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JNCI Journal of the National Cancer Institute 1990 82(12):1050-1054; doi:10.1093/jnci/82.12.1050
© 1990 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 82, No. 12, 1050-1054, June 20, 1990
© 1990 Oxford University Press

Enhanced Chromatid Damage in Blood Lymphocytes After G2 Phase X Irradiation, a Marker of the Ataxia-Telangiectasia Gene

Katherine K. Sanford*, Ram Parshad, Floyd M. Price, Gary M. Jones, Robert E. Tarone, Lindsay Eierman, Paula Hale, Thomas A. Waldmann

Laboratory of Cellular and Molecular Biology National Cancer Institute Bethesda, MD
Biostatistics Branch National Cancer Institute Bethesda, MD
Metabolism Branch National Cancer Institute Bethesda, MD
Department of Pathology, Howard University College of Medicine Washington, DC
Department of Pediatrics, Robert Wood Johnson Medical School New Brunswick, NJ

*Correspondence to: Katherine K. Sanford, Ph.D., Bldg. 37, Rm. 2D15, National Institutes of Health, Bethesda, MD 20892

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 threefold 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. [J Natl Cancer Inst 82:1050–1054, 1990]

Manuscript received March 7, 1990; revised April 2, 1990; accepted April 6, 1990.


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