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dc.contributor.authorBostwick, David G
dc.contributor.authorMeiers, Isabelle
dc.contributor.authorShanks, Jonathan H
dc.date.accessioned2009-06-19T13:50:23Z
dc.date.available2009-06-19T13:50:23Z
dc.date.issued2007-09
dc.identifier.citationGlutathione S-transferase: differential expression of alpha, mu, and pi isoenzymes in benign prostate, prostatic intraepithelial neoplasia, and prostatic adenocarcinoma. 2007, 38 (9):1394-401 Hum. Pathol.en
dc.identifier.issn0046-8177
dc.identifier.pmid17555796
dc.identifier.doi10.1016/j.humpath.2007.02.008
dc.identifier.urihttp://hdl.handle.net/10541/71041
dc.description.abstractGlutathione S-transferases (GST) comprise a family of enzymes which are critical for inactivation of toxins and carcinogens. We examined the cellular expression of multiple subclasses of GST immunohistochemically in 25 radical prostatectomy specimens with clinically localized prostate cancer. Gleason scores ranged from 5 to 9, and pathologic stages varied from pT2a to pT3b (all N0M0). Antibodies were directed against GST Ya, Yc, and Yk (alpha subclass), Yb1 (micro subclass), and YPr (pi subclass). The percentage of positive cells and intensity of staining was assessed for benign epithelium, high-grade prostatic intraepithelial neoplasia (PIN), and adenocarcinoma. GSTalpha (Ya) was detected in 30% of cells (mean) in benign acini, 4.9% of cells in high-grade PIN, and 4.5% of cells in adenocarcinoma. The corresponding results for alpha (Yk), micro (Yb1), and pi (Yp) were 12.7%, 10.9%, and 3.5%; 8.7%, 5.2%, and 0.6%; and 66.7,% 0%, and 0%, respectively. GST Yc (alpha subclass) displayed the lowest level of expression, with diffuse weak staining in scattered benign secretory cells and only single cells (<1%) in high-grade PIN and carcinoma. These results demonstrate consistent reduction or loss of expression of all subclasses of GST with progression of prostatic neoplasia from benign epithelium to high-grade PIN and carcinoma. We hypothesize that carcinogenesis in the prostate results from impaired cellular handling of mutagenic agents owing to reduction or loss of expression of multiple GST and other detoxifying and antimutagenesis agents.
dc.language.isoenen
dc.subjectProstate Canceren
dc.subject.meshAdenocarcinoma
dc.subject.meshAdult
dc.subject.meshAged
dc.subject.meshCarcinoma
dc.subject.meshGene Expression Regulation, Enzymologic
dc.subject.meshGene Expression Regulation, Neoplastic
dc.subject.meshGlutathione S-Transferase pi
dc.subject.meshGlutathione Transferase
dc.subject.meshHumans
dc.subject.meshIsoenzymes
dc.subject.meshMale
dc.subject.meshMiddle Aged
dc.subject.meshProstate
dc.subject.meshProstatic Neoplasms
dc.titleGlutathione S-transferase: differential expression of alpha, mu, and pi isoenzymes in benign prostate, prostatic intraepithelial neoplasia, and prostatic adenocarcinoma.en
dc.typeArticleen
dc.contributor.departmentBostwick Laboratories, Glen Allen, VA 23060, USA. bostwick@bostwicklaboratories.comen
dc.identifier.journalHuman Pathologyen
html.description.abstractGlutathione S-transferases (GST) comprise a family of enzymes which are critical for inactivation of toxins and carcinogens. We examined the cellular expression of multiple subclasses of GST immunohistochemically in 25 radical prostatectomy specimens with clinically localized prostate cancer. Gleason scores ranged from 5 to 9, and pathologic stages varied from pT2a to pT3b (all N0M0). Antibodies were directed against GST Ya, Yc, and Yk (alpha subclass), Yb1 (micro subclass), and YPr (pi subclass). The percentage of positive cells and intensity of staining was assessed for benign epithelium, high-grade prostatic intraepithelial neoplasia (PIN), and adenocarcinoma. GSTalpha (Ya) was detected in 30% of cells (mean) in benign acini, 4.9% of cells in high-grade PIN, and 4.5% of cells in adenocarcinoma. The corresponding results for alpha (Yk), micro (Yb1), and pi (Yp) were 12.7%, 10.9%, and 3.5%; 8.7%, 5.2%, and 0.6%; and 66.7,% 0%, and 0%, respectively. GST Yc (alpha subclass) displayed the lowest level of expression, with diffuse weak staining in scattered benign secretory cells and only single cells (<1%) in high-grade PIN and carcinoma. These results demonstrate consistent reduction or loss of expression of all subclasses of GST with progression of prostatic neoplasia from benign epithelium to high-grade PIN and carcinoma. We hypothesize that carcinogenesis in the prostate results from impaired cellular handling of mutagenic agents owing to reduction or loss of expression of multiple GST and other detoxifying and antimutagenesis agents.


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