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Part of the book series: Cancer Treatment and Research ((CTAR,volume 78))

Abstract

The failure of chemotherapy to achieve complete and durable responses has been attributed in large part to the phenomenon of drug resistance. In the laboratory, tumor cells can be selected for resistance to a particular cytotoxin by repeated exposure to that drug. The selected cells often display crossresistance to a number of functionally and structurally distinct drugs. This drug-resistant phenotype is referred to as multidrug resistance (MDR). Currently, the best understood mechanism of multidrug resistance is that which is mediated by the mdr 1 gene product, P-glycoprotein (P-gp). P-gp is a plasma membrane protein that functions as a multidrug transporter capable of effluxing a variety of antineoplastic agents, predominantly those derived from natural products (see tables 3-1). Cells which express P-gp accumulate less cytotoxin and, hence, are resistant to these drugs [16].

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Fisher, G.A., Lum, B.L., Sikic, B.I. (1995). The reversal of multidrug resistance. In: Muggia, F.M. (eds) Concepts, Mechanisms, and New Targets for Chemotherapy. Cancer Treatment and Research, vol 78. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2007-8_3

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