Cyclooxygenase-2 expression is higher in ovarian cancer tissue adjacent to endometriosis than in ovarian cancer without comorbid endometriosis

被引:11
|
作者
Chou, YC
Chen, YJ
Lai, CR
Wang, PH
Hsin-Chan
Yuan, CC
机构
[1] Taipei Vet Gen Hosp, Dept Obstet & Gynecol, Taipei 11217, Taiwan
[2] Natl Yang Ming Univ, Taipei, Taiwan
[3] Taipei Vet Gen Hosp, Dept Pathol, Taipei, Taiwan
关键词
endometriosis; ovarian cancer; malignant transformation; cyclooxygenase-2 (COX-2);
D O I
10.1016/j.ejogrb.2005.06.019
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Objectives: The purpose of this study was to examine if COX-2, CK7 and CK20 are involved in the malignant transformation of endometriosis. Methods: We compared COX-2, CK7 and CK20 expressions between isolated endometriosis lesions and endometriosis lesions adjacent to ovarian carcinoma and between isolated ovarian carcinoma and ovarian carcinoma with implants of endometriosis. Immunoreactivity was quantified using an immunohistochemical scoring system that corresponds to an image analysis-based system. Results: There was no difference in COX-2, CK7 and CK20 expressions between the isolated endometriosis lesions and the endometriosis lesions adjacent to ovarian carcinoma. Similarly, CK7 and CK20 were equally expressed between the isolated ovarian carcinoma and the ovarian carcinoma with implants of endometriosis. The COX-2 over-expression rate was greater in ovarian carcinoma that was associated with endometriosis than in isolated ovarian carcinoma (27.8% versus 5.6%, P = 0.083). In endometrioid type ovarian carcinoma, the difference in COX-2 expression was statistically significant (50% versus 0%, P = 0.023). Conclusions: COX-2 over-expression may be a result of the malignant transformation of endometriosis to endometrioid type ovarian cancer or may represent an interaction between the two cellular components. With respect to cytokeratins, neither CK7 nor CK20 appear to be involved in the malignant transformation of endometriosis. (c) 2005 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:101 / 105
页数:5
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