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Clinical Cancer Research Vol. 5, 2018-2024, August 1999
© 1999 American Association for Cancer Research


Molecular Oncology, Markers, Clinical Correlates

Overexpression of Cyclooxygenase-2 in Carcinoma of the Pancreas1

Jiro Okami, Hirofumi Yamamoto, Yoshiyuki Fujiwara, Masaki Tsujie, Motoi Kondo, Shingo Noura, Satoshi Oshima, Hiroaki Nagano, Keizo Dono, Koji Umeshita, Osamu Ishikawa, Masato Sakon, Nariaki Matsuura, Shoji Nakamori2 and Morito Monden

Department of Surgery II, Osaka University Medical School, Osaka 565-0871, Japan [J. O., H. Y., Y. F., M. T., M. K., S. No., S. O., H. N., K. D., K. U., M. S., S. Na., M. M.]; Department of Surgery, Osaka Medical Center for Cancer and Cardiovascular Disease, Osaka 537-8511, Japan [O. I.]; and Department of Pathology, School of Allied Health Science, Faculty of Medicine, Osaka University, Osaka 565-0871, Japan [N. M.]

The level of cyclooxygenase (COX)-2 has been investigated recently in various human carcinomas. In the present study, we examined the distribution and extent of COX-2 protein in human pancreatic tumors using immunohistochemistry. A strong expression of COX-2 protein was present in 23 of 52 (44%) pancreatic carcinomas, a moderate expression was present in 24 of 52 (46%) pancreatic carcinomas, and a weak expression was present in 5 of 52 (10%) pancreatic carcinomas. In contrast, benign tumors showed weak expression or no expression of COX-2, and only islet cells displayed COX-2 expression in normal pancreatic tissues. Overexpression of COX-2 in carcinoma tissues was also confirmed by Western blot analysis. Furthermore, consistent with the results at protein levels, reverse transcription-PCR analyses indicated that COX-2 mRNA was overexpressed in 7 of 13 (54%) carcinomas, but in none of 3 benign tumors. Our findings suggest that COX-2 inhibitors might be potentially effective against pancreatic carcinomas and that COX-2 may be involved in certain biological processes in pancreatic islets.




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Copyright © 1999 by the American Association for Cancer Research.