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Carcinogenesis, Vol. 23, No. 10, 1617-1624, October 2002
© 2002 Oxford University Press

CANCER BIOLOGY

Deficiency in the repair of UV-induced DNA damage in human skin fibroblasts compromised for the ATM gene

Mohammed A. Hannan1,*, Ali Hellani2, Fahad M. Al-Khodairy1, Mohammed Kunhi1, Yunis Siddiqui1, Noujud Al-Yussef1, Nancy Pangue-Cruz1, Monica Siewertsen1, Mohammed N. Al-Ahdal1 and Abdelilah Aboussekhra1,3

1 King Faisal Specialist Hospital and Research Center Biological and Medical Research Department, MBC 03-66 and
2 Department of Pathology and Laboratory Medicine, ART Section, MBC 10, PO Box 3354, Riyadh 11211, Saudi Arabia

Ataxia-telangiectasia (A-T), is an autosomal recessive disease characterized by neurological and immunological symptoms, radiosensitivity and cancer predisposition. A-T cells exhibit a greatly decreased survival and a reduction in DNA synthesis inhibition as well as p53 induction in response to ionizing radiation. Occasionally, some strains of A-T cells have been reported to manifest a slightly enhanced sensitivity with no consistent observations of a deficiency in either cell cycle control or the repair of DNA damage after treatment with ultraviolet (UV) light. In the present study it is shown that skin fibroblasts from four A-T patients, compared with the control, display enhanced sensitivity to the killing effect of UV-light, moderate radioresistant DNA synthesis, and a reduction in viral recovery in the host cell reactivation (HCR) assay. PCR based analysis indicated that three of these UV-sensitive A-T cell strains bear a large deletion in the ATM gene, and no ATM polypeptide was detected in their cell free extracts. Moreover, it is shown that, in non-replicative conditions, these A-T cells are less efficient than normal cells in repairing the T4 endonuclease V sensitive sites. These results constitute the first clear evidence showing the deficiency of A-T cells in the repair of UV-induced DNA damage, and provide further information on the relationship between cell cycle control and DNA repair in human cells.


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