Suppression of gene amplification in human cell hybrids.
Gene amplification, one example of genetic instability, is of prognostic and clinical importance in neoplasia. In tumorigenic cells, gene amplification occurs at a very high frequency, whereas in normal diploid fibroblasts the event is undetectable by the clonogenic assay. To investigate genetic control of gene amplification, amplification frequency was measured in hybrids of tumorigenic cells and normal diploid cells. The ability to amplify an endogenous gene behaved as a recessive genetic trait, and control of gene amplification potential segregated independently of tumorigenicity and immortality.
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Lineberger Comprehensive Cancer Center, Department of Pathology and Curriculum in Genetics, School of Medicine, University of North Carolina, Chapel Hill 27599.
White
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Sanchez
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D001221:Aspartate Carbamoyltransferase / Q000037:antagonists & inhibitors / Q000235:genetics; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D002460:Cell Line; D002471:Cell Transformation, Neoplastic / Q000235:genetics*; D004351:Drug Resistance / Q000235:genetics; D005784:Gene Amplification / Q000235:genetics*; D015971:Gene Expression Regulation, Enzymologic; D005799:Genes, Dominant; D005808:Genes, Recessive; D006801:Humans; D006822:Hybrid Cells / Q000187:drug effects / Q000201:enzymology; D009154:Mutation; D010641:Phenotype; D010746:Phosphonoacetic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D013489:Suppression, Genetic; D014407:Tumor Cells, Cultured
D001224:Aspartic Acid; C013195:sparfosic acid; D001221:Aspartate Carbamoyltransferase; D010746:Phosphonoacetic Acid