Abstract
“The problem of resistance in neoplastic cells, as in microorganisms, will remain a most important perpetual threat to the successful use of therapeutic agents” (Law, 1956). It also has been said, that as long as cancer cells are able to divide, Darwinian evolution is inevitable. The basis for these statements can be found by examining mechanisms by which a population of cells (microorganisms or neoplastic cells) adapt to the presence of a drug. Physiologic adaptation, in which the drug induces a change in the population, does not involve a genetic change and is not a stable characteristic. Genetic adaptation, in which mutants arising independently of the drug are selected in the presence of the drug, is characterized by stability of resistance. These mechanisms are not mutually exclusive, as pointed out by Bryson and Szybalski (1955), Dean and Hinshelwood (1957), Peters (1970), and others. Agents that are mutagenic, in some cases the anticancer drug itself, may increase the probability of the development of resistance by increasing the mutation frequency in a population of treated cells.
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Brockman, E.W. (1974). Mechanisms of Resistance. In: Sartorelli, A.C., Johns, D.G. (eds) Antineoplastic and Immunosuppressive Agents Part I. Handbuch der experimentellen Pharmakologie / Handbook of Experimental Pharmacology, vol 38 / 1. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-65678-1_19
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