Radiation-induced chromatid breaks and deficient DNA repair in cancer predisposition

Abstract Deficient repair of DNA double-strand breaks, resulting in an abnormally high frequency of chromatid breaks after G 2 exposure of cells to radiation, appears to be associated with cancer predisposition. Unrepaired DNA strand breaks contribute to genomic instability. Unrepaired chromatid breaks representing DNA strand breaks can result in chromosome deletions, translocations and gene amplifications seen in human cancers. This cytogenetic response of cells to radiation may be useful as a marker of cancer susceptibility and in identifying individuals at risk of developing cancer in cancer families.