外来物的解毒。
为了评估 GSTM1 和/或 GSTT1 是否有助于前列腺癌（CaP）的病因，我们研究了 110 例新发病例和 122 例对照。
在 GSTT1 纯合缺失（无功能）基因型的男性中，患 CaP 的可能性增加（OR=2.17；95%CI=1-3.79），但在 GSTM1 中并非如此（OR=0.89；95%CI=0.66-1.88）。因此，与 GSTT1 基因座至少有一个活性等位基因的个体相比，缺乏 GSTT1 基因的个体患前列腺癌的风险约高两倍。
这些结果表明 GSTT1 与 CaP 风险相关。与 GSTT10/0 基因型相关的吸烟影响并未发现会影响前列腺癌的风险。
