Dihydropyrimidinase and β-ureidopropionase gene variation and severe fluoropyrimidine-related toxicity

Pharmacogenomics. 2015;16(12):1367-77. doi: 10.2217/pgs.15.81. Epub 2015 Aug 5.

Abstract

Aims: To assess the association of DPYS and UPB1 genetic variation, encoding the catabolic enzymes downstream of dihydropyrimidine dehydrogenase, with early-onset toxicity from fluoropyrimidine-based chemotherapy.

Patients & methods: The coding and exon-flanking regions of both genes were sequenced in a discovery subset (164 patients). Candidate variants were genotyped in the full cohort of 514 patients.

Results & conclusions: Novel rare deleterious variants in DPYS (c.253C > T and c.1217G > A) were detected once each in toxicity cases and may explain the occurrence of severe toxicity in individual patients, and associations of common variants in DPYS (c.1-1T > C: p(adjusted) = 0.003; OR = 2.53; 95% CI: 1.39-4.62, and c.265-58T > C: p(adjusted) = 0.039; OR = 0.61; 95% CI: 0.38-0.97) with 5-fluorouracil toxicity were replicated.

Keywords: 5-fluorouracil; DPYS; UPB1; capecitabine; dihydropyrimidinase; fluoropyrimidine; gene variation; pharmacogenomics; toxicity; β-ureidopropionase.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Aged, 80 and over
  • Amidohydrolases / genetics*
  • Antimetabolites, Antineoplastic / adverse effects
  • Case-Control Studies
  • Drug-Related Side Effects and Adverse Reactions / genetics*
  • Exons / genetics
  • Female
  • Fluorouracil / adverse effects
  • Genetic Variation / genetics*
  • Genotype
  • Humans
  • Male
  • Middle Aged
  • Pyrimidines / adverse effects*
  • Young Adult

Substances

  • Antimetabolites, Antineoplastic
  • Pyrimidines
  • Amidohydrolases
  • beta-ureidopropionase
  • dihydropyrimidinase
  • Fluorouracil