dihydropyrimidine dehydrogenase

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di·hy·dro·py·rim·i·dine de·hy·dro·gen·ase

(dī-hī'drō-pī-rim'ĭ-dēn dē-hī'drō-jen-ās'), [MIM*274270]
An enzyme in pyrimidine biosynthesis that reacts 5,6-dihydrouracil with NADP+ to form uracil and NADPH; it also acts on dihydrothymine; a deficiency of this enzyme can result in hyperuracil thyminuria.
References in periodicals archive ?
Thymidylate synthase and dihydropyrimidine dehydrogenase are related to histological effects of 5-fluorouracil and cisplatin neoadjuvant chemotherapy for primary gastric cancer patients.
Importance of dihydropyrimidine dehydrogenase (DPD) deficiency in patients exhibiting toxicity following treatment with 5-fluorouracil.
Patients with a dihydropyrimidine dehydrogenase deficiency had concentrations of the pyrimidine de novo metabolites that were within reference values.
Dihydropyrimidine dehydrogenase pharmacogenetics in Caucasian subjects.
Eniluracil, an oral dihydropyrimidine dehydrogenase (DPD) inhibitor, is being developed to improve the tolerability and effectiveness of 5-fluorouracil (5-FU), one of the most widely used oncology drugs in the world.
Dihydropyrimidine dehydrogenase (DPYD) is the initial and rate-limiting enzyme in the metabolism of the chemotherapeutic drug 5-fluorouracil (5-FU), thus affecting its pharmacokinetics, efficacy, and toxicity (1).
Catabolism of the pyrimidine bases thymine and uracil consists of three consecutive steps: (a) thymine and uracil are catabolized by dihydropyrimidine dehydrogenase (DPD; EC 1.
Quantitation of dihydropyrimidine dehydrogenase expression by real-time reverse transcription polymerase chain reaction.
The human dihydropyrimidine dehydrogenase gene (DPYD) encodes dihydropyrimidine dehydrogenase (DPD; EC 1.
Correlation between dihydropyrimidine dehydrogenase activity in peripheral mononuclear cells and systemic clearance of fluorouracil in cancer patients.
Therefore, eniluracil not only irreversibly inhibits the enzyme dihydropyrimidine dehydrogenase (DPD) which breaks down 5-fluorouracil (5-FU), it can also reversibly inhibit the activation of 5-FU, thereby limiting the effectiveness of 5-FU as an anti-cancer agent when not dosed properly.

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