Abstract
We have identified a group of 8 (among 39) human tumour cell strains deficient in the ability to support the growth of adenovirus 5 preparations treated with N-methyl-N′-nitro-N-nitrosoguanidine (MNNG), but able to support the growth of non-treated adenovirus normally1,2. This deficient behaviour defines the Mer− phenotype2. Strains having the Mer− phenotype were found to arise from tumours originating in four different organs. Relative to Mer+ strains, Mer− tumour strains showed greater sensitivity to MNNG-produced killing, greater MNNG-stimulated ‘DNA repair’ synthesis and a more rapid MNNG-produced decrease in semi-conservative DNA synthesis2. Here we report that (1) Mer− strains are deficient in removing O6-methylguanine (O6-MeG) from their DNA after [Me-14C]MNNG treatment (Table 1); (2) Mer− tumour strains originate from tumours arising in patients having Mer+ normal fibroblasts (Fig. 1a, b); (3) SV40 transformation of (Mer+) human fibroblasts often converts them to Mer− strains (Fig. 1c, d): (4) MNNG produces more sister chromatid exchanges (SCEs) in Mer− than in Mer+ cell strains (Fig. 2).
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Day, R., Ziolkowski, C., Scudiero, D. et al. Defective repair of alkylated DNA by human tumour and SV40-transformed human cell strains. Nature 288, 724–727 (1980). https://doi.org/10.1038/288724a0
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DOI: https://doi.org/10.1038/288724a0
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