PURPOSE: Glutathione S-transferase (GST) enzymes may prevent carcinogenesis through inactivation of reactive electrophiles by conjugation to reduced glutathione. Recently, it was reported that most prostate cancers fail to express GST-pi despite an abundant presence in benign prostate tissue, suggesting a common genetic alteration. To define its presence in prostate tissue, we evaluated GST-pi expression in a variety of prostate tissues. MATERIALS AND METHODS: Immunostaining with anti-GST-pi antibody was performed on 69 benign prostates, 44 malignant prostates, 12 incidental prostate carcinomas and 17 prostatic intraepithelial neoplasia (PIN) specimens. Specimens were evaluated for the presence and percent of GST-pi. Within benign tissue, GST-pi immunostaining was distinguished between basal cells and secretory acinar epithelium. RESULTS: In benign epithelium, the basal cells demonstrated intense staining in all cases. The mean percent staining among the basal cells was 67% (R 40-90%). The acinar epithelium stained weakly positive in 94% (65/69) of specimens, however the mean percent staining was only 5% (R 0-25%). GST-pi was detected in only 3.5% (2/56) of the prostate cancers. No incidental prostate cancers and only one (6%) high grade PIN stained positive. CONCLUSIONS: Our study confirms the absence of GST-pi expression in prostate cancer and high grade PIN. Furthermore, GST-pi expression correlates well with the basal cell phenotype, but not with benign epithelial cells. The lack of staining among prostate cancer cells may reflect the absence of a basal cell layer, suggesting that GST-pi is involved more in epithelial differentiation and questioning its role in the malignant transformation of prostatic acinar cells.
PURPOSE:Glutathione S-transferase (GST) enzymes may prevent carcinogenesis through inactivation of reactive electrophiles by conjugation to reduced glutathione. Recently, it was reported that most prostate cancers fail to express GST-pi despite an abundant presence in benign prostate tissue, suggesting a common genetic alteration. To define its presence in prostate tissue, we evaluated GST-pi expression in a variety of prostate tissues. MATERIALS AND METHODS: Immunostaining with anti-GST-pi antibody was performed on 69 benign prostates, 44 malignant prostates, 12 incidental prostate carcinomas and 17 prostatic intraepithelial neoplasia (PIN) specimens. Specimens were evaluated for the presence and percent of GST-pi. Within benign tissue, GST-pi immunostaining was distinguished between basal cells and secretory acinar epithelium. RESULTS: In benign epithelium, the basal cells demonstrated intense staining in all cases. The mean percent staining among the basal cells was 67% (R 40-90%). The acinar epithelium stained weakly positive in 94% (65/69) of specimens, however the mean percent staining was only 5% (R 0-25%). GST-pi was detected in only 3.5% (2/56) of the prostate cancers. No incidental prostate cancers and only one (6%) high grade PIN stained positive. CONCLUSIONS: Our study confirms the absence of GST-pi expression in prostate cancer and high grade PIN. Furthermore, GST-pi expression correlates well with the basal cell phenotype, but not with benign epithelial cells. The lack of staining among prostate cancer cells may reflect the absence of a basal cell layer, suggesting that GST-pi is involved more in epithelial differentiation and questioning its role in the malignant transformation of prostatic acinar cells.
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