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JNCI Journal of the National Cancer Institute 1999 91(17):1501-1504; doi:10.1093/jnci/91.17.1501
© 1999 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 91, No. 17, 1501-1504, September 1, 1999
© 1999 Oxford University Press


BRIEF COMMUNICATION

Enhancement of Tumor Response to {gamma}-Radiation by an Inhibitor of Cyclooxygenase-2 Enzyme

Luka Milas, Kazushi Kishi, Nancy Hunter, Kathryn Mason, Jaime L. Masferrer, Philip J. Tofilon

Affiliations of authors: L. Milas, K. Kishi, N. Hunter, K. Mason, P. J. Tofilon, Department of Experimental Radiation Oncology, The University of Texas M. D. Anderson Cancer Center, Houston; J. L. Masferrer, Pharma Research and Development, Searle, Monsanto, St. Louis, MO.

Correspondence to: Luka Milas, M.D., Ph.D., Department of Experimental Radiation Oncology, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd., Box 066, Houston, TX 77030-4095 (e-mail: lmilas@mdanderson.org).

Prostaglandins are arachidonate metabolites produced in virtually all mammalian tissues and possess diverse biologic capabilities, including vasoconstriction, vasodilatation, stimulation or inhibition of platelet aggregation, and immunomodulation, primarily immunosupression (1-4). They are implicated in the promotion of development and growth of malignant tumors (4-7). They are also involved in the response of tumor and normal tissues to cytotoxic agents such as ionizing radiation (8). Prostaglandin production is mediated by two cyclooxygenase enzymes: cyclooxygenase-1 and cyclooxygenase-2. Cyclooxygenase-1 is constitutively expressed and is ubiquitous, and cyclooxygenase-2 is induced by diverse inflammatory stimuli (7,9).

Nonsteroidal anti-inflammatory drugs (NSAIDs) or agents inhibit cyclooxygenase enzymes and consequently can prevent, inhibit, or abolish the effects of prostaglandins. Increasing evidence shows that NSAIDs can inhibit the development of cancer in both experimental animals and in humans (7), can reduce the size of . . . [Full Text of this Article]

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