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dc.contributor.authorTurner, S D
dc.contributor.authorRafferty, Joseph A
dc.contributor.authorFairbairn, Leslie J
dc.contributor.authorAshby, J
dc.contributor.authorTinwell, H
dc.contributor.authorEckert, H G
dc.contributor.authorBaum, C
dc.contributor.authorLashford, Linda S
dc.date.accessioned2009-11-23T10:50:36Z
dc.date.available2009-11-23T10:50:36Z
dc.date.issued2000-10
dc.identifier.citationThe 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 Leukemiaen
dc.identifier.issn0887-6924
dc.identifier.pmid11021755
dc.identifier.urihttp://hdl.handle.net/10541/86674
dc.description.abstractWe 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.
dc.language.isoenen
dc.subject.meshAnimals
dc.subject.meshAntineoplastic Agents, Phytogenic
dc.subject.meshBone Marrow
dc.subject.meshDrug Administration Routes
dc.subject.meshDrug Administration Schedule
dc.subject.meshEtoposide
dc.subject.meshFemale
dc.subject.meshGene Transfer, Horizontal
dc.subject.meshMale
dc.subject.meshMice
dc.subject.meshMicronucleus Tests
dc.subject.meshP-Glycoprotein
dc.titleThe effects of dose, route of administration, drug scheduling and MDR-1 gene transfer on the genotoxicity of etoposide in bone marrow.en
dc.typeArticleen
dc.contributor.departmentDepartment of Experimental Haematology, Paterson Institute for Cancer Research, Manchester, UK.en
dc.identifier.journalLeukemiaen
html.description.abstractWe 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.


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