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Volume 192, Issue 4, Pages 1262-1271 (April 2005)


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Correlation of cyclooxygenase-2 (COX-2) and aromatase expression in human endometrial cancer: Tissue microarray analysis

Jeffrey M. Fowler, MDaCorresponding Author Informationemail address, Nilsa Ramirez, MDb, David E. Cohn, MDa, Nicole Kelbick, PhDc, James Pavelka, MDa, Inbar Ben-Shachar, MDa, Carl Morrison, MD, DVMb

Received 31 December 2004; received in revised form 6 January 2005; accepted 6 January 2005.

Objective

The objective of this study was to compare the prevalence of cyclooxygenase-2 (COX-2), aromatase, and hormone receptor immunohistochemical (IHC) expression to well defined clinical-pathologic prognostic factors in a large group of surgically staged endometrial cancer patients.

Study design

A tissue microarray (TMA) was constructed from 336 separate specimens of endometrial cancer. IHC was perfomed for estrogen (ER) and progesterone (PR) receptor, COX-2, COX-1, and aromatase.

Results

The majority of tumors expressed COX-2 (59%) and aromatase (65%). COX-2 staining significantly correlated with aromatase expression (P < .014) but did not correlate with ER and PR. COX-2 expression was correlated with worsening histologic grade (P < .026) and approached statistical significance for deep myometrial invasion (P < .055). After applying multivariate analysis, no single IHC or combination of IHCs correlated with intrauterine poor prognostic factors or advanced stage. Only myometrial invasion >50% (OR 6.98, P < .001) and nonendometrioid histology (OR 4.933, P < .001) were predictive of advanced stage after multivariate analysis.

Conclusion

COX-2 and aromatase are expressed in the majority of endometrial cancer patients. COX-2 expression was not associated with the great majority of surgical-pathologic prognostic factors. COX-2 expression did significantly correlate with aromatase expression, suggesting that intratumoral production of estrogen in endometrial cancer may be an important mechanism in tumorigenesis.

a Division of Gynecologic Oncology

b Department of Pathology

c Center for Biostatistics, and The Arthur James Cancer Hospital and Richard Solove Research Institute, The Ohio State University Medical School, Columbus, Ohio

Corresponding Author InformationReprint requests: Jeffrey M. Fowler, MD, Director, Division of Gynecologic Oncology, JG Boutselis Professor in Gynecologic Oncology, 210-M SL, 320 W 10th Ave, Columbus, OH 43210.

 Presented at the 23rd Annual Meeting of the American Gynecological and Obstetrical Society, September 9-11, 2004, Bolton Landing, NY.

PII: S0002-9378(05)00072-4

doi:10.1016/j.ajog.2005.01.009


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