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Evidence That Inflammation Encourages Pulmonary Adenocarcinoma Formation in Mice*: Clinical Implications

Alvin M. Malkinson, PhD
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*From the University of Colorado Cancer Center, University of Colorado Health Sciences Center, Denver, CO.

Correspondence to: Alvin M. Malkinson, PhD, The University of Colorado Cancer Center, University of Colorado Health Sciences Center, 4200 E Ninth Ave, Denver, CO 80262; e-mail: al.malkinson@uchsc.edu



Chest. 2004;125(5_suppl):154S-155S. doi:10.1378/chest.125.5_suppl.154S-a
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Epidemiologic associations between inflammation and lung cancer include an increased cancer risk in COPD and asthma patients, familial clustering of pulmonary inflammatory diseases and lung cancer, and a decreased cancer incidence among long-term aspirin users. Experimental evidence that inflammation enhances the development of lung tumors in mice includes the following: chromosomal sites that determine susceptibilities to lung injury/inflammation in response to environmental toxins also regulate lung tumor susceptibility; reduced or raised tumorigenesis in mice that are null for, or that overexpress, enzymes that synthesize inflammatory mediators and their receptors; decreased tumor formation following the administration of antiinflammatory drugs such as budesonide and indomethacin; biochemical markers of inflammation such as the elevated expression of enzymes catalyzing eicosanoid biosynthesis and nitric oxide formation within and adjacent to tumor sites; and the incursion of activated inflammatory cells into and peripheral to the tumor mass.

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