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    Cell death, chromosome damage and mitotic delay in normal human, ataxia telangiectasia and retinoblastoma fibroblasts after x-irradiation.

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    Authors
    Zampetti-Bosseler, F
    Scott, David
    Affiliation
    Paterson Laboratories, Christie Hospital & Holt Radium Institute, Manchester, M20 9BX, U.K.
    Issue Date
    1981-05
    
    Metadata
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    Abstract
    We recently showed (Scott and Zampetti-Bosseler 1980) that X-ray sensitive mouse lymphoma cells sustain more chromosome damage, mitotic delay and spindle defects than X-ray resistant cells. We proposed that (a) chromosome aberrations contribute much more to lethality than spindle defects, and (b) that DNA lesions are less effectively repaired in the sensitive cells and give rise to more G2 mitotic delay and chromosome aberrations. Our present results on human fibroblasts with reported differential sensitivity to ionizing radiation (i.e. normal donors and patients with ataxia telangiectasia and retinoblastoma) support the first hypothesis since we observed a positive correlation between chromosome aberration frequencies and cell killing and no induced spindle defects. Our second hypothesis is however not substantiated since X-ray sensitive fibroblasts from the ataxia patient suffered less mitotic delay than cells from normal donors. A common lesion for mitotic delay and chromosome aberrations can still be assumed by adopting the hypothesis of Painter and Young (1981) that the defect in ataxia cells is not in repair but in a failure of DNA damage to initiate mitotic delay. In contrast to other reports, we found the retinoblastoma cells to be of normal radiation sensitivity (cell killing and aberration).
    Citation
    Cell death, chromosome damage and mitotic delay in normal human, ataxia telangiectasia and retinoblastoma fibroblasts after x-irradiation. 1981, 39 (5):547-58 Int J Radiat Biol Relat Stud Phys Chem Med
    Journal
    International Journal of Radiation Biology and Related Studies in Physics, Chemistry, and Medicine
    URI
    http://hdl.handle.net/10541/134850
    DOI
    10.1080/09553008114550651
    PubMed ID
    6972365
    Type
    Article
    Language
    en
    ISSN
    0020-7616
    ae974a485f413a2113503eed53cd6c53
    10.1080/09553008114550651
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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