Induction and expression of mutations at multiple drug-resistance marker loci in Chinese hamster ovary cells

1983 ◽  
Vol 5 (2) ◽  
pp. 161-175 ◽  
Author(s):  
Gerald M. Adair ◽  
June H. Carver
Keyword(s):  
Drug Resistance ◽  
Chinese Hamster Ovary ◽  
Multiple Drug Resistance ◽  
Chinese Hamster Ovary Cells ◽  
Chinese Hamster ◽  
Multiple Drug ◽  
Resistance Marker ◽  
Ovary Cells ◽  
Marker Loci ◽  
Drug Resistance Marker

Increased mutational rates in Chinese hamster ovary cells serially selected for drug resistance

1983 ◽  
Vol 3 (10) ◽  
pp. 1882-1885
Author(s):  
E Drobetsky ◽  
M Meuth
Keyword(s):  
Drug Resistance ◽  
Chinese Hamster Ovary Cell ◽  
Chinese Hamster Ovary ◽  
Chinese Hamster Ovary Cells ◽  
Chinese Hamster ◽  
Cytotoxic Drugs ◽  
Ovary Cell ◽  
Cell Populations ◽  
Ovary Cells ◽  
Serial Cultivation

Chinese hamster ovary cell populations exposed to the pressures of prolonged serial cultivation in cytotoxic drugs have increased mutational rates at independent genetic loci. Evidence suggests that the alterations generating these mutations may be independent of the lesions conferring drug resistance.

Clustered base substitutions in CTP synthetase conferring drug resistance in Chinese hamster ovary cells

1993 ◽  
Vol 3 (4) ◽  
pp. 317-322 ◽  
Author(s):  
Jeremy Whelan ◽  
Geraldine Phear ◽  
Masatake Yamauchi ◽  
Mark Meuth
Keyword(s):  
Drug Resistance ◽  
Chinese Hamster Ovary ◽  
Chinese Hamster Ovary Cells ◽  
Chinese Hamster ◽  
Ctp Synthetase ◽  
Ovary Cells ◽  
Base Substitutions

scholarly journals New ara-C resistant mutants of the Chinese hamster ovary cells

1985 ◽  
Vol 45 (3) ◽  
pp. 265-277 ◽  
Author(s):  
N. C. Mishra ◽  
Kathryn Hinnant ◽  
Emily Cason
Keyword(s):  
Drug Resistance ◽  
Chinese Hamster Ovary ◽  
Chinese Hamster Ovary Cells ◽  
Chinese Hamster ◽  
Wild Type ◽  
Cho Cell ◽  
Ovary Cells ◽  
Mutant Cells ◽  
Antitumour Drug

SummaryMutants of Chinese hamster ovary (CHO) cell resistant to cytosine arabinoside (ara-C), an inhibitor of DNA synthesis and antitumour drug, have been isolated and characterized both biochemically and genetically. Mutants occurring spontaneously and those induced by treatment with N-methyl-N′-Nitro-N-nitrosoguanidine (MNG), were obtained at a frequency of 0·24 × 10−6 and 3·4 10−6 respectively. The mutants showed a stable ara-C resistant phenotype which was inherited as a dominant trait in genetic crosses. The wild type (CHO K-1) and the mutant (103, 002 and 003) cells showed no differences in the levels of the uptake of ara-C or of its degradation. Results of biochemical studies further excluded the involvement of deaminase, kinase and ribonucleotide reductase as the possible factor(s) in conferring drug resistance to the mutant cells. However, the wild type and mutant DNA polymerases differed in the level of the in vitro incorporation of specific dNMP in the presence of ara-CTP. These data suggested that the wild-type DNA polymerase which becomes error prone in the presence of ara-CTP may cause the drug sensitivity of the wild-type cells and that a change in the mutant enzyme making it resistant (or less prone) to ara-CTP induced errors in dNMP incorporation may control the drug resistance of the mutant cells.

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