DHFR 19-bp insertion/deletion polymorphism and MTHFR C677T in adult acute lymphoblastic leukaemia: Is the risk reduction due to intracellular folate unbalancing?

Donato Gemmati, Monica De Mattei, Linda Catozzi, Matteo Della Porta, Maria L. Serino, Cristina Ambrosio, Antonio Cuneo, Simonetta Friso, Mauro Krampera, Elisa Orioli, Giulia Zeri, Alessia Ongaro

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Abstract

Folate and its derivatives are pivotal for cell cycle and proliferation. They facilitate the crosstalk between DNA synthesis and methylation crucial processes in cancer establishment [1]. Dietary folate or supplements (e.g., folic acid) must be fully reduced by dihydrofolate reductase (DHFR) before entering cell metabolism [1]. DHFR is responsible for dihydrofolate (DHF) to tetrahydrofolate (THF) conversion, as well as for assisting the generation of additional partially reduced folates (i.e., methylene-THF and formyl-THF), which are then transformed into the fully active folate (i.e., methyl-THF) with the help of methylenetetrahydrofolate reductase (MTHFR). As the main folate isoforms involved in DNA synthesis and methylation are handled by these two key enzymes, alterations in DHFR and/or in MTHFR functions may have detrimental effects on DNA stability and cancer susceptibility [2-5].

Original languageEnglish
Pages (from-to)526-529
Number of pages4
JournalAmerican Journal of Hematology
Volume84
Issue number8
DOIs
Publication statusPublished - Aug 2009

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ASJC Scopus subject areas

  • Hematology

Cite this

Gemmati, D., De Mattei, M., Catozzi, L., Della Porta, M., Serino, M. L., Ambrosio, C., Cuneo, A., Friso, S., Krampera, M., Orioli, E., Zeri, G., & Ongaro, A. (2009). DHFR 19-bp insertion/deletion polymorphism and MTHFR C677T in adult acute lymphoblastic leukaemia: Is the risk reduction due to intracellular folate unbalancing? American Journal of Hematology, 84(8), 526-529. https://doi.org/10.1002/ajh.21451