Epigenetic silencing of glutathione S-transferase π (GSTP1) is a hallmark of transformation from normal prostatic epithelium to adenocarcinoma of the prostate.
Prostate adenocarcinoma with hypermethylation of each of ASC, COX2, RARB, TNFRSF10C, MDR1, TIG1, RBP1, NEUROG1, RASSF1A, and GSTP1 showed a significantly lower methylation level of Alu or LINE-1 than prostate adenocarcinoma without hypermethylation.
We present a real-time, methylation specific protocol to detect hypermethylation in the promoter region of the GSTP1 gene in benign hyperplasia and adenocarcinoma of the prostate.
Paraffin tissue samples from 45 patients with minute foci of intermediate grade prostatic adenocarcinoma or benign disease on needle biopsy were tested for GSTP1 hypermethylation using quantitative fluorogenic real-time methylation specific polymerase chain reaction.
A total of 7 of 18 (39%) patients with prostate adenocarcinoma identified on their initial biopsy had detectable urinary GSTP1 methylation (58% sensitivity among informative cases).
Epigenetic DNA alterations such as promoter hypermethylation of glutathione S-transferase P1 (GSTP1) in prostatic adenocarcinoma frequently constitute tumour biomarkers.
We used a fluorogenic real-time methylation-specific polymerase chain reaction (MSP) assay to analyze cytidine methylation in the GSTP1 promoter in prostate tissue samples from 69 patients with early-stage prostatic adenocarcinoma (28 of whom also had prostatic intraepithelial neoplasia lesions) and 31 patients with benign prostatic hyperplasia.