DNA repair activity may be associated with risk of lung cancer

September 02, 2003

People with reduced DNA repair activity, as determined by a blood test, appear to be at a higher risk of developing lung cancer than people with average DNA repair activity, according to a study in the September 3 issue of the Journal of the National Cancer Institute. The findings suggest a genetic predisposition to lung cancer in some individuals and may explain why only a fraction of smokers develop the disease.

Tobacco smoke contains many carcinogens that are known to damage DNA. Reduced ability to repair damaged DNA has been associated with a predisposition to lung cancer in previous studies. To examine the association between a specific DNA repair enzyme and risk of lung cancer, Zvi Livneh, Ph.D., and Tamar Paz-Elizur, Ph.D., of the Weizmann Institute of Science in Rehovot, Israel, and their colleagues measured the activity of the DNA repair enzyme OGG in blood samples of 68 patients with non-small-cell lung cancer and 68 healthy people.

OGG activity was statistically significantly lower in lung cancer patients than in controls and was the same in smokers and non-smokers. After adjusting for age and smoking status, people in the bottom third of OGG activity had 4.8 times the risk of lung cancer as people in the top third of OGG activity.

In addition, the authors found that smoking and low OGG activity were independent risk factors for lung cancer and that people who smoked and had low OGG activity had the greatest risk of lung cancer. Whereas nonsmokers with very low OGG activity had seven times the lung cancer risk of nonsmokers with normal OGG activity, smokers with low OGG activity were more than 100 times the risk of lung cancer of smokers with normal OGG.

The findings suggest that "a substantial fraction of lung cancer cases might result from a combination of smoking and reduced OGG activity," the authors write. "If so, then screening for smokers with low OGG activity, followed by smoking cessation in these individuals, may lead to a decrease in the incidence of lung cancer."

In an accompanying editorial, Neil Caporaso, M.D., of the National Cancer Institute, says that it will be important to examine in greater detail whether OGG activity is influenced by exposures (for example, among never, former, and current smokers) and disease (for example, in treated and untreated subjects and by histology and stage).

He concludes that integrated large studies will help establish the role of oxidative repair phenotypes in human disease and cancer. "Regardless of how refined a picture emerges from human and animal models, large-scale work in human populations will be required to confirm effects in realistic settings and to gauge public health implications," he writes.
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Contact: Zvi Livneh, Weizmann Institute of Science, 972-54-774-637 or 972-8-934-3203 (no later than 5pm ET or midnight GMT) zvi.livneh@weizmann.ac.il.

Editorial: NCI Press Office, 301-496-6641, ncipressofficers@mail.nih.gov.

Paz-Elizur T, Krupsky M, Blumenstein S, Elinger D, Schechtman E, Livneh Z. DNA repair activity for oxidative damage and risk of lung cancer. J Natl Cancer Inst 2003;95:1312-19.

Editorial: Caporaso N. The molecular epidemiology of oxidative damage to DNA and cancer. J Natl Cancer Inst 2003;95:1263-65.

Note: The Journal of the National Cancer Institute is published by Oxford University Press and is not affiliated with the National Cancer Institute. Attribution to the Journal of the National Cancer Institute is requested in all news coverage.

Journal of the National Cancer Institute

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