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Fanconi anaemia cells are not uniformly deficient in unhooking of DNA interstrand crosslinks, induced by mitomycin C or 8-methoxypsoralen plus UVA

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Summary

Fanconi anaemia (FA) cells are extremely sensitive to crosslinking agents, e. g. mitomycin C, but only moderately sensitive to trimethylpsoralen plus UVA. Evidence has been reported suggesting that there is a deficient DNA crosslink repair mechanism in FA cells, but others failed to confirm this conclusion using other methods and other crosslinking agents. We reinvestigated the mitomycin C and 8-methoxypsoralen crosslink repair in FA cells with a high sensitivity to mitomycin C. Although an essentially similar methodology was used to that previously described, no difference between the control and FA cell strains was observed, neither for mitomycin C- nor for 8-methoxypsoralen-induced crosslinks.

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Authors and Affiliations

  1. Institute of Human Genetics, Faculty of Medicine, Free University, P.O.Box 7161, NL-1007 MC, Amsterdam, The Netherlands

    E. H. A. Poll, F. Arwert, H. T. Kortbeek & A. W. Eriksson

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  1. E. H. A. Poll
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  2. F. Arwert
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  3. H. T. Kortbeek
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  4. A. W. Eriksson
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Poll, E.H.A., Arwert, F., Kortbeek, H.T. et al. Fanconi anaemia cells are not uniformly deficient in unhooking of DNA interstrand crosslinks, induced by mitomycin C or 8-methoxypsoralen plus UVA. Hum Genet 68, 228–234 (1984). https://doi.org/10.1007/BF00418393

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  • DOI: https://doi.org/10.1007/BF00418393

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