On the localization of mitomycin C-induced aberrations in normal human and Fanconi's anaemia cells |
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Authors: | J R Savage K S Reddy |
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Affiliation: | 1. GET Information Technology GmbH, Rudolf-Diesel-Strasse 14, 41516 Grevenbroich, Germany;2. Peter the Great St.Petersburg Polytechnic University, Polytechnicheskaya 29, St. Petersburg, 195351, Russia;1. Applied Geotechnologies Group, Dept. Natural Resources and Environmental Engineering, University of Vigo, Campus Lagoas-Marcosende, CP 36310 Vigo, Spain;2. GIS Technology, OTB Research Institute for the Built Environment, Delft University of Technology, Julianalaan 134, 2628 BL Delft, The Netherlands |
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Abstract: | This paper summarizes the results of a series of experiments with primary cultures of normal human fibroblasts and lymphocytes designed to investigate chromatid aberration 'break-point' localization after a 1-h pulse of mitomycin C. For discontinuities and interchanges, 60-70% of the inferred 'break-points' were localized to defined paracentric heterochromatin and the centromeric regions (i.e. approximately 21% by length of the normal karyotype), irrespective of 'dose', aberration frequency, sample time or cycle sub-phase as determined by replication banding. Chromatid intrachanges are non-(or negatively) localized because of an inescapable scoring bias. SCE in fibroblasts show no such localization. Cells from a number of Fanconi's anaemia subjects were examined. In poorly growing cultures, localization was as high as in normal cells but in vigorous cultures localization was reduced to approximately 30%. It is suggested that the enhanced aberration sensitivity of this syndrome could arise because non-localized aberrations, usually eliminated before division in normal cells, are allowed to reach mitosis in FA cells. |
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