Abstract
The description of a decrease in the intracellular accumulation of a number of cytostatics, such as anthracyclines, vinca alkaloids, epipodophyllotoxins, and actinomycin D, in drug-resistant malignant cells — first demonstrated for colchicine in hamster ovary cells [4] caused by an energy-dependent outward pump in connection with the expression of the 170 000-dalton plasma membrane glycoprotein PI 70 [2] — has substantially contributed to the understanding of “multidrug resistance” [6]. Accordingly, the responsiveness of malignant cells to these cytotoxic drugs may more critically depend on their cellular tumor pharmacokinetics and metabolism than on their plasma pharmacokinetics, which in general only poorly correlates with their pharmacodynamics [7].
Supported by the Deutsche Forschungsgemeinschaft, Bonn-Bad Godesberg:Sonderforschungsbereich 102
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Scheulen, M.E., Kramer, B., Skorzec, M., Reich, W.K. (1990). Cellular Pharmacokinetics of Daunomycin in Human Leukemic Blasts In Vitro and In Vivo. In: Büchner, T., Schellong, G., Hiddemann, W., Ritter, J. (eds) Acute Leukemias II. Haematology and Blood Transfusion / Hämatologie und Bluttransfusion, vol 33. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-74643-7_22
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DOI: https://doi.org/10.1007/978-3-642-74643-7_22
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