Comparison of cyclooxygenase-2 and p53 expression in normal endometrium, endometrial hyperplasia and endometrial cancer.
- Author:
Sang Wook YOO
1
;
Ok Kyong KIM
;
Jae Yun SONG
;
Soon Cheol HONG
;
Nak Woo LEE
;
Kyu Wan LEE
Author Information
1. Department of Obstetrics and Gynecology, College of Medicine, Korea University, Seoul, Korea. pumplee@kumc.or.kr
- Publication Type:Original Article
- Keywords:
COX-2;
p53;
Endometrial cancer;
Endometrial hyperplasia
- MeSH:
Cyclooxygenase 2*;
Endometrial Hyperplasia*;
Endometrial Neoplasms*;
Endometrium*;
Female;
Hyperplasia
- From:Korean Journal of Gynecologic Oncology
2006;17(3):234-240
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVE: The purpose of this study is to compare the expression rate of cyclooxygenase-2 (COX-2), p53 in endometrial hyperplasia, endometrial cancer and normal endometrium and to correlate COX-2 with the clinicopathological factors and p53 in endometrial cancer. METHODS: Immunohistochemical stain of COX-2, p53 was performed on samples from a series of 19 cases of normal proliferative endometrium, 20 cases of complex endometrial hyperplasia and 19 cases of endometrial cancer. And then we analyzed the expression of COX-2 correlated the findings with clinicopathological factors and p53. Expression of COX-2 was scored according to the proportion of positive-staining cells: negative, no staining; 1+, <10%; 2+, 10-50%; 3+, >50. For p53 overexpression, when there were at least 10% of tumor cells stained, it was considered as positive. RESULTS: Overexpression of COX-2 (> or =2+) was seen in 5 (26.3%) of the endometrial cancers, 6 (30%) of the complex endometrial hyperplasia, and 4 (21.1%) of the normal endometria. The expression rates of COX-2 in endometrial cancer, hyperplasia and normal endometrium were not different statistically significant (p=0.93). COX-2 was not correlated with clinicopathological factors but correlated with p53 significantly (p=0.021). CONCLUSION: In this study, the immunohistochemical analysis showed no difference statistically in COX-2 expression between endometrial cancer and hyperplasia compared to normal endometria. COX-2 was significantly correlated with p53. This finding may represent that tumor suppressor p53 upregulates COX-2 expression.