Chromatid damage after G2 phase x-irradiation of cells from cancer-prone individuals implicates deficiency in DNA repair.

Publisher Website
Google Scholar
Abstract
Ten lines of skin fibroblasts [GM2548, PC-109, GM0449A, BH, DWsr, CRl1158, GM2415, CRL1162, CRL1223, CRL1261] from individuals with genetic disorders predisposing to a high risk of cancer were compared with 9 lines [CR-1188, CRL-1191, CRL-1221, CRL-1222, CRL-1224, CRL-1232, RJH-4, KD, GM0500] from normal adult donors with respect to chromatid damage after x-irradiation [25, 50 and 100 rad (0.25, 0.50 and 1 gray)] during G2 phase. The 10 cell lines represented 5 genetic disorders: Bloom syndrome, familial polyposis, Fanconi anemia, Gardner syndrome and xeroderma pigmentosum, complementation groups A(XP-A), C(XP-C), E(XP-E) and variant (XP-Va). The incidence of chromatid breaks in all cancer-prone lines except XP-E and XP-A was significantly higher than in the normal lines. The incidence of chromatid gaps in all cancer-prone lines except XP-A and XP-Va was significantly higher than in the normal lines. Because each chromatid apparently contains a single continuous DNA double strand, chromatid breaks and gaps represent unrepaired DNA strand breaks arising directly or indirectly during excision repair of X-ray-induced DNA damage. These cytogenetic data together with results from use of the DNA repair inhibitor arabinofuranosyl cytosine (cytosine arabinoside) suggest that cells from all of these cancer-prone individuals are deficient in some step of DNA repair, predominantly excision repair operative during the G2-prophase period of the cell cycle. These DNA repair deficiencies are associated with a genetic predisposition to a high risk of cancer.

This publication has 25 references indexed in Scilit: