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[Cancer Research 60, 4342-4345, August 15, 2000]
© 2000 American Association for Cancer Research

Advances in Brief

A Deficiency in DNA Repair and DNA-PKcs Expression in the Radiosensitive BALB/c Mouse1

Ryuichi Okayasu2, Katsutoshi Suetomi, Yongjia Yu, Andy Silver, Joel S. Bedford, Roger Cox and Robert L. Ullrich

Department of Radiological Health Sciences, Colorado State University, Fort Collins, Colorado 80523-1673 [R. O., J. S. B.]; Department of Radiation Oncology-Biology Division, University of Texas Medical Branch, Galveston, Texas 77555-0656 [R. O., K. S., Y. Y., R. L. U.]; and National Radiological Protection Board, Chilton, Didcot, Oxon OX11 0RQ, United Kingdom [A. S., R. C.]

We have studied the efficiency of DNA double strand break (DSB) rejoining in primary cells from mouse strains that show large differences in in vivo radiosensitivity and tumor susceptibility. Cells from radiosensitive, cancer-prone BALB/c mice showed inefficient end joining of {gamma} ray-induced DSBs as compared with cells from all of the other commonly used strains and F1 hybrids of C57BL/6 and BALB/c mice. The BALB/c repair phenotype was accompanied by a significantly reduced expression level of DNA-PKcs protein as well as a lowered DNA-PK activity level as compared with the other strains. In conjunction with published reports, these data suggest that natural genetic variation in nonhomologous end joining processes may have a significant impact on the in vivo radiation response of mice.




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