RT Journal Article
SR Electronic
T1 Inactivation of Glutathione <em>S</em>-Transferase <em>P1</em> Gene by Promoter Hypermethylation in Human Neoplasia
JF Cancer Research
JO Cancer Res
FD American Association for Cancer Research
SP 4515
OP 4518
VO 58
IS 20
A1 Esteller, Manel
A1 Corn, Paul G.
A1 Urena, Jesus M.
A1 Gabrielson, Edward
A1 Baylin, Stephen B.
A1 Herman, James G.
YR 1998
UL http://cancerres.aacrjournals.org/content/58/20/4515.abstract
AB Glutathione S-transferases (GSTs) are a family of isoenzymes that play an important role in protecting cells from cytotoxic and carcinogenic agents. The π-class GST has been associated with preneoplastic and neoplastic changes. Recently, it has been reported that regulatory sequences near the GSTP1 gene, which encodes the human π-class GST, are commonly hypermethylated in prostatic carcinomas. In the present study, we studied more than 300 primary human tumors originating in other organs for aberrant methylation of GSTP1 using methylation-specific PCR. GSTP1 hypermethylation was most frequent in breast and renal carcinoma, showing aberrant methylation in 30 and 20% of the cases, respectively. Other tumor types showed promoter methylation only rarely or not at all. Hypermethylation of GSTP1 was associated with loss of expression demonstrated by immunohistochemistry. Our results suggest that aberrant methylation of GSTP1 may contribute to the carcinogenetic process in breast and renal carcinomas. ©1998 American Association for Cancer Research.