2004
DOI: 10.1007/s00280-004-0844-8 View full text |Buy / Rent full text
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Abstract: OSI-7836 (4'-thio-beta-D-arabinofuranosylcytosine) is a novel nucleoside analog in phase I clinical development for the treatment of cancer. As with other nucleoside analogs, the proposed mechanism of action involves phosphorylation to the triphosphate form followed by incorporation into cellular DNA, leading to cell death. This hypothesis has been examined by measuring and comparing the incorporation of ara-C, OSI-7836, and gemcitabine (dFdC) into DNA of cultured cells and by investigating the role of deoxycy… Show more

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“…T-araC has also demonstrated better activity than gemcitabine against various human tumor xenografts in mice. Although the basic mechanism of action of T-araC is similar to that of araC (both compounds are phosphorylated to their respective triphosphates (T-araCTP or araCTP) and inhibit DNA synthesis), there are several quantitative differences in the metabolism and biochemical activity of these two compounds that can explain their differences in antitumor activity. Most importantly, the half-life of T-araCTP in solid tumor cells is approximately 10 times longer than that of araCTP, and T-araCTP is a much more potent inhibitor of DNA synthesis than is araCTP .…”
Section: New Compoundsmentioning
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“…T-araC has also demonstrated better activity than gemcitabine against various human tumor xenografts in mice. Although the basic mechanism of action of T-araC is similar to that of araC (both compounds are phosphorylated to their respective triphosphates (T-araCTP or araCTP) and inhibit DNA synthesis), there are several quantitative differences in the metabolism and biochemical activity of these two compounds that can explain their differences in antitumor activity. Most importantly, the half-life of T-araCTP in solid tumor cells is approximately 10 times longer than that of araCTP, and T-araCTP is a much more potent inhibitor of DNA synthesis than is araCTP .…”
Section: New Compoundsmentioning
“…TaraC was a better substrate for nuclear DNA polymerase ␣ and ␦ than either araC or gemcitabine, and its incorporation into DNA resulted in strong chain termination in comparison with that of araC and gemcitabine, which resulted in minimal termination (Richardson et al, 2004). In recent studies in which mice bearing human lung cancer xenografts (Calu-6, A549) were treated with graded doses of TaraC, TaraC was incorporated into internal nucleotide linkages in a manner that was dose-and time-dependent, leading to the conclusion that DNA synthesis may play a role in TaraC cytotoxicity (Richardson et al, 2005).…”
mentioning
“…The mechanism of TaraC cytotoxicity differs from that of either cytarabine or gemcitabine. Although TaraC cytotoxicity is dependent upon DNA synthesis [189], in comparison with cytarabine and gemcitabine, TaraCTP is a better substrate for nuclear DNA polymerase α and δ, and its incorporation into DNA results in stronger chain termination than araCTP and dFdCTP [190].…”
Section: Pyrimidine Nucleoside Drugsmentioning