By Randall Johnson, Fred Valeriote (auth.), Frederick A. Valeriote, Laurence H. Baker (eds.)
Biochemical Modulation this day defines a space of research within which the intracellular metabolism of a given anti melanoma agent is modulated (usually by way of a noncytotoxic agent or a cytotoxic agent at sufficiently low dosage to make it non cytotoxic) so one can both elevate the effectiveness of the actual agent opposed to tumor cells or reduce its cytotox icity opposed to basic cells. the foremost concentration of modulation has been the brokers 5-fluorouracil (FUra), arabinofuranosylcytosine (ara-C), methotrexate (MTX) and some alkylating brokers. the main thrust of the reports has been to extend the stream of the anticancer agent alongside the pathway liable for the formation of the cytotoxic species: for instance, FUra to FUTP or ara-C to ara-CTP. whereas more often than not the applying of study re sults to medical trials doesn't require the next exper tise of the laboratory researchers, software of biochemical modulatory schemes to medical protocols necessitate a dramatic holiday with the earlier systems. As proven within the laboratory scientific loop under, shut collaboration among the laboratory and scientific investigator is key. whereas the laboratory REDEFINE expertise, checks OR QUESTIONS FOR extra healing enhance medical EXPERIMENTAL PROTOCOL (LABORATORY) study stories outline AND try out acceptable clinical PARAMETERS effects outline rationally-based regimens, it truly is crucial that the medical protocols comprise the requirement that medical fabric (either tumor or common tissues) be sampled to discourage mine no matter if the biochemical modulation being proposed is in truth beinq accomplished.
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Additional info for Biochemical Modulation of Anticancer Agents: Experimental and Clinical Approaches: Proceedings of the 18th Annual Detroit Cancer Symposium Detroit, Michigan, USA — June 13–14, 1986
These results suggest that inhibition of dUMP synthesis might be a worthwhile approach toward modulating the activity of FU. The second step in the formation of the ternary complex is the reaction of MTHF with TS-FdUMP (equation 3), and therefore the k on depends on the concentration of MTHF, according to the following equation (28): 34 k2 [MTHF] ( 6) This equation predicts a hyperbolic function with two limiting conditions. When the term k3 [MTHF] is small compared to kl' the k on of ternary complex formation will be linear with MTHF concentration.
Pharmacol. 31:2929-2935, 1982. Moran RG, Werkheiser WC, Zakrzewski SF: Folate metabolism in mammalian cells in culture. I. Partial characterization of the folate derivatives present in L1210 mouse leukemia cells. J. BioI. Chem. 251:3569-3575, 1976. Houghton JA, Houghton PJ: On the mechanism of cytotoxicity of fluorinated pyrimidines on four human colon adenocarcinoma xenografts maintained in immune-deprived mice. Cancer 45:1159-1167, 1980. 42 39. 40. yin MB, Zakrzewski SF, Hakala MT: Relationship of cellular folate cofactor pools to activity of 5-FU.
The idea was that if the uracil analog were also preferentially taken up by tumors, selective toxicity toward tumors might be achieved. The modification that was chosen was to SUbstitute one of the hydrogens of uracil with a fluorine atom because of the similarity in size between hydrogen and fluorine. On this basis, Heidelberger predicted that FU would be incorporated into RNA as an analog of uracil, but would not be incorporated into DNA (5). Instead, FU was expected to inhibit DNA synthesis because the exceptional stability of carbon-fluorine bond would 24 prevent the methylation of compound at the C-5 position, thereby allowing it to act as an inhibitor of the biosynthesis of thymine for DNA (5).