Comparison of cyclooxygenase-2 and p53 expression in normal endometrium, endometrial hyperplasia and endometrial cancer
Sang Wook Yoo, Ok Kyong Kim, Jae Yun Song, Soon–Cheol Hong, Nak Woo Lee, Kyu Wan Lee
Abstract
Sang Wook Yoo, Ok Kyong Kim, Jae Yun Song, Soon–Cheol Hong, Nak Woo Lee, Kyu Wan Lee
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 (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.
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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 (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.
Key concepts: Endometrial cancer, Endometrium, Endometrial hyperplasia, Cyclooxygenase, Medicine, Gynecology, Internal medicine, Cancer