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Celecoxib Decreases Ki-67 Proliferative Index in Active Smokers

Authors' Affiliations: ¹ Division of Pulmonary and Critical Care Medicine, Departments of ² Pathology and Laboratory Medicine, and ³ Surgery, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California

Requests for reprints: Jenny T. Mao, Division of Pulmonary and Critical Care, CHS 37-131, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, CA 90095-1690. Phone: 310-825-3100; Fax: 310-206-8622; E-mail: jmao{at}mednet.ucla.edu.

Purpose: This study evaluated the feasibility of cyclooxygenase-2 (COX-2) inhibition for lung cancer chemoprevention. We hypothesized that treatment with oral Celecoxib, a selective COX-2 inhibitor, would favorably alter the biomarkers of lung cancer risk as measured by the Ki-67 proliferative labeling index (Ki-67 LI).

Experimental Design: Twenty active heavy smokers were enrolled into a pilot study and treated with Celecoxib for 6 months. Bronchoscopies with bronchial biopsies were done before and after 6 months of Celecoxib treatment. H&E stain for histologic grading and immunohistochemical examination for Ki-67 LI, COX-2, and survivin were carried out on serially matched biopsy samples to determine responses to treatment.

Results: Treatment with Celecoxib significantly reduced Ki-67 LI in smokers by 35% (P = 0.016), and increased the expression of nuclear survivin by 23% (P = 0.036) without significantly changing that of cytoplasmic survivin.

Conclusions: Our findings suggest that oral Celecoxib may be capable of modulating the proliferation indices and apoptotic balance in bronchial tissue of active smokers.

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