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Cancer Res Treat. 2005 Jun;37(3):165-170. English. Original Article.
Nam E , Lee SN , Im SA , Kim DY , Lee KE , Sung SH .
Ewha Medical Research Center, Departments of Internal Medicine, Ewha Womans University College Medicine, Seoul, Korea. snlee@ewha.ac.kr
Daejin Medical Center, Pundang Jesaeng General Hospital, Ewha Womans University College Medicine, Seoul, Korea.
Ewha Womans University College of Medicine, Ewha Womans University College Medicine, Seoul, Korea.
Seoul National University College of Medicine, Ewha Womans University College Medicine, Seoul, Korea.
Dongguk University College of Medicine, Ewha Womans University College Medicine, Seoul, Korea.
Department of Pathology, Ewha Womans University College Medicine, Seoul, Korea.
Abstract

PURPOSE: Previous epidemiologic studies have demonstrated that nonsteroidal anti-inflammatory drugs can reduce the risk of breast cancer, and this possibly happens via cyclooxygenase (COX) inhibition. Moreover, growth factor-inducible COX-2, which is overexpressed in neoplastic tissue, is an attractive therapeutic target. Thus, we evaluated the expression of COX-2 in breast cancer tissues, and we assessed the association between COX-2 expression and HER-2/neu expression and also with several clinicopathological features. MATERIALS AND METHODS: We analyzed the surgical specimens from 112 women with breast cancer who had undergone lumpectomy or mastectomy. The expressions of COX-2, HER-2/neu, MMP-2 and TIMP-2 were determined immunohistochemically. The correlations between COX-2 expression and several variables, including clinicopathological factors, HER-2/neu expression, MMP-2 expression and TIMP-2 expression were analyzed. Survival analysis was also performed with respect to COX-2 overexpression. RESULTS: The overexpression of COX-2 protein was observed in 28.6% of the breast cancer tissues. Tumors with lymph node metastasis more frequently showed COX-2 overexpression than did those tumors without metastasis (p=0.039), and the increased COX-2 expression correlated positively with HER-2/neu overexpression (p=0.000). No significant differences were found for the MMP-2 or TIMP-2 expression rates in the COX-2 positive and negative groups. The survival analysis revealed no significant differences according to the COX-2 expression. CONCLUSION: This study results suggest that increased COX-2 expression is related with the progression of breast cancer, e.g., with lymph node invasion. COX-2 overexpression found to be related with HER-2/neu overexpression, but not with MMP-2 or TIMP-2 expression. These results support the potential use of selective agents that inhibit COX-2 or HER-2/neu for the management of breast cancer.

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