The γ-ray sensitivity of skin fibroblasts from six members of a cancer family was investigated using a colony-forming assay. Fibroblasts from the three members with cancer (two sisters with acute myelogenous leukemia and the mother with cervical carcinoma) showed a significant (p < 0.05) increase in radiosensitivity, while three members without cancer (the father and two sons) showed a normal radioresponse. The possibility that the increased γ-ray sensitivity was due to defective DNA repair was investigated using assays for DNA repair replication, single-strand break rejoining, and removal of enzyme-sensitive sites in γ-irradiated DNA. Results of these assays indicate that the kinetics of enzymatic repair of radiogenic DNA damage in general, and the rejoining of single-strand scissions and excision repair of base and sugar radioproducts in particular, were the same in the cell lines from the sensitive and clinically normal family members.

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Supported in part by Contract NO1-CP-81002 with the Clinical Epidemiology Branch, National Cancer Institute, NIH, Bethesda, Md.

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©1981 American Association for Cancer Research.
1981
Cancer Research, Inc.