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[Cancer Research 58, 3761-3764, September 1, 1998]
© 1998 American Association for Cancer Research
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Increased Expression of Cyclooxygenase 2 Occurs Frequently in Human Lung Cancers, Specifically in Adenocarcinomas1

Toyoaki Hida2,3,, Yasushi Yatabe2, Hiroyuki Achiwa, Hideki Muramatsu, Ken-ichi Kozaki, Shigeo Nakamura, Makoto Ogawa, Tetsuya Mitsudomi, Takahiko Sugiura and Takashi Takahashi

Departments of Internal Medicine [T. H., H. A., H. M., M. O., T. S.], Pathology and Clinical Laboratories [Y. Y., S. N.], and Thoracic Surgery [T. M.], Aichi Cancer Center Hospital, and Laboratory of Ultrastructure Research, Aichi Cancer Center Research Institute [K-i. K., T. T.], Nagoya 464-8681, Japan

Cyclooxygenase (COX)-2 expression was immunohistochemically examined in 59 human lung cancers as well as in normal and premalignant lung specimens. In contrast to scattered weak reactivity seen in normal peripheral airway epithelial cells, markedly up-regulated COX-2 expression was detected in about one-third of atypical adenomatous hyperplasias and carcinoma in situ specimens, and a significant increase in COX-2 expression was observed in 70% of invasive adenocarcinoma cases. Interestingly, the proportion of adenocarcinoma cells with marked COX-2 expression was much greater in lymph node metastases than in the corresponding primary tumors. In contrast, small cell carcinomas showed virtually negligible expression, and squamous cell carcinomas showed infrequent and low expression. These findings suggest that an increase in COX-2 expression may be associated with the development of adenocarcinomas and possibly with acquisition of an invasive and metastatic phenotype.

1 This work was supported in part by a Grant-in-Aid for Cancer Research from the Ministry of Health and Welfare of Japan; by a grant for Biomedical Research from Bristol Myers Squibb; by a grant from the Smoking Research Foundation; and by a Grant-in-Aid for Encouragement of Young Scientists from the Ministry of Education, Science, Sports and Culture, Japan.

2 These authors contributed equally to this work.

3 To whom requests for reprints should be addressed, at Aichi Cancer Center Hospital, Department of Internal Medicine, 1-1 Kanokoden, Chikusa-ku, Nagoya 464-8681, Japan.

Received 6/ 4/98. Accepted 7/17/98.




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