By William T. Beck, Mary K. Danks (auth.), Igor B. Roninson (eds.)
The skill of neoplastic cells to outlive publicity to numerous chemotherapeutic medicinal drugs represents the most crisis to winning melanoma chemotherapy. This booklet bargains with a selected form of resistance in tumor cells that represents a unmarried yet specially very important point of the multifaceted challenge of melanoma drug resistance. this sort of resistance, referred to as multidrug or pleiotropic drug resistance, is characterised by means of cross-resistance of cells to numerous diversified sessions of cytotoxic medications, together with one of the most standard anticancer brokers. over the past a number of years, there was a veritable explosion of genetic, biochemical, and scientific details on multidrug resistance, which the id and cloning of the genes chargeable for this phenotype and the isolation of monoclonal antibodies opposed to P-glycoproteins, the goods of those genes. Elucida tion of the molecular mechanism of multidrug resistance has ended in the formula of novel ways to the prediction of tumor reaction to chemotherapeutic medicinal drugs and extending the efficacy of melanoma treatment. research of the constitution and serve as of P glycoproteins from multidrug-resistant mammalian cells has additionally validated a prototype for a singular classification of eukaryotic membrane proteins, that have now been linked to numerous delivery procedures in several organisms. This booklet summarizes the result of molecular organic, pharmacological, bio chemical, cytogenetic, immunological, and pathological reports on multidrug resistance in mammalian cells. many of the chapters deal not less than to some degree with the constitution and expression of P-glycoprotein and its position in multidrug resistance.
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Extra info for Molecular and Cellular Biology of Multidrug Resistance in Tumor Cells
In general, the primary resistance of the human lines appears to be similar, ranging from ca. five- to several hundred-fold. There are only a few examples of human MDR lines of very high resistance, such as have been reported by Peterson et ai. (1983) for their MDR Chinese hamster lung cells. It is unlikely that this indicates some fundamental difference between rodent and human expressions of MDR, since the recent studies by Keizer and Joenjie (1989) and by Bradley et ai. (1989) report human cell lines of 2000- to 25,OOO-fold resistance or cross-resistance.
1986) Cell line DNA (MDR gene copy number) mRNA Expression of Pgp-MDR markersa Table IV. , 1986) t t t t by WB by WB by WB P2 10 and PI80 reactive with C219 (anti-Pgp) PI70 not detected by WB (McGrath and Center, 1987); t PI50 by 32p and 1251 labeling ! ! t (continued) p 72; ! , 1985b) p72; ! , 1989a) ! , 1989) ~ 'I '" n ~ ::l :I: ~ S III S· (I) n ::l .... '" III ~. ~ OQ ~ 5: ... , 1988) mRNA Expression of Pgp-MDR markersa Table IV. , 1989). Alteration of other GSH-metabolizing enzymes. 7x t nonprotein SH in R cells, which !
II> ~ I:l p.. II> ~ t:C co n ~ a ~ ;. , 1986b) OV1IVCR cont. OVI/VCR discont. > n ::s ~ ~ ~. ~ OQ r:: 5: .... ~ g. 32 William T. Beck and Mary K. 6-fold for I hr of exposure and continuous drug exposure, respectively). , cell type), and the physical (lipid solubility, size), chemical (charge), or biochemical (protein binding) properties of the drug may also contribute. To the best of our know ledge, experiments designed to address these questions directly have not been reported. , 1988). Finally, it is possible that the differences between primary resistance and crossresistance are due to stochastic processes: whatever the biochemical or molecular basis, the selection of one cross-resistance pattern over another may be randomly generated.