Celebrex (Celecoxib) and Cancer

A substantial amount of research has been carried out into the potential role celecoxib might play in reducing cancer rates.

Celecoxib exerts its pain relieving effects by inhibiting the enzyme cycloxygenase-2 (COX-2). This inhibition of COX-2 has been shown to cause several adverse heart effects, which has prevented the use of celecoxib as an anticancer agent.

Celecoxib and colon and rectum cancer

Research findings have suggested that celecoxib and other non steroidal anti-inflammatory drugs (NSAIDs) reduce the risk of bowel cancer.

Several small clinical studies on humans showed that patients at high risk of colorectal cancer due to a family history of familial adenomatous polyposis benefit from taking celecoxib, which prevented the growth of polyps in these patients. This led to large-scale clinical trials being conducted to further test the effects of the drug.

According to the landmark study by Arber and Bertagnolli published in 2006 in the New England Journal of Medicine, the rate of polyp recurrence was reduced by between 33% and 45% in people who took daily celecoxib (400 to 800 mg). On the other hand, treatment with celecoxib was associated with a significantly increased rate of adverse cardiovascular events compared with the use of placebo.

Celecoxib and cancer treatment

Currently, it is unclear whether the inhibition of COX-2 by celecoxib may be a useful approach in the treatment (rather than prevention) of cancer. However, studies have shown that celecoxib may interact with other cell components aside from the intended target, COX-2. This discovery contradicted the initial assumption that celecoxib primarily exerts its anticancer effects through inhibition of COX-2.

Further studies showed that although the anti-inflammatory effects of celecoxib were indeed linked to inhibition of COX-2, the drug’s anticancer mechanism was not clear. One study of malignant tumor cells showed that celecoxib did reduce the growth of these cells but that this effect could also be achieved using cancer cells that did not even contain COX-2.