Potential of dihydropyrimidine dehydrogenase genotypes in personalizing 5-fluorouracil therapy among colorectal cancer patients

Teh LK 1 , Hamzah S , Hashim H , Bannur Z , Zakaria ZA , Hasbullani Z Show all authors , Shia JK , Fijeraid H , Md Nor A , Zailani M , Ramasamy P , Ngow H , Sood S , Salleh MZ

Affiliations 

  • 1 *Pharmacogenomics Centre, Faculty of Pharmacy, Universiti Teknologi MARA; †Department of Biomedical Science, Faculty of Medicine and Health Sciences, University Putra Malaysia, Selangor, Malaysia; ‡Department of Surgery, Kulliyah of Medicine, International Islamic University Malaysia, Kuantan, Malaysia; and §Department of Surgery, Faculty of Medicine, Universiti Teknologi MARA, Selangor, Malaysia
Ther Drug Monit, 2013 Oct;35(5):624-30.
PMID: 23942539 DOI: 10.1097/FTD.0b013e318290acd2

Abstract

Dihydropyrimidine dehydrogenase (DPD) is a pyrimidine catabolic enzyme involved in the initial and rate-limiting step of the catabolic pathway of toxic metabolites of 5-fluorouracil (5-FU). Several studies have reported that deficiency of DPD and polymorphisms of its gene are related to 5-FU toxicities and death. Association between serum concentration of 5-FU and its related toxicity has also been previously demonstrated. Hence, this study aims to understand the role of DPYD variants in serum level of 5-FU and the risk of developing toxicity to prevent adverse reactions and maximize therapy outcome for personalized medicine.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.

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