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Repair of DNA damaged by alkylating carcinogens is defective in xeroderma pigmentosum-derived fibroblasts


THE human hereditary skin disease xeroderma pigmentosum (XP) is characterised by extreme sensitivity to sunlight and a high incidence of sunlight-induced skin cancer. These symptoms seem to be correlated with a defect in the excision repair of ultraviolet-induced dimers1. Repair of DNA damage caused by chemical carcinogens belonging to the group of monofunctional alkylating agents was thought to be normal in XP cells, however, because after treatment with these agents the amounts of repair replication2,3 and the numbers of chromosome aberrations4 were similar in normal and XP cells. Contrary to this indirect evidence, it is reported here that direct measurement of the amounts of two products formed by alkylating carcinogens in the DNA and of the rate at which they are eliminated indicates that XP cells have a defect in this type of repair also.

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GOTH-GOLDSTEIN, R. Repair of DNA damaged by alkylating carcinogens is defective in xeroderma pigmentosum-derived fibroblasts. Nature 267, 81–82 (1977).

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