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  • Docetaxel  (1)
  • Ehrlich ascites carcinoma  (1)
  • 1
    ISSN: 1432-0843
    Keywords: Key words Cisplatin ; Docetaxel ; Paclitaxel
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The purpose of this study was to determine the mechanism of the pharmacodynamic interaction between docetaxel/paclitaxel and cisplatin. Cisplatin-induced DNA-adducts and cisplatin accumulation were quantitated in peripheral blood leukocytes (WBC). The WBC were obtained from patients treated with docetaxel or paclitaxel in phase I/II studies and were incubated in vitro with cisplatin. In addition, blank whole-blood samples were obtained from patients and healthy subjects and incubated in vitro with cisplatin or docetaxel/paclitaxel and cisplatin. The cisplatin-induced DNA-adduct levels measured in WBC after treatment with docetaxel or paclitaxel were significantly lower than those determined in non-pretreated WBC. Docetaxel and paclitaxel reduced the intracellular accumulation of cisplatin in WBC by 46–47%. If the pharmacodynamic interaction between docetaxel/paclitaxel and cisplatin also occurs in other normal tissues such as bone marrow, it may well contribute to the sequence dependent toxicity that has been observed in clinical studies.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-4935
    Keywords: cell adhesion ; Ehrlich ascites carcinoma ; lectin ; mistletoe ; signaling inhibitor ; thymocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract Initial ligand selection and the intermolecular spatial arrangement ofglycan-lectin complexes are assumed to be essential to induce formationof stable cell aggregates by a lectin. To distinguish effects of thesetwo processes, the tetrameric mistletoe lectin and its isolated B-chainwere used. A reduced impact of multivalency for Ehrlich ascites tumorcells in contrast to rat thymocytes was revealed. Signaling is thusinitiated in a cell-type-dependent manner. Using selective metabolicinhibitors to reduce signal transfer for aggregate stability, decreasein cellular SH-group level was shown to be a common effect accompanyingsuppression of lectin-dependent aggregate stability. The resultsunderscore an intrinsic variability in the relative importance oflectin-dependent glycan aggregation on the cell surface for triggeringpost-binding lectin effects.
    Type of Medium: Electronic Resource
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