Abstract
Recent studies indicate that nonsteroidal anti-inflammatory drugs have a chemopreventive effect against colorectal neoplasia. Nonsteroidal anti-inflammatory drugs inhibit cyclooxygenases, principal enzymes that mediate the formation of prostanoids. To determine whether prostanoids are involved in the pathogenesis of colorectal adenomas, we compared the levels of five major stable metabolic products of the cyclooxygenase pathway in the normal-appearing mucosa and in adenomas of patients with familial adenomatosis polyposis. Of 12 patients tested, 6 had elevated levels of at least one prostanoid in the adenomas. More importantly, the relative levels of three prostanoids [prostaglandin (PG)D2, PGE2, and 6-keto-PGF1α] were elevated in adenomas compared to normal-appearing mucosa from the same patients, and the resulting ratios were correlated with the size of the adenoma. These results suggest a role for prostanoids in progression of colorectal polyposis in familial adenomatosis polyposis patients.
Footnotes
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↵1 This work was in part supported by the Clayton Fund and by Grants CA53801, CA62924, and CA63721 from the NIH.
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↵2 To whom requests for reprints should be addressed, at Department of Medicine, Ross 918, The Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD 21205. Phone: (410) 955-9691; Fax: (410) 955-9677; E-mail: vyang@welchlink.welch.jhu.edu.
- Received October 1, 1997.
- Accepted February 18, 1998.
- ©1998 American Association for Cancer Research.
Volume 58, Issue 8
