An introduction to aspirin, NSAids, and COX-2 inhibitors for the primary prevention of cardiovascular events and cancer and their potential preventive role in bladder carcinogenesis: part II.
Aspirin and the nonselective nonsteroidal anti-inflammatory drugs (NSAIDs) have been commercially available for decades, and their ability to reduce pain and inflammation are well known. The ability of some of these agents to also reduce a primary or secondary cardiovascular event or to potentially reduce the risk of colorectal cancer has also been documented. These observations collectively have initiated a wide variety of investigations to determine whether or not these agents may have an ability to reduce the risk or progression of numerous cancers. Some urologic cancers have been included in these recent studies. For example, prostate cancer may be sensitive to these compounds based on a small number of preliminary studies. Bladder cancer may also be sensitive to the effects of these agents. Older patients and those with more aggressive tumors may benefit most from these initial studies. Many cancers also demonstrate a greater upregulation of cyclooxygenase-2 (COX-2), and this has lead to recent interest, especially in colorectal cancer, to test the ability of these selective agents against the development of precancerous colon polyps. High-risk patients for colorectal cancer may have benefited by taking a selective COX-2 inhibitor in a recent randomized trial, but whether or not this benefit continues to occur after the COX-2 inhibitor is removed remains controversial and needs further study. Prostate and bladder cancer also seem to demonstrate an upregulation of COX-2, and laboratory studies suggest that these selective NSAIDs may have a greater effect on reducing the development of these tumors. Randomized clinical trials are needed, but because numerous individuals are currently using COX-2 inhibitors, a large volume of data should make at least retrospective studies more plausible in the near future. The challenge for researchers and clinicians is to further understand which NSAIDs and what dosage and duration may provide the optimal benefit (if any), and to accurately construe the available current data on these agents for patients inquiring about these compounds.
Moyad
M A
MA
Department of Surgery, University of Michigan Medical Center, Ann Arbor 48109-0330, USA.
D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D001241:Aspirin / Q000627:therapeutic use*; D015179:Colorectal Neoplasms / Q000453:epidemiology / Q000517:prevention & control*; D051546:Cyclooxygenase 2; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors / Q000627:therapeutic use*; D006801:Humans; D015994:Incidence; D007527:Isoenzymes / Q000037:antagonists & inhibitors* / Q000378:metabolism; D008297:Male; D008565:Membrane Proteins; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D011471:Prostatic Neoplasms / Q000517:prevention & control*; D012307:Risk Factors; D001749:Urinary Bladder Neoplasms / Q000139:chemically induced / Q000453:epidemiology / Q000517:prevention & control*
D000894:Anti-Inflammatory Agents, Non-Steroidal; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors; D007527:Isoenzymes; D008565:Membrane Proteins; D010975:Platelet Aggregation Inhibitors; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases; D001241:Aspirin