Quantitative GSTP1 methylation clearly distinguishes benign prostatic tissue and limited prostate adenocarcinoma

Susan V. Harden, Zhongmin Guo, Jonathan Ira Epstein, David Sidransky

Research output: Contribution to journalArticle

Abstract

Purpose: Hypermethylation of the glutathione S-transferase gene (GSTP1) is the most common (greater than 90%) reported epigenetic alteration in prostate cancer. It occurs early in cancer progression and it is a promising marker for detecting organ confined disease. To evaluate its use as a diagnostic tool for cancer we used quantitative GSTP1 methylation to test for the presence of cancer in 45 prostate needle biopsy samples. Materials and Methods: 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. This assay was performed in blinded fashion without previous knowledge of the histopathological diagnosis. Results: DNA from 29 of the 45 paraffin samples was amenable to polymerase chain reaction amplification. In these 29 samples GSTP1 methylation was detected in 11 of 15 cases of limited cancer and in 0 of 14 of benign disease (2-sided Fisher's exact test, p

Original languageEnglish (US)
Pages (from-to)1138-1142
Number of pages5
JournalJournal of Urology
Volume169
Issue number3
DOIs
StatePublished - Mar 1 2003

Fingerprint

Methylation
Prostate
Adenocarcinoma
Needle Biopsy
Paraffin
Neoplasms
Polymerase Chain Reaction
Glutathione Transferase
Epigenomics
Prostatic Neoplasms
DNA
Genes

Keywords

  • Gene expression
  • Glutathione transferase
  • Prostate
  • Prostatic neoplasms
  • Tumor markers, biological

ASJC Scopus subject areas

  • Urology

Cite this

Quantitative GSTP1 methylation clearly distinguishes benign prostatic tissue and limited prostate adenocarcinoma. / Harden, Susan V.; Guo, Zhongmin; Epstein, Jonathan Ira; Sidransky, David.

In: Journal of Urology, Vol. 169, No. 3, 01.03.2003, p. 1138-1142.

Research output: Contribution to journalArticle

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