Transformation of chromosome breakage syndrome fibroblasts by SV40 DNA transfection.
SV40 DNA was transfected into three Fanconi's anemia, two classical ataxia-telangiectasia, two variant ataxia-telangiectasia, three Bloom's syndrome, and three normal fibroblast cultures in order to study T-antigen expression, growth transformation, and survival of the crisis phase. Although Fanconi's anemia cells exhibited an initially higher frequency of uptake of transfected DNA compared with all the other cell strains studied, they did not acquire the transformed phenotype any faster than the others. Classical ataxia-telangiectasia fibroblasts, on the other hand, showed approximately the same rate of initial uptake of SV40, but were significantly slower than all other cell strains in expressing the transformed phenotype. The uptake and growth transformation properties of Bloom's syndrome and variant ataxia-telangiectasia cells were similar to those of normals. Serial subculturing of transfected cells was found to accelerate the appearance of growth-transformed cells. Although a number of transformed sublines of Fanconi's anemia, classical and variant ataxia-telangiectasia, and Bloom's syndrome strains apparently survived the crisis phase, no immortalized strains emerged from them.
D000957:Antigens, Viral, Tumor / Q000032:analysis; D001260:Ataxia Telangiectasia / Q000235:genetics; D001816:Bloom Syndrome / Q000235:genetics; D002471:Cell Transformation, Neoplastic; D002472:Cell Transformation, Viral; D002478:Cells, Cultured; D002869:Chromosome Aberrations; D005199:Fanconi Anemia / Q000235:genetics; D005260:Female; D005347:Fibroblasts / Q000648:ultrastructure; D006801:Humans; D008297:Male; D009154:Mutation; D009857:Oncogenes; D010641:Phenotype; D013539:Simian virus 40 / Q000235:genetics*; D014162:Transfection
D000957:Antigens, Viral, Tumor