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Comparison of Virus Reactivation, DNA Base Damage, and Cell Cycle Effects in Autologous Human Melanoma Cells Resistant to Methylating Agents¹

Queensland Institute of Medical Research, Herston, Brisbane, Australia 4006

A human melanoma cell line (MM253c1-3D) having an induced stable resistance to the methylating agents 5-(3'-methyl-1-triazeno)imidazole-4-carboxamide, methylnitrosourea, and N-methyl-N'-nitro-N-nitrosoguanidine gave more efficient replication of 5-(3'-methyl-1-triazeno)imidazole-4-carboxamide-treated adenovirus 5 than did the methylation-sensitive parent line (MM253c1). Analysis of DNA hydrolysates from melanoma cells treated with [³H]methylnitrosourea for 1.6 hr showed similar initial levels of 7-methylguanine and 3-methyladenine in both cell lines and substantial excision of the latter lesion after 19 hr. O⁶-Methylguanine in the DNA of MM253c1 cells also decreased during this period, but in MM253c1-3D cells the initial yield of this lesion was too low for subsequent decrease to be detected. 5-(3'-Methyl-1-triazeno)imidazole-4-carboxamide induced a significant arrest of MM253c1 cells in the G₂ phase of the cell cycle. These results show that MM253c1 is a variant of the Mer^- phenotype, the resistance of MM253c1-3D cells being attributed to reversion to Mer⁺ and expressed as very rapid repair of O⁶-methylguanine lesions.

¹ This work was assisted by a grant from the National Health and Medical Research Council, Canberra, Australia.

² To whom requests for reprints should be addressed.

Received 12/ 6/82. Accepted 9/21/83.