By William T. Beck, Mary K. Danks (auth.), Igor B. Roninson (eds.)
The skill of neoplastic cells to outlive publicity to varied chemotherapeutic medicinal drugs represents the most difficulty to profitable melanoma chemotherapy. This ebook bargains with a selected kind of resistance in tumor cells that represents a unmarried yet specially very important element of the multifaceted challenge of melanoma drug resistance. this kind of resistance, referred to as multidrug or pleiotropic drug resistance, is characterised via cross-resistance of cells to numerous diversified periods of cytotoxic medicines, together with essentially the most regular 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 answerable 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 resulted in the formula of novel ways to the prediction of tumor reaction to chemotherapeutic medicinal drugs and lengthening the efficacy of melanoma remedy. research of the constitution and serve as of P glycoproteins from multidrug-resistant mammalian cells has additionally proven a prototype for a singular type of eukaryotic membrane proteins, that have now been linked to numerous delivery methods in numerous organisms. This ebook summarizes the result of molecular organic, pharmacological, bio chemical, cytogenetic, immunological, and pathological experiences on multidrug resistance in mammalian cells. lots of the chapters deal not less than to a point with the constitution and expression of P-glycoprotein and its position in multidrug resistance.
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Additional info for Molecular and Cellular Biology of Multidrug Resistance in Tumor Cells
1989, P-glycoprotein expression in multidrug-resistant human ovarian carcinoma cell lines. Cancer Res. 49:2790-2796. , Giuliani, F. , 1988, Intracellular doxorubicin concentrations and drug-induced DNA damage in a human colon adenocarcinoma cell line and in a drug-resistant subline, Biochem. Pharmacol. 37:4423-4431. Broxterman, H. , Pinedo, H. , Kuiper, C. , Kaptein, L. C. , Schuurhuis, G. , 1988, Induction by verapamil of a rapid increase in ATP consumption in multidrug-resistant tumor cells, FASEB J.
1984) R inherent in lines; no selection pressure Several weeks at each drug concentration G-MCF. G-CCM. G-UVW (Merry et al.. 1984) SK VLB (series VLBO. 004-VLB 1) (Bradley et al.. 1989) HN-I/VPz (B. T. Hill et al.. 1988) LoVo/OX (Grandi et al.. 1986) 14 months H69AR (Mirski et al.. CA8 hr 24 hr; same as S line; but lag phase of 24 hr for LoVo and 40 hr for LoVolDX =26 hr. same as S line =24 hr. same as S line 2: 10 passages >6 months in drugfree medium Lost 40% of resistance between 1 and 6 months No Yes Yes Yes No (continued) Parent line SKOV3: hypodiploid to hypotetraploid (Fogh and Trempe.
1987b, Different mechanisms of multiple drug resistance in two human leukemic cell lines, in: Mechanisms of Drug Resistance in Neoplastic Cells (P. Wolley and K. ), Academic Ptess, New York, pp. 211-222. Beck, W. , Cirtain, M. , Glover, C. , Felsted, R. , and Safa, A. , 1988, Effects of indole alkaloids on multidrug resistance and labeling of P-glycoprotein by a photoaffinity analog of vinblastine, Biochem. Biophys. Res. Commun. 153:959-966. Bell, D. , Gerlach, 1. , Buick, R. , 1985, Detection of P-glycoprotein in ovarian cancer: A molecular marker associated with multidrug resistance, J.