This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Hittelman, W. N. Articles by Sen, P. Search for Related Content PubMed PubMed Citation Articles by Hittelman, W. N. Articles by Sen, P.

Heterogeneity in Chromosome Damage and Repair Rates after Bleomycin in Ataxia Telangiectasia Cells¹

Department of Medical Oncology, The University of Texas M. D. Anderson Hospital and Tumor Institute, and the U. T. Graduate School of Biomedical Sciences, Houston, Texas 77030

Cells derived from patients with ataxia telangiectasia (AT) are known to be exceptionally sensitive to ionizing radiation and chemotherapeutic agents such as bleomycin (BLM), neocarzinostatin, and etoposide. This increased sensitivity is manifested by high chromosome aberration frequencies after treatment. In order to probe the underlying basis for this phenomenon, the technique of premature chromosome condensation was used to determine whether the increased chromosome damage observed after bleomycin treatment is due to increased initial chromosome damage or to a decreased capability of these cells to repair chromosome damage. Five AT cell lines were brought to quiescence and treated with BLM, and initial chromosome damage and repair rates were determined in the G₁ prematurely condensed chromosomes. AT cells exhibited increased aberration frequencies compared to normal human fibroblasts immediately after BLM treatment. The five AT cell lines were heterogeneous in the fast component of chromosome break repair, varying from a nearly normal fast repair component in one cell line to a nearly defunct fast repair component in two other AT cell lines. Thus, while the AT cell lines were heterogeneous in the basis for their chromosome breakage sensitivity, all AT cell lines tested showed increased residual chromosome damage after BLM treatment while still in the quiescent phase.

¹ Supported in part by Grants R01-CA 27931, R01-CA 39534, and P01-CA06294 from the National Cancer Institute, NIH, Bethesda, MD.

² To whom requests for reprints should be addressed.

Received 6/29/87. Revised 10/16/87. Accepted 10/19/87.

This article has been cited by other articles:

				X. Wu, S. M. Lippman, J. J. Lee, Y. Zhu, Q. V. Wei, M. Thomas, W. K. Hong, and M. R. Spitz Chromosome Instability in Lymphocytes: A Potential Indicator of Predisposition to Oral Premalignant Lesions Cancer Res., May 1, 2002; 62(10): 2813 - 2818. [Abstract] [Full Text] [PDF]

				M. L. Bondy, L.-E. Wang, R. El-Zein, M. de Andrade, M. S. Selvan, J. M. Bruner, V. A. Levin, W. K. Alfred Yung, P. Adatto, and Q. Wei {gamma}-Radiation Sensitivity and Risk of Glioma J Natl Cancer Inst, October 17, 2001; 93(20): 1553 - 1557. [Abstract] [Full Text] [PDF]

				L. Dumenco, E Allay, K Norton, and S. Gerson The prevention of thymic lymphomas in transgenic mice by human O6-alkylguanine-DNA alkyltransferase Science, January 8, 1993; 259(5092): 219 - 222. [Abstract] [PDF]