A deficiency in DNA repair and DNA-PKcs expression in the radiosensitive BALB/c mouse

R. Okayasu, K. Suetomi, Yongjia Yu, A. Silver, J. S. Bedford, R. Cox, R. L. Ullrich

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Abstract

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 γ 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.

Original languageEnglish (US)
Pages (from-to)4342-4345
Number of pages4
JournalCancer Research
Volume60
Issue number16
StatePublished - Aug 15 2000

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ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Okayasu, R., Suetomi, K., Yu, Y., Silver, A., Bedford, J. S., Cox, R., & Ullrich, R. L. (2000). A deficiency in DNA repair and DNA-PKcs expression in the radiosensitive BALB/c mouse. Cancer Research, 60(16), 4342-4345.