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[Cancer Research 62, 5405-5407, October 1, 2002]
© 2002 American Association for Cancer Research

Advances in Brief

Celecoxib, a Selective Cyclooxygenase 2 Inhibitor, Protects against Human Epidermal Growth Factor Receptor 2 (HER-2)/neu-induced Breast Cancer1

Louise R. Howe2, Kotha Subbaramaiah, Jay Patel, Jaime L. Masferrer, Aparna Deora, Clifford Hudis, Howard T. Thaler, William J. Muller, Baoheng Du, Anthony M. C. Brown and Andrew J. Dannenberg

Departments of Cell and Developmental Biology [L. R. H., A. M. C. B.] and Medicine [K. S., B. D., A. J. D.], Weill Medical College of Cornell University, New York, New York 10021; Strang Cancer Research Laboratory at the Rockefeller University, New York, New York 10021 [L. R. H., K. S., J. P., A. M. C. B., A. J. D.]; Pharmacia Corporation, St. Louis, Missouri 63017 [J. L. M., A. D.]; Departments of Medicine [C. H.] and Epidemiology and Biostatistics [H. T. T.], Memorial Sloan-Kettering Cancer Center, New York, New York 10021; and McGill University, Montreal, Quebec, Canada [W. J. M.]

Cyclooxygenase 2 (HER-2) (Cox-2), an inducible form of Cox, is overexpressed in HER-2/neu-positive human breast cancers. The aim of this study was to determine whether celecoxib, a selective Cox-2 inhibitor, protected against HER-2/neu-induced experimental breast cancer. Cox-2 protein was detected in breast carcinomas from mouse mammary tumor virus (MMTV)/neu mice. Treatment with celecoxib (500 ppm) significantly reduced the incidence of mammary tumors in MMTV/neu mice (P = 0.003) and caused about a 50% reduction in mammary prostaglandin E2 (PGE2) levels. Because mammary glands from MMTV/neu mice expressed all four PGE2 receptor subtypes, we speculate that signaling through PGE2 receptors is important for mammary tumorigenesis. These results strengthen the rationale for developing clinical trials to determine whether selective Cox-2 inhibitors possess anticancer properties in humans at risk for breast cancer.




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