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- W3107795979 abstract "5-fluorouracil (5-FU) is still the backbone in some cancer treatments particularly in digestive cancers. The drug is associated with potential severe adverse events leading in some cases to substantial morbidity and mortality. As the drug is essentially catabolized through an enzymatic process mediated by dihydropyrimidine deshydrogenase (DPD), DPD deficiency is thought to be the main mechanism leading to 5-FU accumulation and toxicity [ [1] Goirand F. Lemaitre F. Launay M. Tron C. Chatelut E. Boyer J.-.C. et al. How can we best monitor 5-FU administration to maximize benefit to risk ratio?. Expert Opin Drug Metab Toxicol. 2018; 14: 1303-1313https://doi.org/10.1080/17425255.2018.1550484 Crossref PubMed Scopus (19) Google Scholar ]. Identifying patients with DPD deficiency and notably patients with complete deficiency, is then a relevant approach to limit the risk of severe adverse event. Recently, the European Agency for Medicine has therefore recommended DPD deficiency screening prior a treatment with fluorouracil or one of these derivatives [ [2] European Medicine Agency. EMA recommendations on DPD testing prior to treatment with fluorouracil, capecitabine, tegafur and flucytosine. 2020. Google Scholar ]." @default.
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- W3107795979 date "2021-02-01" @default.
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- W3107795979 title "When helping the minority of patients may hurt the majority: The case for DPD phenotyping and 5-fluorouracil therapeutic drug monitoring." @default.
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- W3107795979 doi "https://doi.org/10.1016/j.dld.2020.11.004" @default.
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