Abstract
Shortly after the discovery of the cytostatic activity of cis-diamminedichloroplatinum(II) (cisplatin) (1) it was suggested that the mechanism of antitumor activity of cisplatin involves its binding to DNA (for review, see refs. 2–4). In addition, it was suggested that the mechanism of antitumor activity of cisplatin might be analogous to the biologic activity of bifunctional alkylating agents (such as nitrogen mustard), which also exhibit cytostatic effects (5). As the cytostatic effect of di-alkylating agents was generally accepted to be associated with their DNA interstrand crosslinking efficiency, the first hypotheses on the mechanism underlying the cytotoxicity of cisplatin in tumor cells were derived from its ability to form interstrand crosslinks in DNA (6). On the basis of this analogy, cisplatin was sometimes incorrectly called an “alkylating agent.”
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Brabec, V. (2000). Chemistry and Structural Biology of 1,2-Interstrand Adducts of Cisplatin. In: Kelland, L.R., Farrell, N.P. (eds) Platinum-Based Drugs in Cancer Therapy. Cancer Drug Discovery and Development. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-012-4_2
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