ArticleCancer management and research2026
A Pharmacogenomic Basis for Tolerance of 5-Fluorouracil Following Early, Severe Toxicity from Capecitabine in a CDA Ultrarapid Metabolizer Colon Cancer Patient: A Case Report.
Article in Cancer management and research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Capecitabine is an oral prodrug that is converted to 5-FU via three enzyme-catalysed steps: carboxylesterase (CES), cytidine deaminase (CDA), and thymidine phosphorylase (TYMS). Approximately 80-90% of 5-FU, whether from capecitabine or direct administration, is quickly inactivated by dihydropyrimidine dehydrogenase (DPD), encoded by DPYD. Preemptive testing for four pathogenic DPYD variants that reduce DPD activity is advised; however, currently, no evidence for CES, CDA, or TYMS has necessitated a similar recommendation despite polymorphisms in these genes potentially causing treatment toxicity. The current preemptive testing guidelines for 5-FU and capecitabine are similar. Case Presentation: A 74-year-old black woman with a caecal adenocarcinoma diagnosis of pT Conclusion: This case shows that the severe adverse effects of capecitabine therapy in a patient with a CDA ultrametabolizer profile can be successfully switched to 5-FU-based therapy at a normal dose and tolerate this alternative fluoropyrimidine.
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