» Articles » PMID: 8434025

DNA Repair and Aging in Basal Cell Carcinoma: a Molecular Epidemiology Study

Overview
Specialty Science
Date 1993 Feb 15
PMID 8434025
Citations 74
Authors
Affiliations
Soon will be listed here.
Abstract

This molecular epidemiology study examines the DNA-repair capacities (DRCs) of basal cell carcinoma (BCC) skin cancer patients (88) and their controls (135) by using a plasmid/host-cell reactivation assay. In this assay UV-damaged expression vector plasmid is transfected into peripheral blood T lymphocytes from the subjects. The host-cellular repair enzymes repair the photochemical damage in the plasmid, and 40 hr later the plasmid-encoded reporter chloramphenicol acetyltransferase is measured. An age-related decline in this DRC, amounting to approximately 0.61% per yr occurred in the controls from 20 to 60 yr of age. Reduced DRC was a particularly important risk factor for young individuals with BCC and for those individuals with a family history of skin cancer. Young individuals with BCC repaired DNA damage poorly when compared with controls. As the BCC patients aged, however, differences between cases and controls gradually disappeared. The normal decline in DNA repair with increased age may account for the increased risk of skin cancer that begins in middle age, suggesting that the occurrence of skin cancer in the young may represent precocious aging. Patients with reduced DRCs and overexposure to sunlight had an estimated risk of BCC > 5-fold greater than the control group. Such a risk was even greater (10-fold) in female subjects.

Citing Articles

Facial basal cell carcinoma: A retrospective study of 67 cases.

Khalil A, Enezei H, Aldelaimi T, Al-Ani R World J Clin Cases. 2023; 11(7):1488-1497.

PMID: 36926407 PMC: 10011985. DOI: 10.12998/wjcc.v11.i7.1488.


Human Variation in DNA Repair, Immune Function, and Cancer Risk.

Cheong A, Nagel Z Front Immunol. 2022; 13:899574.

PMID: 35935942 PMC: 9354717. DOI: 10.3389/fimmu.2022.899574.


Sex disparities in DNA damage response pathways: Novel determinants in cancer formation and therapy.

Cardano M, Buscemi G, Zannini L iScience. 2022; 25(3):103875.

PMID: 35243237 PMC: 8858993. DOI: 10.1016/j.isci.2022.103875.


DNA repair phenotype and cancer risk: a systematic review and meta-analysis of 55 case-control studies.

Wu H, Kehm R, Santella R, Brenner D, Terry M Sci Rep. 2022; 12(1):3405.

PMID: 35233009 PMC: 8888613. DOI: 10.1038/s41598-022-07256-7.


Let's talk about sex: A biological variable in immune response against melanoma.

Dakup P, Greer A, Gaddameedhi S Pigment Cell Melanoma Res. 2022; 35(2):268-279.

PMID: 35076986 PMC: 9305920. DOI: 10.1111/pcmr.13028.


References
1.
Munch-Petersen B, Frentz G, Squire B, WALLEVIK K, Horn C, REYMANN F . Abnormal lymphocyte response to u.v. radiation in multiple skin cancer. Carcinogenesis. 1985; 6(6):843-5. DOI: 10.1093/carcin/6.6.843. View

2.
Kovacs E, Weber W, Muller H . Age-related variation in the DNA-repair synthesis after UV-C irradiation in unstimulated lymphocytes of healthy blood donors. Mutat Res. 1984; 131(5-6):231-7. DOI: 10.1016/0167-8817(84)90030-0. View

3.
Harris G, Holmes A, Sabovljev S, Cramp W, Hedges M, HORNSEY S . Sensitivity to X-irradiation of peripheral blood lymphocytes from ageing donors. Int J Radiat Biol Relat Stud Phys Chem Med. 1986; 50(4):685-94. DOI: 10.1080/09553008614551091. View

4.
Kraemer K, Lee M, Scotto J . Xeroderma pigmentosum. Cutaneous, ocular, and neurologic abnormalities in 830 published cases. Arch Dermatol. 1987; 123(2):241-50. DOI: 10.1001/archderm.123.2.241. View

5.
Cole J, Green M, James S, Henderson L, Cole H . A further assessment of factors influencing measurements of thioguanine-resistant mutant frequency in circulating T-lymphocytes. Mutat Res. 1988; 204(3):493-507. DOI: 10.1016/0165-1218(88)90044-4. View