Suppression of X-Ray-Induced Chromatid Breaks in Human Tumor Cells by Introduction of Normal Chromosome 4

Abstract

Human tumor cells in culture frequently show an infinite lifespan and are characterized by an abnormally high frequency of chromatid breaks after x-irradiation during G 2 phase of the cell cycle. This abnormally high frequency of persistent chromatid breaks results from deficient repair of the radiation-induced DNA damage. In three of four tumor cell lines, addition of a single human chromosome 4 from normal cells by microcell fusion resulted in efficient repair as evidenced by suppression of radiation-induced chromatid breaks to the level in normal cells. With respect to senescence-related gene (s), two of these four tumor cell lines belonged to complementation group A and one each to groups C and D. Chromosome 4 restored DNA repair efficiency in only one of the two tumor cell lines of complementation group A. These results suggest that chromosome 4 carries a DNA repair gene or gene(s) that complement the repair deficiency in three of these four tumor lines. Furthermore, the gene(s) involved in cellular senescence on chromosome 4 appear to differ from the gene(s) for repair of radiation-induced DNA damage during G 2.