© 2002 by Oxford University Press
Journal of the National Cancer Institute, Vol. 94, No. 10, 749-754,
May 15, 2002
© 2002 Oxford University Press
ARTICLE |
Insulin-Like Growth Factor I, IGF-Binding Protein 3, and Lung Cancer Risk in a Prospective Study of Men in China
Affiliations of authors: S. J. London (Epidemiology Branch and Laboratory of Pulmonary Pathobiology), G. S. Travlos, R. Wilson (Environmental Toxicology Program), National Institute of Environmental Health Sciences, Research Triangle Park, NC; J.-M. Yuan, M. C. Yu, R. K. Ross, Norris Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles; Y.-T. Gao, Shanghai Cancer Institute, Shanghai, China.
Correspondence to: Stephanie London, M.D., Dr.P.H., National Institute of Environmental Health Sciences, P.O. Box 12233, MD A3–05, Research Triangle Park, NC 27709 (e-mail: london2{at}niehs.nih.gov).
Background: Insulin-like growth factor I (IGF-I) stimulates cell proliferation and inhibits apoptosis in the lung and other tissues by interacting with the IGF-I receptor. The major binding protein for IGF-I, insulin-like growth factor-binding protein 3 (IGFBP-3), modulates the effects of IGF-I but also inhibits cell growth and induces apoptosis independent of IGF-I and its receptor. In a prospective study of men in Shanghai, China, we examined the association between serum levels of IGF-I and IGFBP-3 and the subsequent risk of lung cancer. Methods: From 1986 to 1989, serum was collected from 18 244 men aged 45–64 years living in Shanghai without a history of cancer. We analyzed IGF-I and IGFBP-3 levels in serum from 230 case patients who developed incident lung cancer during follow-up and from 740 control subjects. Results: Among 230 case patients and 659 matched control subjects, increased IGF-I levels were not associated with increased risk of lung cancer. However, for subjects in the highest quartile relative to the lowest quartile of IGFBP-3, the odds ratio (OR) for lung cancer, adjusted for smoking and IGF-I, was 0.50 (95% confidence interval [CI] = 0.25 to 1.02). When the analysis was restricted to ever smokers (184 case patients and 344 matched control subjects), the OR for lung cancer in men in the highest quartile of IGFBP-3 relative to those in the lowest quartile, adjusted for smoking and IGF-I, was 0.41 (95% CI = 0.18 to 0.92). Conclusions: In this prospective study of Chinese men, higher serum levels of IGF-I did not increase the risk of lung cancer. However, subjects with higher serum levels of IGFBP-3 were at reduced risk of lung cancer. This finding is consistent with experimental data that indicate that IGFBP-3 can inhibit cellular proliferation and induce apoptosis independent of IGF-I and the IGF-I receptor.
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