Transformation of DNA repair-deficient human diploid fibroblasts with a simian virus 40 plasmid.
Fibroblasts from patients with xeroderma pigmentosum (XP) complementation groups A, C, D, E, and G, as well as Bloom syndrome (BS) and Fanconi anemia (FA) have been transfected with a plasmid, pSV7, containing the early region of Simian virus 40 (SV40). All of the cultures exhibited cytologic changes characteristic of transformed cells and expressed T-antigen. They also contained integrated copies of DNA derived from the vector, and in several cases, extrachromosomally replicated DNA. Not all of the transfected cultures became immortalized. The transformed xeroderma pigmentosum (XP) cultures retained their UV-sensitive phenotype in all but one case. The BS and FA cell lines retained their characteristic phenotype. All of the cultures, except the BS cells, can be readily transfected with the plasmids, pSV2neo and pSV2gpt.
D001816:Bloom Syndrome / Q000235:genetics; D002470:Cell Survival / Q000187:drug effects; D002472:Cell Transformation, Viral; D002478:Cells, Cultured; D002945:Cisplatin / Q000494:pharmacology; D004260:DNA Repair; D005199:Fanconi Anemia / Q000235:genetics; D005347:Fibroblasts / Q000166:cytology; D005816:Genetic Complementation Test; D006801:Humans; D010957:Plasmids; D013539:Simian virus 40 / Q000235:genetics*; D014162:Transfection; D014983:Xeroderma Pigmentosum / Q000235:genetics
D002945:Cisplatin