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© 2006 The American Thoracic Society
doi: 10.1513/pats.200603-089MS
State of the Art. Chronic Obstructive Pulmonary Disease, Inflammation, and Lung Cancer
Pulmonary Center and Department of Medicine, Boston University School of Medicine, Boston, Massachusetts
Correspondence and requests for reprints should be addressed to Jerome S. Brody, M.D., Pulmonary Center, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118. E-mail: jbrody{at}bu.edu
ABSTRACT
Both lung cancer and chronic obstructive pulmonary disease (COPD) are associated with cigarette smoking, which, by generating reactive oxidant species, induces a chronic inflammatory state in the lung. Activation, particularly of nuclear factor-
B, occurs in both cancer and COPD, and expression of a number of genes is altered in both diseases. In lung cancer, DNA damage, lack of DNA repair, and genomic instability predominate, whereas matrix degradation, lack of repair, and an intense immune response predominate in COPD. The reasons for the different responses to a common inflammatory response induced by smoking remain to be determined, but likely lie in genetic polymorphisms in genes that regulate genome integrity in cancer and that regulate the immune response to tissue destruction in COPD.
Key Words: genomic instability • inflammation • lung immune response • reactive oxygen species
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