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• W2040301739 abstract "Folate antagonists have over the last 30 years become increasingly important in the treatment of human cancer ( 18). However, only one of these agents, Methotrexate (MTX), can be considered as established in clinical use. Its use in chemotherapy of solid tumors and in maintenance therapy of lymphoblastic leukemia is widespread (12). MTX mediates its cytotoxic effects through the inhibition of dihydrofolate reductase (DHFR), an enzyme which catalyzes the reduction of dihydrofolic acid to tetrahydrofolic acid. The inhibition of DHFR results in a depletion of reduced folate cofactors. These substances participate as C,-carriers in de novo purine and amino acid synthesis and in the conversion of deoxyuridinemonophosphate to deoxythymidinemonophosphate, the latter reaction being catalyzed by thymidilate synthetase (TS) ( 14). The effectiveness of MTX is often limited by development of acquired resistance. The most common mechanisms of resistance described are defect in membrane transport of the drug and overproduction of DHFR, the target enzyme of MTX (7, 10, 15, 17). Since a number ofantifolate compounds have recently been developed, it is important to determine to which extent such new substances are cross-resistant to tumors resistant to MTX. CB3717 (8), a quinazoline analog of folic acid, acts as an inhibitor of both TS and DHFR. Metoprine (4), a lipophilic diaminopyrimidine, is an inhibitor of DHFR. Cellular uptake of Metoprine is not mediated by the same carrier system as MTX and reduced folates. Because of this Metoprine may be active against tumors which became resistant to MTX due to a deficient transport system. Trimetrexate (l), a tight-binding lipophilic quinazoline inhibitor of DHFR also enters the cell by a mechanism different from the uptake system for MTX. Homofolate (3, 9), an analog of folic acid, which requires metabolic activation through reduction by DHFR, may have an increased activity against MTX-resistant tumor cells with an elevated amount of DHFR. In an attempt to determine the potential value of new non-classical antifolates in overcoming acquired MTX resistance, we tested the antifolates CB3717, Metoprine," @default.
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• W2040301739 date "1984-03-01" @default.
• W2040301739 modified "2023-09-27" @default.
• W2040301739 title "Resistance of human tumor cell lines to antifolates" @default.
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• W2040301739 doi "https://doi.org/10.1016/0305-7372(84)90041-0" @default.
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