Postreplication repair in three murine melanomas, a mammary carcinoma, and a normal mouse lung fibroblast line.

Repair of ultraviolet light-induced damage to DNA was studied in three melanoma lines, a mammary carcinoma line, EMT6, and a normal lung fibroblast line, MLF, all from the mouse. The melanomas were B16CL4, a gamma-ray-resistant clonal line derived from B16; S91H-, an auxotrophic line derived from Cloudman S91; and HP, a freshly isolated line from s.c. grown Harding-Passey melanoma. The melanomas and MFL were found to perform minimal excision repair and photoreactivation. Postreplication repair, on the other hand, was an active process in all five of the lines. All three melanomas exhibited postreplication repair rates that were about twice that of MLF. The freshly isolated HP line evolved during subcultivation, and its postreplication repair rate dropped after 3 months to a rate comparable to EMT6, which was 1.5 times that of MLF. The results suggest that postreplication repair is an important process in melanomas and may be related to radiation response.