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Celecoxib effective in lung chemoprevention
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Using a non-steroidal antiinflammatory drug to inhibit COX-2 may be an important approach in the prevention of lung cancer among current and former smokers.
“The aim of our study was to assess the change in expression of the proliferation marker Ki-67 in the bronchial epithelium from baseline to a three-month visit,” Edward S. Kim, MD, assistant professor at the University of Texas M.D. Anderson Cancer Center, said in his presentation at the 2008 ASCO Annual Meeting.
Kim and colleagues conducted a randomized trial of celecoxib (Celebrex, Pfizer) for chemoprevention of lung cancer in 204 participants with a smoking history of >20 packs per year. The researchers used bronchial biopsy to measure Ki-67 and randomly assigned participants to one of four treatment groups: celecoxib followed by placebo (n=52), celecoxib alone (n=51), placebo followed by celecoxib (n=51) or placebo alone (n=50). Each treatment occurred in three-month intervals.
Initially, researchers administered a low dose (200 mg twice daily, n=81) of celecoxib, then increased the dose to 400 mg twice daily (n=123).
Current smokers had higher Ki-67 expression in both basal (P=.001) and parabasal (P=.005) layers compared with former smokers. Those assigned to high-dose celecoxib, whether current or former smokers, had decreased Ki-67 expression in the basal layer (P=.003) compared with those assigned to low dose (P=.88).
“Overall study compliance was good, and we saw that, histologically, baseline squamous metaplasia correlated with smoking status and increased about threefold in current smokers,” Kim said of the overall results. “We understand that the therapeutic approach to lung cancer is based on our understanding of the cancer development process and the principles of chemoprevention.”
Kim ES. #1501.Presented at: ASCO Annual Meeting; May 30-June 3, 2008; Chicago.
This is an important advance in lung cancer prevention and Dr. Kim and colleagues have performed a rationally designed prevention study targeting one of the salient pathways in the pathogenesis of lung cancer. Particularly important is the perseverance that was necessary in accruing subjects despite the hold that was placed on trials in December 2004. And, importantly, they have defined Ki-67, a marker of epithelial proliferation, as responsive to intervention by COX-2 inhibition.
– Steven M. Dubinett, MD
Director, UCLA Lung Cancer Research Program