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Experimental Evidence From an Animal Model of Adenocarcinoma That Chronic Inflammation Enhances Lung Cancer Risk*

A.M. Malkinson, PhD; A. Bauer; A. Meyer; L. Dwyer-Nield, PhD; K. Koski; R. Keith, MD; M. Geraci, MD; Y.-E. Miller, MD
Author and Funding Information

*From the University of Colorado Health Sciences Center, Denver, CO.

Correspondence to: A. M. Malkinson, PhD, Department of Pharmaceutical Sciences Center, Box C238, 4200 E. 9th Ave., Denver, CO 80262



Chest. 2000;117(5_suppl_1):228S. doi:10.1378/chest.117.5_suppl_1.228S
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Abbreviations: AC = adenocarcinoma; BHT = butylated hydroxytoluene; MCA = 3-methylcholanthrene; PGI2 = prostacyclin; PGE2 = prostaglandin E2

The chronic inflammation associated with COPD enhances lung cancer risk. However, because of the overwhelming contribution of cigarette smoking to lung cancer etiology, this epidemiologic association is not strong. The incidence of adenocarcinoma (AC), which accounts for one third of all lung cancer and is the only kind of lung cancer that develops in nonsmokers (10% of male lung cancer cases and 20% of women), is the fastest rising lung cancer. Early markers for AC do not exist, and the prognosis is dire.

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