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JNCI Journal of the National Cancer Institute 2003 95(17):1263-1265; doi:10.1093/jnci/djg065
© 2003 by Oxford University Press
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© 2003 Oxford University Press

EDITORIAL

The Molecular Epidemiology of Oxidative Damage to DNA and Cancer

Neil Caporaso

Correspondence to: Neil Caporaso, MD, Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Blvd., EPS 7116, Bethesda, MD 20892 (e-mail: caporasn@exchange.nih.gov).

The first 150 words of the full text of this article appear below.

Oxygen is required for respiration and the energetic processes that enable aerobic life. A cost associated with oxygen use is free-radical formation, which damages genome stability and contributes to various processes including aging, degenerative diseases, and cancer (1,2). Foods including fruits, vegetables, tea components, and trans-fats; nutrients including vitamins C and E, selenium, beta-carotene, and dietary fish oil; chemotherapeutic drugs; radiation; infection; environmental exposures including air pollution; and hereditary and acquired conditions broadly contribute to or oppose free-radical formation and genomic damage (2–9). Individually and cooperatively, the action of modulators of oxidative DNA damage is the focus of intense study and controversy (10). Understanding the regulation of free-radical formation and its consequences may provide new insight into the etiology of cancer and lead to the development of effective chemoprevention agents.

Lung cancer is a logical disease for evaluating oxidative . . . [Full Text of this Article]


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