Chromatid Breakage: Differential Effect of Inhibitors of DNA Synthesis during G 2 Phase
- 6 October 1972
- journal article
- other
- Published by American Association for the Advancement of Science (AAAS) in Science
- Vol. 178 (4056) , 62
- https://doi.org/10.1126/science.178.4056.62
Abstract
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.Keywords
This publication has 5 references indexed in Scilit:
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- Chromatid Breakage: Cytosine Arabinoside-Induced Lesions Inhibited by Ultraviolet IrradiationScience, 1971
- Inhibition of DNA Polymerase by -D-Arabinosylcytosine and Reversal of Inhibition by Deoxycytidine-5'-triphosphateExperimental Biology and Medicine, 1968
- Incorporation of 5-Azacytidine into nucleic acids of Escherichia coliBiochimica et Biophysica Acta (BBA) - Nucleic Acids and Protein Synthesis, 1968
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