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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 Antibodies (53) and DPYD Kits (35) and many more products for this protein.
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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 Proteins), DPYD, and HIF1A (show HIF1A Proteins) in tumor tissues at 7 days after the start of CRT (show SLC6A8 Proteins) may be useful for predicting the efficacy of CRT (show SLC6A8 Proteins) 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 Proteins) genotypes. Our results suggested that determination of DPD or UGT1A1 (show UGT1A1 Proteins) 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.
Results suggest that DPYD c.1129-5923 C>G/hapB3 have limited predictive value for severe toxicity to 5-FU based combination chemotherapy.
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