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    The effects of dose, route of administration, drug scheduling and MDR-1 gene transfer on the genotoxicity of etoposide in bone marrow.

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    Authors
    Turner, S D
    Rafferty, Joseph A
    Fairbairn, Leslie J
    Ashby, J
    Tinwell, H
    Eckert, H G
    Baum, C
    Lashford, Linda S
    Affiliation
    Department of Experimental Haematology, Paterson Institute for Cancer Research, Manchester, UK.
    Issue Date
    2000-10
    
    Metadata
    Show full item record
    Abstract
    We have used the bone marrow micronucleus assay (BMMN) as a measure of clastogenicity, in response to etoposide exposure in murine bone marrow. Oral delivery of etoposide resulted in a reduced number of micronucleated polychromatic erythrocytes (MPE) relative to the same dose delivered intraperitoneally (P < 0.001). Daily fractionation of the oral schedule of etoposide led to a more than six-fold increase in cumulative MPE frequency over that observed with the same total, unfractionated dose, with the potency of the response increasing with serial exposure (r = 0.79). Retrovirally-mediated expression of MDR1 in murine bone marrow resulted in partial protection against the clastogenic activity of etoposide relative to mock transduced control mice. The model system developed has indicated a variety of factors able to influence the genotoxicity of etoposide. It should now be possible to further exploit this model in order to define other factors governing haemopoietic sensitivity to etoposide.
    Citation
    The effects of dose, route of administration, drug scheduling and MDR-1 gene transfer on the genotoxicity of etoposide in bone marrow. 2000, 14 (10):1796-802 Leukemia
    Journal
    Leukemia
    URI
    http://hdl.handle.net/10541/86674
    PubMed ID
    11021755
    Type
    Article
    Language
    en
    ISSN
    0887-6924
    Collections
    All Christie Publications
    All Paterson Institute for Cancer Research

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