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Evidence that Xeroderma Pigmentosum Cells do not Perform the First Step in the Repair of Ultraviolet Damage to their DNA
R. B. Setlow, James D. Regan, James German and W. L. Carrier
Proceedings of the National Academy of Sciences of the United States of America
Vol. 64, No. 3 (Nov. 15, 1969), pp. 1035-1041
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/59701
Page Count: 7
You can always find the topics here!Topics: DNA, Dimers, Cell lines, Pyrimidine dimers, Molecular weight, Skin, Genetics, DNA damage, Fibroblasts, Diploidy
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Xeroderma pigmentosum (XP) is a recessively transmitted disorder of man characterized by increased sensitivity to ultraviolet light. Homozygous, affected individuals, upon exposure to sunlight, sustain severe damage to the skin; this damage is characteristically followed by multiple basal and squamous cell carcinomas and not uncommonly by other malignant neoplasia. A tissue culture cell line was derived from the skin of a man with XP. Our measurements of ultraviolet-induced pyrimidine dimers in cellular DNA show that normal diploid human skin fibroblasts excise up to 70 per cent of the dimers in 24 hours, but that fibroblasts derived from the individual with XP excise less than 20 per cent in 48 hours. Alkaline gradient sedimentation experiments show that during the 24 hours after irradiation of normal cells a large number of single-strand breaks appear and then disappear. Such changes are not observed in XP cells. XP cells apparently fail to start the excision process because they lack the required function of an ultraviolet-specific endonuclease. These findings, plus earlier ones of Cleaver on the lack of repair replication in XP cells, raise the possibility that unexcised pyrimidine dimers can be implicated in the oncogenicity of ultraviolet radiation.
Proceedings of the National Academy of Sciences of the United States of America © 1969 National Academy of Sciences