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Active efflux of daunorubicin and adriamycin in sensitive and resistant sublines of P388 leukemia.
There is an active outward transport mechanism for anthracyclines in P388 leukemia cells and that enhanced activity of this efflux process renders cells highly resistant to the cytostatic and cytotoxic effects of ADR and DAU.
Evaluation of antitumor activity in a human breast tumor/nude mouse model with a special emphasis on treatment dose
The results agree with the reported clinical results compared with those with MTD, suggesting the importance of the use of clinically equivalent doses in the evaluation of antitumor efficacy in a human tumor/nude mouse system.
Active efflux common to vincristine and daunorubicin in vincristine-resistant P388 leukemia.
In vivo circumvention of vincristine resistance in mice with P388 leukemia using a novel compound, AHC-52.
The results suggest that combination chemotherapy using a sensitizing agent such as AHC-52 will be effective in not only circumvention of multidrug resistance but also retardation of its occurrence.
Uptake and retention of adriamycin and daunorubicin by sensitive and anthracycline-resistant sublines of P388 leukemia.
Decreased retention of actinomycin D as the basis for cross-resistance in anthracycline-resistant sublines of P388 leukemia.
It is concluded that P388 leukemia resistant to Adriamycin and anthracycline-resistant sublines must retain appreciable concentrations of actinomycin D for several hr in order to be killed.
Induction of hepatic P-glycoprotein enhances biliary excretion of vincristine in rats.
Kinetic analysis of hepatobiliary transport of vincristine in perfused rat liver. Possible roles of P-glycoprotein in biliary excretion of vincristine.
Reduced Activity of Anabolizing Enzymes in 5‐Fluorouracil‐resistant Human Stomach Cancer Cells
- M. Inaba, J. Mitsuhashi, M. Fukushima
- BiologyJapanese journal of cancer research : Gann
- 1 February 1996
The mechanism of resistance to 5‐fluorouracil (5‐FU) was studied with NUGC‐3/5FU/L, a human stomach cancer cell line which had acquired resistance as a consequence of repeated 5‐day exposures to…
Reversal of resistance to vincristine in P388 leukemia by various polycyclic clinical drugs, with a special emphasis on quinacrine.
Quinacrine, an antimalarial drug which had the greatest effect on vincristine uptake and relatively low host toxicity, exhibited potent therapeutic synergism in combination with vINCristine in resistant leukemia-bearing mice.