By Joseph R. Bertino, Andrew J. Dannenberg, Raymond N. DuBois
A number of investigators have came upon elevated degrees of cyclooxygenase-2 (COX-2) in either pre-malignant and malignant tissues. additionally, animals engineered to be COX-2 poor or handled with a selective COX-2 inhibitor confirmed diminished tumor formation and development. the current ebook studies those findings suggesting that COX-2 is a legitimate molecular objective for the prevention and remedy of melanoma. the 1st chapters are dedicated to the epidemiology of nonsteroidal anti inflammatory medicines (NSAIDs) and melanoma, the pharmacology of COX-2 inhibitors and the rules of COX-2 expression in human cancers. along with, the ebook includes a sequence of chapters studying the hyperlink among COX-2 and melanoma in particular organs (e.g. epidermis, breast, cervix, digestive tract, lung, etc.). additionally, a number of medical trials assessing the potential for COX-2 inhibitors for fighting and treating melanoma are defined.
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Additional resources for Cox-2: a new target for cancer prevention and treatment
These data demonstrate the extent of variation that arises from the use of these different assays. Therefore, while these different methods are good predictors of the relative COX-2 selectivity of different drugs, it is difficult to make direct comparisons between different agents based on in vitro and animal model data. Nor are these assays necessarily predictive of the clinical efficacy or tolerability of a selective agent. Pharmacokinetics of COX-2-Specific Inhibitors The oral COX-2 inhibitors including celecoxib, rofecoxib and valdecoxib are all highly lipophilic, neutral, nonacidic molecules with limited solubility in aqueous media.
Farrow DC, Vaughan TL, Hansten PD, Stanford JL, Risch HA, Gammon MD, Chow WH, Dubrow R, Ahsan H, Mayne ST, Schoenberg JB, West AB, Rotterdam H, Fraumeni JF Jr, Blot WJ: Use of aspirin and other nonsteroidal anti-inflammatory drugs and risk of esophageal and gastric cancer. Cancer Epidemiol Biomarkers Prev 1998;7:97–102. Coogan PF, Rosenberg L, Palmer JR, Strom BL, Zauber AG, Stolley PD, Shapiro S: Nonsteroidal anti-inflammatory drugs and risk of digestive cancers at sites other than the large bowel.
If vascular COX-2 was in fact the source of PGI2 then it is possible that without concomitant inhibition of platelet aggregation, therapeutic doses of COX-2-specific inhibitors might increase the risk of thromboembolic events due to inhibition of PGI2 in the vascular endothelium in patients with a history of CV disease who have a particularly high risk from MI or stroke. This hypothetical risk would be obviated by appropriate prophylactic therapy with low-dose aspirin . In addition, COX-2 inhibitors have no effect on other vascular regulators of platelet function, in particular nitric oxide (NO).
Cox-2: a new target for cancer prevention and treatment by Joseph R. Bertino, Andrew J. Dannenberg, Raymond N. DuBois