Objective: To investigate the correlation of peripheral DPYD gene polymorphism with 5-fluorouracil (5-FU) susceptibility and side effect in patients with colon cancer.
Methods: The total DNA of peripheral mononuclear cells was extracted in 100 cases of colon cancer patients. Quantitative PCR was conducted to measure DPYD gene 14G1A, A1627G, T85C 3 loci polymorphism, and analyze the correlation of 5-FU susceptibility, side effects with DPYD gene polymorphism.
Results: Mutations were detected at position 14G1A (mutation rate 14%), A1627G (mutation rate 11%), and T85C (mutation rate 17%). The effective rate of 3 loci of wild type was significantly higher than that of mutant type (P < 0.05). With respect to side effects such as myelosuppression, hand-foot syndrome, diarrhea, and gastrointestinal reactions, the incidence in mutation type was significantly higher than that in the wild type (P < 0.05).
Conclusion: DPYD gene polymorphism plays a guiding role in predicting efficacy and toxicity of 5-FU, which can be used as an important reference index of 5-FU individualized administration scheme.
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Pharmaceutics
December 2024
Personalized Medicine and Mental Health Unit, University Institute for Bio-Sanitary Research of Extremadura, 06080 Badajoz, Spain.
Genetic polymorphism of the dihydropyrimidine dehydrogenase gene () is responsible for the variability found in the metabolism of fluoropyrimidines such as 5-fluorouracil (5-FU), capecitabine, or tegafur. The genotype is linked to variability in enzyme activity, 5-FU elimination, and toxicity. Approximately 10-40% of patients treated with fluoropyrimidines develop severe toxicity.
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Jiangsu Key Laboratory of Marine Pharmaceutical Compound Screening, College of Pharmacy, Jiangsu Ocean University, Lianyungang, 222005, China. Electronic address:
Colorectal cancer (CRC) is a fatal cancer prevalent worldwide, and epithelial-mesenchymal transition (EMT) is a key factor in tumor invasion and metastasis. Piperine, a natural alkaloid known for its antitumor properties, faces limitations in clinical use due to its moderate potency. To address this, our team synthesized and validated a new derivative, HJJ_3_5, which has shown potent antitumor activity against CRC cells.
View Article and Find Full Text PDFWorld J Gastrointest Oncol
January 2025
Department of Clinical Medicine and Surgery, University of Naples Federico II, Naples 80131, Campania, Italy.
Background: Fluoropyrimidines are metabolized in the liver by the enzyme dihydropyrimidine dehydrogenase (DPD), encoded by the gene. About 7% of the European population is a carrier of gene polymorphisms associated with reduced DPD enzyme activity.
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Front Cell Dev Biol
December 2024
Department of Medical Oncology, The First Affiliated Hospital of Anhui Medical University, Hefei, China.
Aim: This study aims to compare the efficiencies and toxicities of pegylated liposomal doxorubicin (PLD) based and epirubicin based chemotherapeutic regimens as neoadjuvant chemotherapy (NAC) for early breast cancer.
Patients And Methods: We retrospectively analyzed 391 patients with stage II-III breast cancer who received NAC in multiple centers. The efficiencies and toxicities of PLD and epirubicin based NAC regimens were compared by using both propensity-score matched (PSM) and unmatched data.
Cancer Chemother Pharmacol
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Service de Génomique des Tumeurs et Pharmacologie, Hôpital Saint-Louis, Assistance Publique Hôpitaux de Paris, Paris, France.
The enzyme dihydropyrimidine dehydrogenase (DPD) is the primary catabolic pathway of fluoropyrimidines including 5 fluorouracil (5FU) and capecitabine. Cases of lethal toxicity have been reported in cancer patients with complete DPD deficiency receiving standard dose of 5FU or capecitabine. DPD is encoded by the pharmacogene DPYD in which more than 200 variants have been identified.
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