Abstract
It is suggested here that the unusually high level of radiation-induced chromosome and chromatid-type aberrations in cells from patients with ataxia telangiectasia, compared with normals, is due to a significantly increased fraction of unrepaired double and single strand breaks. A hypothesis is proposed to explain how unrepaired and misrepaired DNA single or double strand breaks might be the basic lesion leading to the typical chromosome aberrations seen following X-irradiation of both normal or AT cells.
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