Abstract
THE radiosensitivity of patients with ataxia telangiectasia (AT) has been indicated by in vivo studies1–3 and in vitro studies on skin fibroblasts4. We present data here to show that this radiosensitivity is observed at the chromosomal level in blood lymphocytes X irradiated at different stages of the cell cycle and for the same range of doses as our survival experiments4. Our results are consistent with the hypothesis that there is a defect in some form of DNA repair in these patients. From the observation of the types of chromosome aberrations seen in AT lymphocytes after irradiation at G0/early G1, we propose a mechanism for the origin of these aberrations, based on the premise that the G0/early G1 chromosome contains a single DNA double helix, in which one polynucleotide chain can be damaged independently of the other.
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TAYLOR, A., METCALFE, J., OXFORD, J. et al. Is chromatid-type damage in ataxia telangiectasia after irradiation at G0 a consequence of defective repair?. Nature 260, 441–443 (1976). https://doi.org/10.1038/260441a0
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DOI: https://doi.org/10.1038/260441a0
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