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Pretreatment of L5178Y murine leukemia cells with uracil arabinoside (ara-U) enhances the cytotoxicity of cytosine arabinoside (ara-C). This effect is mediated by the cytostatic effect of ara-U, which causes a delay of cell progression through S-phase. Consequently, the specific activity of enzymes that peak during S-phase increases, and deoxycytidine kinase increases 3.6-fold over untreated controls. This allows enhanced anabolism of ara-C to nucleotides, as well as increased incorporation into DNA with ultimate synergistic cytotoxicity. It is postulated that the systemic metabolism of high-dose ara-C to sustained high levels of ara-U in patients with acute leukemia may enhance the activity of subsequent doses of ara-C, and thus contribute to a means for pharmacologic self-potentiation, contributing to the unique therapeutic activity of high-dose ara-C.
J L Yang, and
E H Cheng, and
R L Capizzi, and
Y C Cheng, and
T Kute
May 1968,
Biochemical pharmacology,
J L Yang, and
E H Cheng, and
R L Capizzi, and
Y C Cheng, and
T Kute
July 1968,
Biochimica et biophysica acta,
J L Yang, and
E H Cheng, and
R L Capizzi, and
Y C Cheng, and
T Kute
January 1995,
Acta poloniae pharmaceutica,
J L Yang, and
E H Cheng, and
R L Capizzi, and
Y C Cheng, and
T Kute
June 1973,
Biochemical and biophysical research communications,
J L Yang, and
E H Cheng, and
R L Capizzi, and
Y C Cheng, and
T Kute
January 1990,
Cancer chemotherapy and pharmacology,
J L Yang, and
E H Cheng, and
R L Capizzi, and
Y C Cheng, and
T Kute
October 1988,
Cancer research,
J L Yang, and
E H Cheng, and
R L Capizzi, and
Y C Cheng, and
T Kute
June 1985,
Seminars in oncology,
J L Yang, and
E H Cheng, and
R L Capizzi, and
Y C Cheng, and
T Kute
June 1989,
Clinical chemistry,
J L Yang, and
E H Cheng, and
R L Capizzi, and
Y C Cheng, and
T Kute
January 1974,
Bulletin du cancer,
J L Yang, and
E H Cheng, and
R L Capizzi, and
Y C Cheng, and
T Kute
January 1987,
Cancer investigation,
