By Joseph R. Bertino, Andrew J. Dannenberg, Raymond N. DuBois

Quite a few investigators have discovered elevated degrees of cyclooxygenase-2 (COX-2) in either pre-malignant and malignant tissues. furthermore, animals engineered to be COX-2 poor or taken care of with a selective COX-2 inhibitor confirmed diminished tumor formation and development. the current ebook stories those findings suggesting that COX-2 is a sound molecular goal for the prevention and remedy of melanoma. the 1st chapters are dedicated to the epidemiology of nonsteroidal anti inflammatory medications (NSAIDs) and melanoma, the pharmacology of COX-2 inhibitors and the rules of COX-2 expression in human cancers. along with, the e-book incorporates a sequence of chapters reading the hyperlink among COX-2 and melanoma in particular organs (e.g. dermis, breast, cervix, digestive tract, lung, etc.). moreover, numerous medical trials assessing the opportunity of COX-2 inhibitors for fighting and treating melanoma are defined.

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A preliminary study in healthy adults that compared the effects of naproxen 500 mg bid for 10 days versus celecoxib 200 mg bid for 5 days followed by 400 mg bid for a further 10 days, demonstrated similar significant decreases from baseline in urinary PGs (PGE2 and 6-keto-PGF1␣) in both treatment groups and similar small transient decreases in urinary sodium excretion [127]. However, treatment with naproxen resulted in a greater decrease from baseline in GFR compared with celecoxib and this difference became significant after 6 days of treatment [127].

Derivatives of salicylic acid were characterized as the active components of these plants in the 18th century and were chemically synthesized for the first time in 1860. In 1971, inhibition of the enzyme cyclooxygenase (COX, also known as prostaglandin endoperoxide synthase) was characterized as the mechanism of action of NSAIDs [1]. COX is the ratelimiting enzyme in the production of prostaglandins (PGs), catalyzing the conversion of arachidonic acid to the PG precursor PGH2. PGH2 is then converted to a variety of other PGs including PGE2, PGI2, PGD2 and thromboxane (TxA2).

Most of the celecoxib metabolites are excreted in the feces, with Isakson 32 only 2% of celecoxib excreted in the urine unchanged [55]. None of the metabolites of celecoxib have appreciable activity on COX-1 or COX-2. Rofecoxib is metabolized by an uncharacterized cytosolic reductase to cisdihydro and trans-dihydro derivatives, most likely in the liver; these metabolites can undergo further hepatic biotransformation to carboxylic acid and glucuronidate derivatives. Most of a single daily dose is excreted in the urine within 17 h of administration, and less than 1% of excreted drug is unchanged [57].

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Cox-2: a new target for cancer prevention and treatment by Joseph R. Bertino, Andrew J. Dannenberg, Raymond N. DuBois
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