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*6 rs1801160 and *2A rs3918290 DPYD variant alleles were significantly associated with time to neutropenia in colon cancer.
Results have shown crosstalk among the EGFR (show EGFR Proteins) cascade and Sp1 (show PSG1 Proteins) and DPD expressions in EGFR (show EGFR Proteins) mutant non-small-cell lung cancer cell lines. EGF (show EGF Proteins)-induced Sp1 (show PSG1 Proteins) up-regulation resulted in both DPYD mRNA and DPD protein expressions.
Carriers of the rare allelic variants DPYD*2A, DPYD*13, and DPYD D949V are more likely to experience severe adverse reactions during fluoropyrimidine-based therapy.
Exploring an extended set of deleterious DPYD variants improves the performance of DPYD genotyping for predicting both grade 3-4 and grade 4 toxicities (digestive and/or neurologic and/or hematotoxicities) related to capecitabine, as compared to conventional genotyping restricted to consensual variants *2A, *13 and D949V
Combined expression analyses of hENT1, TS, and DPD may predict long-term outcomes in patients with borderline resectable pancreatic cancer after neoadjuvant chemoradiotherapy
We demonstrated that real-time DPYD genotyping using TaqMan probes is cost effective in all fluoropyrimidine-based treatments
In pancreatic neuroendocrine neoplasms, biochemical response (p = 0.005) and high dihydropyrimidine-dehydrogenase expression (p = 0.018) were predictive markers of response to 5-FU-based chemotherapy. Thymidylate-Synthase (show TYMS Proteins) deficiency was an independent risk factor for shorter progression-free survival.
ERCC1 (show ERCC1 Proteins)-SNP in combination with mRNA ERCC1 (show ERCC1 Proteins), DPYD, and ERBB2 (show ERBB2 Proteins) from pretherapeutic endoscopic biopsies can predict minor response to chemoradiation, as a basis for individualized therapy of advanced esophageal cancer.
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
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