2005
DOI: 10.1007/s00280-005-0126-0 View full text |Buy / Rent full text
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Abstract: 4'-Thio-arabinofuranosylcytosine (T-araC) is a new cytosine analog, which exhibits excellent antitumor activity against various solid tumor xenografts in mice. T-araC is a structural analog of arabinofuranosylcytosine (araC), which is known to be marginally active against solid tumors. We have continued to study the biochemical pharmacology of T-araC in solid tumor cells to further characterize the mechanism of action of this new agent and to elucidate why these compounds show a profound difference in antitumo… Show more

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“…In a previous report, we showed that T-ara-C is a poorer substrate than ara-C for deoxycytidine kinase, and as a result, at equimolar concentrations, less T-ara-C monophosphate is formed versus ara-C monophosphate (62). However, we have also recently reported that the half-life of T-ara-C triphosphate was 10-fold over that of ara-C triphosphate in HCT 116 cells (63). It is clear from our data that after an acute treatment, T-ara-C at 10 Amol/L is more cytotoxic than ara-C at the same concentration (Fig.…”
Section: Discussionmentioning
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“…In a previous report, we showed that T-ara-C is a poorer substrate than ara-C for deoxycytidine kinase, and as a result, at equimolar concentrations, less T-ara-C monophosphate is formed versus ara-C monophosphate (62). However, we have also recently reported that the half-life of T-ara-C triphosphate was 10-fold over that of ara-C triphosphate in HCT 116 cells (63). It is clear from our data that after an acute treatment, T-ara-C at 10 Amol/L is more cytotoxic than ara-C at the same concentration (Fig.…”
Section: Discussionmentioning
“…However, treatment with T-araC (a cytotoxic 4′-thionucleoside analog with a natural cytosine base but containing a 4-thioarab-inose sugar [22]), did not demethylate the p15 CpG indicating that the 4-thio-2-deoxyribose was essential for this effect. Incorporation of T-araC into DNA is known to result in profound inhibition of DNA synthesis [36], due to its ability to cause DNA chain termination [37]. …”
Section: Resultsmentioning
“…It was shown earlier that TaraC was markedly more cytotoxic than araC when high concentrations of the compounds were given for short periods (Someya et al, 2005), presumably because of the longer intracellular half-life of TaraCTP than araCTP. Once TaraC enters cells by mediated transport, its metabolites are trapped inside, resulting in prolonged cytotoxic action; in contrast, araC cytotoxicity requires continued influx of araC because of its susceptibility to degradation.…”
Section: Discussionmentioning
“…The prolonged retention time of TaraC-5Ј-monophosphate resulting from its high rate of phosphorylation by UMP/CMP kinase has been suggested as a more important determinant for its activity against solid tumors than its resistance to cytidine and dCMP deaminase activities (Parker et al, 2000;Someya et al, 2005). Preliminary studies indicated that the mechanism of TaraC cytotoxicity differs from that of either araC or gemcitabine, a difluoro-2Ј-deoxycytidine analog with activity against solid tumors (Blajeski et al, 2002).…”
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