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• W2141878889 abstract "The identification of genetic factors associated with either responsiveness or resistance to 5-fluorouracil (5-FU) chemotherapy, as well as genetic factors predisposing patients to the development of severe 5-FU-associated toxicity, is increasingly being recognised as an important field of study. Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Although the role of tumoral levels as a prognostic factor for clinical responsiviness has not been firmly established, there is ample evidence that a deficiency of DPD is associated with severe toxicity after the administration of 5-FU. Patients with a partial DPD deficiency have an increased risk of developing grade IV neutropenia. In addition, the onset of toxicity occurred twice as fast compared with patients with a normal DPD activity. To date, 39 different mutations and polymorphisms have been identified in DPYD. The IVS14+1G>A mutation proved to be the most common one and was detected in 24–28% of all patients suffering from severe 5-FU toxicity. Thus, a deficiency of DPD appears to be an important pharmacogenetic syndrome." @default.
• W2141878889 created "2016-06-24" @default.
• W2141878889 creator A5072840045 @default.
• W2141878889 date "2004-05-01" @default.
• W2141878889 modified "2023-10-02" @default.
• W2141878889 title "Dihydropyrimidine dehydrogenase and the efficacy and toxicity of 5-fluorouracil" @default.
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• W2141878889 doi "https://doi.org/10.1016/j.ejca.2003.12.004" @default.
• W2141878889 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15093568" @default.
• W2141878889 hasPublicationYear "2004" @default.
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