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[Cancer Research 33, 362-369, February 1, 1973]
© 1973 American Association for Cancer Research

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DNA Repair with Purines and Pyrimidines in Radiation- and Carcinogen-damaged Normal and Xeroderma Pigmentosum Human Cells1

J. E. Cleaver

Laboratory of Radiobiology, University of California, San Francisco, California 94122

Repair replication of DNA in cells exposed to UV, X-rays, or chemical carcinogens involves incorporation of both purine and pyrimidine precursors. Previous reports stating that purines are not involved in repair must be due to insufficient resolution in the reported experiments. Hypoxanthine was more efficiently incorporated by repair replication than other precursors such as adenine, deoxyadenosine, and guanine. Hydroxyurea did not inhibit hypoxanthine incorporation by repair replication. Cells from patients with the hereditary high-cancer disease xeroderma pigmentosum show reduced repair after exposure to UV, 4-nitroquinoline 1-oxide, and 1,3-bis(2-chloroethyl)-1-nitrosourea; they show normal repair after exposure to agents such as N-methyl-N'-nitro-N-nitrosoguanidine. These results allow agents to be classified according to whether or not xeroderma pigmentosum cells respond normally to them and illustrate the values and limitations of the use of xeroderma pigmentosum cells or measurements of DNA repair as test systems for carcinogens.

1 Work performed under the auspices of the U. S. Atomic Energy Commission.

Received 8/21/72. Accepted 11/ 2/72.




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1973 by the American Association for Cancer Research.