CHROMOSOMAL RADIOSENSITIVITY OF LYMPHOCYTES FROM SKIN CANCER-PRONE PATIENTS

Citation
R. Elzein et al., CHROMOSOMAL RADIOSENSITIVITY OF LYMPHOCYTES FROM SKIN CANCER-PRONE PATIENTS, Mutation research. Section on environmental mutagenesis and related subjects, 335(2), 1995, pp. 143-149
Citations number
18
Categorie Soggetti
Genetics & Heredity","Environmental Sciences
ISSN journal
01651161
Volume
335
Issue
2
Year of publication
1995
Pages
143 - 149
Database
ISI
SICI code
0165-1161(1995)335:2<143:CROLFS>2.0.ZU;2-5
Abstract
Frequencies of spontaneous and radiation-induced chromosome aberration s were documented in lymphocytes from patients with basal cell nevus s yndrome (BCNS) and from those with epidermodysplasia verruciformis (EV ). Cells were irradiated with single or double doses of gamma-rays or UV light. For the double dose irradiation protocol, the two doses were separated from each other by 60 min. After irradiation of cells with 4 or 2 + 2 J/m(2) UV light, lymphocytes from seven BCNS patients had a similar number of aberrant cells compared with normal controls, while cells from three EV patients showed a significantly increased number of cells containing aberrations, particularly chromatid-type aberratio ns, compared to controls (p < 0.03, Student's t-test). Similar results were observed whether the cells were irradiated with single or double doses of UV light. In addition, lymphocytes from EV patients had sign ificantly lower mitotic indices than controls whether the cultures wer e irradiated with UV light or unirradiated (p < 0.05; Student's t-test ). After irradiation with 100, 100 + 100 or 50 + 50 cGy gamma-rays, th e mean chromosome aberration frequencies from nine BCNS patients and t wo EV patients were not significantly different from the controls. The spontaneous chromosome aberration frequencies were similar for the pa tients and the controls. Our data indicate that BCNS and EV lymphocyte s irradiated with gamma-rays have a normal DNA repair response. Howeve r, cells from EV patients have an abnormal repair response to UV light induced DNA damage. This abnormality is probably caused by deficiency in DNA repair and it is consistent with the patients' sensitivity to UV light induced cutaneous squamous cell carcinomas.