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首页> 外文期刊>The EPMA journal. >Dihydropyrimidine dehydrogenase polymorphisms and fluoropyrimidine toxicity: ready for routine clinical application within personalized medicine?
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Dihydropyrimidine dehydrogenase polymorphisms and fluoropyrimidine toxicity: ready for routine clinical application within personalized medicine?

机译：二氢嘧啶脱氢酶的多态性和氟嘧啶毒性：准备用于个性化药物的常规临床应用吗？

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Fluoropyrimidines, including 5-fluorouracil (5-FU), are widely used in the treatment of solid tumors and remain the backbone of many combination regimens. Despite their clinical benefit, fluoropyrimidines are associated with gastrointestinal and hematologic toxicities, which often lead to treatment discontinuation. 5-FU undergoes complex metabolism, dihydropyrimidine dehydrogenase (DPD) being the rate-limiting enzyme of inactivation of 5-FU and its prodrugs. Several studies have demonstrated significant associations between severe toxicities by fluoropyrimidines and germline polymorphisms of DPD gene. To date, more than 30 SNPs and deletions have been identified within DPD, the majority of these variants having no functional consequences on enzymatic activity. However, the identification of deficient DPD genotypes may help identify poor-metabolizer patients at risk of developing potentially life-threatening toxicities after standard doses of fluoropyrimidines.
机译：氟嘧啶类药物，包括5-氟尿嘧啶（5-FU），广泛用于治疗实体瘤，并且仍然是许多联合治疗方案的骨干。尽管它们具有临床益处，但氟嘧啶与胃肠道和血液学毒性有关，常常导致治疗中断。 5-FU经历复杂的代谢，二氢嘧啶脱氢酶（DPD）是5-FU及其前药失活的限速酶。数项研究表明，氟嘧啶的严重毒性与DPD基因的种系多态性之间存在显着关联。迄今为止，已在DPD中鉴定出30多个SNP和缺失，这些变体中的大多数对酶活性没有功能性影响。但是，鉴定缺陷型DPD基因型可能有助于鉴定代谢不良的患者，这些患者在标准剂量的氟嘧啶后有发展潜在威胁生命的毒性的风险。

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