Overexpression of p53 Protein in Endometrial Hyperplasia and Adenocarcinoma.
- Author:
Yun Sin KIM
;
Mi Sook LEE
;
Sung Chul LIM
;
Jang Shin SOHN
;
Chae Hong SUH
- Publication Type:Original Article
- Keywords:
p53 protein;
Endometrial hyperplasia;
Adenocarcinoma
- MeSH:
Adenocarcinoma*;
Adenomyosis;
Carcinogenesis;
Cell Proliferation;
Crowding;
Endometrial Hyperplasia*;
Female;
Genes, p53;
Humans;
Hyperplasia;
Prognosis
- From:Korean Journal of Pathology
1997;31(7):655-661
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Proliferations of the endometrial glands form a continuum from focal glandular crowding through simple hyperplasia, complex hyperplasia and atypical hyperplasia to frank adenocarcinoma. But objective criteria to distinguish these proliferative endometrial lesions are not clear-cut and terminology is confusing. The p53 protein is a nuclear phosphoprotein that can regulate cell proliferation and suppress tumor growth. Mutation in the p53 gene have been reported in a variety of human tumors, and in selected malignancies overexpression of p53 has been associated with poor prognosis. In this study we examined a series of endometrial proliferative lesion, including hyperplasia, adenocarcinoma, and adenomyosis to determine whether or not p53 is overexpressed in these lesions. In the result, p53 immunoreactivity was observed in 3 of 17 (17.6%) simple hyperplasia, one of 6 (16.6%) complex hyperplasia, none of 3 (O%) atypical hyperplasia, 6 of 13 (46.1%) adenocarcinoma and none of 10 (O%) adenomyosis. In conclusion, p53 mutation seems to play a role in oncogenesis of endometrial adenocarcinoma in early phase but there was no significant relationship between p53 overexpression and histologic grade of adenocarcinoma.
