Proceedings of the National Academy of Sciences · 1990 · 191 citations · 49 references
MedicineCell BiologyMolecular BiologyCancer GeneticsCarcinogenesisOncogenesAnimal Cell CultureOncogene ActivationOncogene AmplificationOncogene MutationsAmplificationCellular OncogenesCopy Number Alteration AnalysisDna Amplification MechanismsMolecular Drug ResistanceNucleic Acid AmplificationOncogenic TransformationReductase Gene Amplification
Three types of normal human cells were selected in tissue culture with three drugs without observing a single amplification event from a total of 5 x 10(8) cells. No drug-resistant colonies were observed when normal foreskin keratinocytes were selected with N-(phosphonacetyl)-L-aspartate or with hydroxyurea or when normal mammary epithelial cells were selected with methotrexate. Some slightly resistant colonies with limited potential for growth were obtained when normal diploid fibroblast cells derived from fetal lung were selected with methotrexate or hydroxyurea but careful copy-number analysis of the dihydrofolate reductase and ribonucleotide reductase genes revealed no evidence of amplification. The rarity of DNA amplification in normal human cells contrasts strongly with the situation in tumors and in established cell lines, where amplification of oncogenes and of genes mediating drug resistance is frequent. The results suggest that tumors and cell lines have acquired the abnormal ability to amplify DNA with high frequency.
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Amplification of P-glycoprotein genes in multidrug-resistant mammalian cell lines
John R. Riordan, Kathryn L. Deuchars, Norbert Kartner et al. · Nature · 1985 · 841 citations
Sally Hammond, R G Ham, Martha R. Stampfer · Proceedings of the National Academy of Sciences · 1984 · 445 citations · Full text