Epidemiology of Ultraviolet-DNA Repair Capacity and Human Cancer
Lawrence Grossman
Department of Biochemistry, The Johns Hopkins University,
Baltimore, Maryland
Abstract
The following conclusions are derived from an epidemiological study. Reduced repair of ultraviolet (UV)-induced DNA damage contributes directly to basal cell carcinoma (BCC) in individuals with prior sunlight overexposure. A family history of BCC is a predictor of low DNA repair. Repair of UV-damaged DNA declines at a fixed rate of approximately 1% per annum in noncancerous controls. The DNA repair differences between young BCC cases and their controls disappear as they age. Hence, BCC, in terms of DNA repair, is a premature aging disease. The persistence of photochemical damage because of reduced repair results in point mutations in the p53 gene and allelic loss of the nevoid BCC gene (Gorlin's syndrome) located on chromosome 9q. The fact that environmental vulnerability is gender oriented implicates hormones in regulating DNA repair. Xeroderma pigmentosum appears to be a valid paradigm for the role of DNA repair in BCC in the general population. -- Environ Health Perspect 105(Suppl 4):927-930 (1997)
Key words: DNA repair capacity, molecular epidemiology, basal cell carcinoma, adenoma carcinoma of the lung, DNA repair capacity and aging, nevoid basal cell carcinoma, Gorlin's syndrome
This paper is based on a presentation at the symposium on Mechanisms and Prevention of Environmentally Caused Cancers held 21-25 October 1995 in Santa Fe, New Mexico. Manuscript received at EHP 16 April 1996; accepted 25 June 1996.
Address correspondence to Dr. L. Grossman, Department of Biochemistry, Johns Hopkins University, School of Hygiene and Public Health, 615 North Wolfe Street, Baltimore, MD 21205. Telephone: (410) 614-4226. Fax: (410) 955-2926.
E-mail: lg@welchlink.welch.jhu.edu
Abbreviations used: BCC, basal cell carcinoma; DRC, DNA repair capacity; UDS, unscheduled DNA synthesis; UV, ultraviolet; XP, xeroderma pigmentosum.
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