1986
DOI: 10.1073/pnas.83.24.9328
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Similar biochemical changes associated with multidrug resistance in human breast cancer cells and carcinogen-induced resistance to xenobiotics in rats.

Abstract: MCF7 human breast cancer cells selected for resistance to doxorubicin (adriamycin; DoxR) have developed the phenotype of multidrug resistance. Multidrug resistance in DoxR MCF7 cells (called AdrR MCF7 cell line in previous publications) is associated with biochemical changes similar to those induced by carcinogens in rat hyperplastic liver nodules (HNs) and associated with resistance to xenobiotics in that system. In HNs and DoxR cells, exposure to a single agent results in the selection of cells that are cros… Show more

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Cited by 223 publications
(139 citation statements)
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“…Rhabdomyosarcoma (RMS) RH-30 cell line was a gift from St. Jude Children's Research Hospital (Memphis, TN). Both DOX-selected multidrug resistant (MDR) cell subline K562/A02 13 and MCF-7/ADR 14,15 were purchased from the Institute of Hematology, Chinese Academy of Medical Sciences (Tianjin, China). The VCR-selected MDR KB/VCR 16 subline was obtained from Zhongshan University of Medical Sciences (Guangzhou, China).…”
Section: Cell Lines and Culturementioning
confidence: 99%
“…Rhabdomyosarcoma (RMS) RH-30 cell line was a gift from St. Jude Children's Research Hospital (Memphis, TN). Both DOX-selected multidrug resistant (MDR) cell subline K562/A02 13 and MCF-7/ADR 14,15 were purchased from the Institute of Hematology, Chinese Academy of Medical Sciences (Tianjin, China). The VCR-selected MDR KB/VCR 16 subline was obtained from Zhongshan University of Medical Sciences (Guangzhou, China).…”
Section: Cell Lines and Culturementioning
confidence: 99%
“…As CDDP exerts its cytoxicity by producing intrastrand crosslinks in DNA strands (Sundquist & Lippard, 1990), whilst adriamycin intercalates between neighbouring DNA bases (Muller, 1975), the mechanisms of induced drug resistance are different. In the case of CDDP increased resistance of tumour cells was shown to result often from a higher cellular efficiency in excising Pt-DNA adducts (Masuda et al, 1988, Eastman & Schulte, 1988Sekiya et al, 1989), whereas in cells resistant to adriamycin an enhanced capacity for drug transport out of the cells was supposed to be the main mechanism responsible for drug resistance (Inaka et al, 1979;Cowan et al, 1986). it is conceivable that this property of adriamycin-resistant cells is associated with alterations in membrane metabolism and, thus, could explain the decreased concentrations of the PMEs and PDEs, which are both metabolites of membrane-bound phospholipids (for an overview see Van den Bosch, 1974;Cohen, 1988).…”
Section: Uninfluenced Tumour Growthmentioning
confidence: 99%
“…(Hayes & Wolf 1988). In certain cases concomitant over expression of both GST pi and mdr-1 mRNA have been observed (Cowan et al, 1986). Over expression of both mdr-l and GST has also been seen in carcinogen-induced preneoplastic lesions in rat liver indicating that there may be co-ordinate expression of these proteins (Kitahara et al, 1984).…”
mentioning
confidence: 99%