Overexpression of p53 Protein in Endometrial Hyperplasia and Adenocarcinoma

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.