@article{oai:niigata-u.repo.nii.ac.jp:00006594,
 author = {Kakihara, Toshio},
 issue = {3},
 journal = {Acta medica et biologica, Acta medica et biologica},
 month = {Sep},
 note = {Two human myelomonocytie leukemia cell lines highly resistant to 1-β-D-arabinofuranosyleytosine (ara-C) were established. One line, designated KY-Ra, has been proliferating with 1 × 10^<-4> M ara-C for over one year. The other one, KY-Rb, has proliferated with 1 × 10^<-5> M N^4-behenoyl-1-β-D-arabinofuranosylcytosine (BH-AC) after it reached a proliferative capacity with 1×10^<-6> M ara-C. These two area-C-resistant cell lines have shown approximately 5,900 fold and 18,000 fold resistance to ara-C over the parental KY-821 cell line. The deoxycytidine kinase activity of each cell line was 0.39 (dCMP/min/μg protein) for KY-Ra, 0.26 for KY-Rb, 1.23 for KY-821. Deoxycytidine deaminase activities were almost identical. In drug accumulations, arac-C resistant cell lines showed a reduced uptake of ara-C during a 4 h exposure to 1 nM ara-C. After loading almost the same intracellular contents of drugs, ara-CTP accumulation decreased in two ara-C resistant cell lines, and the efflux rate was increased in KY-Ra. These results indicate that the decreased deoxycytidine kinase activity, which resulted in a decreased ara-CTP accumulation, is one of major mechanisms of the resistance, and suggest the possibility that an increase of the outward flux of ara-C is one mechanism of resistance. These cell lines may be useful for studying the refractoriness encountered in ara-C administration.},
 pages = {119--127},
 title = {The Characterization of Highly Resistant Human Leukemic Cell Lines to 1-β-D-Arabinofuranosylcytosine},
 volume = {39},
 year = {1991}
}