1. Enhanced chromatid damage in blood lymphocytes after G2 phase x irradiation, a marker of the ataxia-telangiectasia gene
- Author
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Gary M. Jones, Robert E. Tarone, Thomas A. Waldmann, Paula Hale, Katherine K. Sanford, Floyd M. Price, Lindsay Eierman, and Ram Parshad
- Subjects
Adult ,Male ,Cancer Research ,Heterozygote ,Adolescent ,DNA repair ,DNA damage ,Lymphocyte ,Biology ,Chromatids ,Radiation Tolerance ,chemistry.chemical_compound ,Ataxia Telangiectasia ,medicine ,Humans ,Radiosensitivity ,Lymphocytes ,Child ,Interphase ,Aged ,Middle Aged ,medicine.disease ,Molecular biology ,medicine.anatomical_structure ,Oncology ,chemistry ,Demecolcine ,Immunology ,Ataxia-telangiectasia ,Chromatid ,Female ,Radiation Induced DNA Damage ,DNA Damage - Abstract
An assay for ataxia-telangiectasia (A-T) heterozygotes, i.e., healthy carriers of the A-T gene(s), requiring only a small sample (3.5 mL) of peripheral blood, is described. Frequencies of chromatid aberrations in phytohemagglutinin-stimulated blood lymphocytes collected by demecolcine from 0.5 hour to 1.5 hours after x irradiation with 58 roentgens were twofold to threefold higher in A-T heterozygotes than in clinically normal controls and twofold to three-fold higher in A-T patients (homozygotes) than in A-T gene carriers. The persistence of chromatid breaks and gaps in lymphocytes following radiation-induced DNA damage during G2 suggests a deficiency or deficiencies in DNA repair that may be the defect at the molecular level that results in the enhanced radiosensitivity and cancer proneness characterizing A-T gene carriers and patients.
- Published
- 1990