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. 2019 Jul 22;18(3):3115–3127. doi: 10.3892/ol.2019.10650

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Copyright: © Organista-Nava et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 4. — Model of the possible role of folate pathway gene expression levels involved in the transport and metabolism of MTX in patients with AL with relapse. The decreased levels of RFC1 could favor inhibition of MTX internalization into the cell, while the increase in GGH levels favors MTX depolyglutamation, preventing MTX from exerting its activity, which also affects the levels of ATIC and TS (overexpression). Moreover, high expression levels of ABCB1 and ABCC1 cause the efflux of MTX from the cell. All of these processes favor cell proliferation and survival. RFC1, reduced folate carrier; GGH, γ-glutamyl hydrolase; FPGS, folylpolyglutamate synthetase; TS, thymidylate synthase; ATIC, 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase; MTHFR, methylenetetrahydrofolate reductase; MTHFD1, methylenetetrahydrofolate dehydrogenase 1; MTRR, 5-methyltetrahydrofolate-homocysteine methyltransferase reductase; MS, methionine synthase; ABCB1, ATP-binding cassette subfamily B member 1; ABCC1, ATP-binding cassette subfamily C member 1.