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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Comparison of virus reactivation, DNA base damage, and cell cycle effects in autologous human melanoma cells resistant to methylating agents.

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]


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