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HOME > J Pathol Transl Med > Volume 31(7); 1997 > Article
Original Article Overexpression of p53 Protein in Endometrial Hyperplasia and Adenocarcinoma.
Yun Sin Kim, Mi Sook Lee, Sung Chul Lim, Jang Shin Sohn, Chae Hong Suh
Journal of Pathology and Translational Medicine 1997;31(7):655-661
DOI: https://doi.org/
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Department of Pathology, Medical College, Chosun University, Kwangju Christian Hospital, Kwangju 501-140, Korea.

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.

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