A Study of p53 Overexpression in Endometrial Disorder, Endometrial Hyperplasia, and Endometrial Carcinoma.
- Author:
Yoo Sun MIN
1
;
Woo Gyeong KIM
;
Kyung Bok LEE
;
Ki Tae KIM
Author Information
1. Department of Obstetrics & Gynecology, Pusan Paik Hospital, College of Medicine, Inje University, Korea.
- Publication Type:Original Article
- Keywords:
p53;
Endometrial carcinoma;
Endometrial hyperplasia;
Immunohistochemistry
- MeSH:
Carcinogenesis;
Endometrial Hyperplasia*;
Endometrial Neoplasms*;
Endometrium;
Estrogens;
Female;
Genes, p53;
Genes, Tumor Suppressor;
Genitalia;
Humans;
Hyperplasia;
Immunohistochemistry;
Incidence;
Korea;
Molecular Biology;
Progesterone;
Proto-Oncogenes
- From:Korean Journal of Gynecologic Oncology and Colposcopy
1998;9(2):144-150
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Endometrial carcinoma is the most common female genital organ malignancy in western countries and the incidence is increasing in Korea. Endometrial carcinoma frequently develops under the condition of excessive prolonged estrogenic stimulation in the absence of progesterone but the molecular mechanisms of carcinogenesis remain unknown. Recent advances in molecular biology have led to the concept that carcinoma arise from the accumulation of a series of gene alterations involving activation of proto-oncogenes and inactivation of tumor suppressor genes. The p53, one of tumor suppressor genes, is located on chromosome 17p. Alteration of p53 gene is observed in a wide variety of human cancer. Immunohistochemistry is considered as a simple and useful method to detect p53 overexpression in surgical pathologic specimens and close correlation of p53 expression with the presence of mutations in the gene has been demonstrated. In order to observe the expression of p53 protein, immunohistochemical studies were performed in 28 cases of endometrial carcinoma, 33 cases of endometrial hyperplasia, and 8 cases of disordered proliferative phase endometrium were used as a control group. The results were as follows: 1. The expression rate of p53 protein were 57.1% (16/28) in endometrial carcinoma and 12.1% (4/33) in endometrial hyperplasia but 8 cases of disordered proliferative phase endome-trium revealed negative reaction. 2. The expression rates of p53 protein were 47.4% (9/19) in early stage and 77.8% (7/9) in advanced stage of endometrial carcinoma. 3. According to histologic grade of endometrial carcinoma, the expression rates of p53 protein were 58.4% (10/7) in G1, 62.0% (5/8) in G2, and 33.3% (1/3) in G3. 4. The expression of p53 protein of simple hyperplasia were 12.5% (2/16) and that of complex hyperplasia were 11.8% (2/17). In conclusion, it could be suggested that p53 gene alteration might play a role in carcinogenesis of endometrium and mutation of p53 gene might be a relatively late event in tumor progression. Further study will be required to clarify the role of p53 in the carcinogenesis of the endometrium.
