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 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 Gg phase. All of these agents except guanazole also induce breakage in S phase.
Original language | English (US) |
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Pages (from-to) | 62 |
Number of pages | 1 |
Journal | Science |
Volume | 178 |
Issue number | 4056 |
State | Published - 1972 |
ASJC Scopus subject areas
- General