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The protein encoded by DPYD is a pyrimidine catabolic enzyme and the initial and rate-limiting factor in the pathway of uracil and thymidine catabolism. Additionally we are shipping DPYD Kits (36) and DPYD Proteins (7) and many more products for this protein.
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Fourteen out of 275 cancer patients (5.1%) carried a DPYD variant and received a 25-50% dose reduction recommendation for 5-fluorouracil or capecitabine. None of the patients with a DPYD variant treated with a reduced dose developed toxicities.
findings showed that almost 57.1% of Chinese colorectal cancer patients had at least one variant of DPYD*5A and DPYD*9A
High levels of intratumoral DPD expression have a negative impact on sensitivity to 5-fluorouracil in gastric cancer patients, but no prognostic value for long-term survival was uncovered. (Meta-analysis)
Reprot strong functional effect of a DPYD haplotype upon a phenotypic marker of individual 5-FU metabolism to improve toxicity prediction.
we believe that developing functional testing at the bedside could probably help to better picture the actual DPD status of patients scheduled for fluorouracil-based therapy, so as to propose subsequent appropriate adaptive dosing strategies.
DPYD genotyping for alleles 7, *2A, *13 and Y186C was not helpful in the identification of patients with severe DPD deficiency in this series of patients
Our results revealed that the C allele of the DPYD 85T > C polymorphism might be associated with susceptibility to pediatric acute lymphoblastic leukemia
Increases in gene expression levels of TYMP (show TYMP Antibodies), DPYD, and HIF1A (show HIF1A Antibodies) in tumor tissues at 7 days after the start of CRT (show SLC6A8 Antibodies) may be useful for predicting the efficacy of CRT (show SLC6A8 Antibodies) including S-1 or UFT
There were not statistical significant differences between carriers of KRAS mutated alleles between SD and PD groups. No significant difference was found between response rates and toxicity and DPD or UGT1A1 (show UGT1A1 Antibodies) genotypes. Our results suggested that determination of DPD or UGT1A1 (show UGT1A1 Antibodies) genotypes could not be useful for predicting severe toxicity of irinotecan in our population.
Study shows that somatic mutations of DPYD cause a switch in pyrimidine metabolism and promote gene expression of pyrimidine enzymes toward malignant progression.
DPD gene expression is regulated first at the mRNA level when the hepatocytes enter the cell cycle. There is little regulation at the translational level. Cell proliferation rate is influences the enzyme activity modification.
Data show that dihydropyrimidine dehydrogenase residue H673 is required for active site closure, while S670 is important for substrate recognition.
The protein encoded by this gene is a pyrimidine catabolic enzyme and the initial and rate-limiting factor in the pathway of uracil and thymidine catabolism. Mutations in this gene result in dihydropyrimidine dehydrogenase deficiency, an error in pyrimidine metabolism associated with thymine-uraciluria and an increased risk of toxicity in cancer patients receiving 5-fluorouracil chemotherapy. Two transcript variants encoding different isoforms have been found for this gene.
, dihydropyrimidine dehydrogenase [NADP(+)]
, dihydrothymine dehydrogenase
, dihydrouracil dehydrogenase
, dihydropyrimidine dehydrogenase