Sir: DNAtopoisomerases are nuclear enzymes that catalyze the concerted breaking and rejoining of DNAstrands, thereby controlling the topological states of DNA1}. There is now good evidence showing that topoisomerase I is the principal intracellular target for clinically important antitumor drugs, camptothecin and its derivatives2 ~4). These drugs, referred as to "topoisomerase I poisons" interfere with the breakage-rejoining reaction of topoisomerase I by stabilizing a tight topoisomerase I-DNAcomplex termed "cleavable complex" which prevents the final rejoining step of the reaction. Exposure of this cleavable complex to a denaturant leads to the formation of DNAsingle strand breaks5). Several lines of evidence indicate that the ability to induce topoisomerase I mediated DNA cleavage is responsible for the antitumor activity of these drugs2~5). In order to identify a specific new topoisomerase I poison, we have screened cultures of actinomycetes and fungi for their ability to stabilize cleavable complex in vitro. Wefound that saintopin6) and bulgarein7) are potent inducers of topoisomerase I mediated DNA cleavege, and have now isolated UCE6, a novel compound with topoisomerase I mediated DNA cleavage activity, from a culture broth of actinomycetes.
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