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[Cancer Research 61, 6025-6028, August 15, 2001]
© 2001 American Association for Cancer Research

Advances in Brief

Age-related Radical-induced DNA Damage Is Linked to Prostate Cancer1

Donald C. Malins2, Paul M. Johnson, Thomas M. Wheeler, Edward A. Barker, Nayak L. Polissar and Mark A. Vinson

Molecular Epidemiology Program, Pacific Northwest Research Institute, Seattle, Washington 98122 [D. C. M., P. M. J., M. A. V.]; Baylor College of Medicine, Houston, Texas 77030 [T. M. W.]; Molecular Oncology International, Seattle, Washington 98109 [E. A. B.]; and Mountain-Whisper-Light Statistical Consulting, Seattle, Washington 98112; and Department of Biostatistics, University of Washington, Seattle, Washington 98195 [N. L. P.]

We measured concentrations and ratios of mutagenic (8-OH) lesions to putatively nonmutagenic formamidopyrimidine (Fapy) lesions of adenine (Ade) and guanine (Gua) to elucidate radical (·OH)-induced changes in DNA of normal, normal from cancer, and cancer tissues of the prostate. The relationship between the lesions was expressed using the mathematical model log10[(8-OH-Ade + 8-OH-Gua)/(FapyAde + FapyGua)]. Logistic regression analysis of the log ratios for DNA of normal and cancer tissues discriminated between the two tissue groups with high sensitivity and specificity. Correlation analysis of log ratios for normal prostates revealed a highly significant increase in the proportion of mutagenic base lesions with age. Data from correlation analysis of the log ratios for normal tissues from cancer were consistent with an age-dependent, dose-response relationship. The slopes for both correlations intersected at ~61 years, an age when prostate cancer incidence is known to rise sharply. The age-related increase in the proportion of ·OH-induced mutagenic base lesions is likely a significant factor in prostate cancer development.




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Copyright © 2001 by the American Association for Cancer Research.