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Science 6 October 1972:
Vol. 178. no. 4056, p. 62
DOI: 10.1126/science.178.4056.62
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Articles

Chromatid Breakage: Differential Effect of Inhibitors of DNA Synthesis during G2 Phase

Myron Karon 1 and William F. Benedict 1

1 Division of Hematology, Childrens Hospital of Los Angeles, University of Southern California School of Medicine, Los Angeles 90054

The cell cycle specificity of chromatid breakage induced by inhibitors of DNA synthesis depends on the mechanism of drug action. 5-Hydroxy-2-formylpyridine thiosemicarbazone, hydroxyurea, and guanazole, compounds that inhibit ribonucleotide reductase, do not cause chromatid breakage during G2 phase. In contrast, two active antitumor agents, arabinosylcytosine and 5-azacytidine, which are either incorporated into polynucleotides or affect DNA polymerase, produce chromatid breakage during G2 phase. All of these agents except guanazole also induce breakage in S phase.


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
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Molecular analysis of 5-azacytidine-induced variants in mammalian cells.
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5-Azacytidine: A New Anticancer Drug with Effectiveness in Acute Myelogenous Leukemia.
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