Chromatid breakage: differential effect of inhibitors of DNA synthesis during G 2  phase.
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 G(2) 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 G(2) phase. All of these agents except guanazole also induce breakage in S phase.
D000818:Animals; D001374:Azacitidine / Q000494:pharmacology; D001375:Azaguanine / Q000494:pharmacology; D002460:Cell Line; D002842:Chromatids / Q000187:drug effects*; D002869:Chromosome Aberrations; D006224:Cricetinae; D003561:Cytarabine / Q000494:pharmacology; D003562:Cytidine / Q000494:pharmacology; D004247:DNA / Q000096:biosynthesis*; D004254:DNA Nucleotidyltransferases / Q000037:antagonists & inhibitors; D006918:Hydroxyurea / Q000494:pharmacology; D008168:Lung; D008938:Mitosis; D010088:Oxidoreductases / Q000037:antagonists & inhibitors; D011725:Pyridines; D012265:Ribonucleotides; D013882:Thiosemicarbazones / Q000494:pharmacology; D014227:Triazines / Q000494:pharmacology
D011725:Pyridines; D012265:Ribonucleotides; D013882:Thiosemicarbazones; D014227:Triazines; D003561:Cytarabine; D003562:Cytidine; D004247:DNA; D010088:Oxidoreductases; D004254:DNA Nucleotidyltransferases; D001374:Azacitidine; D001375:Azaguanine; D006918:Hydroxyurea