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Cyclooxygenase enzymes cancer

As shown in a paper by Conderoy et al. (2008), there is an increasing amount of evidence that-suggests an association between cancer and the cyclooxygenase (COX) enzyme (5) hence, the COX-expressing cell line fiT-29 was studied in this present work. [Pg.584]

Prostaglandins and Cyclooxygenase COX-2 Expression and Cancer Underlying Mechanisms of COX-2 Enzyme and Its Inhibitors on Cancers Effect of COX or Selective COX-2 Inhibitors on Cancer Prevention... [Pg.391]

Milas L, Kishi K, Hunter N, et al. Enhancement of tumor response to y-radiation by an inhibitor of cyclooxygenase-2 enzyme. J Natl Cancer Inst 1999 91 1501-1504. [Pg.408]

The prostaglandins are lipid mediators implicated, not only in inflammation, but also, in other pathological processes, such as edema, fever, hyperalgia, cancer or Alzheimer s disease. The cyclooxygenase (COX) is the rate-limiting enzyme in the synthesis of PGE2, TXB2 and prostacyclines from arachidonic acid. [Pg.700]

Johnson, A.J., Song,X., Hsu, A., and Chen, C. (2001) Apoptosis Signaling Pathways Mediated by Cyclooxygenase-2 Inhibitors in Prostate Cancer Cells, Adv. Enzyme Regul. 41, 221-235. [Pg.177]

More than 15 years ago, Jimg et aL reported the synthesis of the dicobalthex-acarbonyl derivative 31 (Q)-ASS) of the well-known analgesic aspirin (acetylsali-cylic acid (ASS)) [107]. Non-steroidal anti-inflammatory drugs (NSAIDs) such as ASS are known to bind to cyclooxygenases (COXs). This family of enzymes is responsible for the formation of prostaglandin H2 from arachidonic acid. Three subtypes of COX are known, namely COX-1, COX-2, and COX-3, which is a splice variant of COX-1. COX-1 is constitutionally expressed, while COX-2 is overexpressed in many cancer cell lines. ASS is a selective inhibitor of the COX-1 subtype and its analgetic and antiaggregating effects stem from this interaction. [Pg.41]

Figure 4, Kinin generating cascade and various vascular mediators in cancer tissues affecting the EPR effect. Mediators, enzymes, and inhibitors are shown. See text for details. M, macrophage PMN, polymorphoneuclear cells COXs, cyclooxygenases PCs, prostaglandins. SBTl, soybean trypsin inhibitor (Kunitz type) ONOO", peroxynitrite NO, nitric oxid MMP, matrix metalloproteinases. Figure 4, Kinin generating cascade and various vascular mediators in cancer tissues affecting the EPR effect. Mediators, enzymes, and inhibitors are shown. See text for details. M, macrophage PMN, polymorphoneuclear cells COXs, cyclooxygenases PCs, prostaglandins. SBTl, soybean trypsin inhibitor (Kunitz type) ONOO", peroxynitrite NO, nitric oxid MMP, matrix metalloproteinases.

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