A genetic basis for tumour suppression.
The technique of somatic cell hybridization has established the phenomenon of tumour suppression and provided evidence for a genetic basis for suppression. Further refinements aimed at eventually identifying 'tumour suppressor' genes include the use of monochromosome transfer via microcell hybridization. The application of this technique to the study of tumour suppression in tumorigenic HeLa cell x fibroblast hybrids, Wilms' tumour, retinoblastoma and osteosarcoma cells is described. The issue of whether tumour suppression involves a direct effect on expression of activated oncogenes is discussed. Transformation of normal human cells in culture by activated cellular oncogenes is an extremely rare event. This may be due to a relatively greater genomic stability of human cells compared to rodent cells. We describe the use of a spontaneously immortalized human keratinocyte cell line, HaCaT, for studies of the effects of introduction of activated c-Ha-ras oncogene into these cells, with particular reference to tumorigenic conversion.
Stanbridge
E J
EJ
Department of Microbiology and Molecular Genetics, California College of Medicine, University of California, Irvine 92717.
D000818:Animals; D005347:Fibroblasts; D005786:Gene Expression Regulation; D011905:Genes, ras; D006367:HeLa Cells; D006801:Humans; D006822:Hybrid Cells; D051379:Mice; D008819:Mice, Nude; D009369:Neoplasms / Q000235:genetics*; D012516:Osteosarcoma / Q000235:genetics; D012175:Retinoblastoma / Q000235:genetics; D013489:Suppression, Genetic; D014162:Transfection; D009396:Wilms Tumor / Q000235:genetics