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Data show that dihydropyrimidine dehydrogenase residue H673 is required for active site closure, while S670 is important for substrate recognition.
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.
Results still showed UGT1A1 (show UGT1A1 Proteins)*6 and UGT1A1 (show UGT1A1 Proteins)*28 to be partially associated with irinotecan-induced toxicity and clinical response. An examination of more UGT1A (show UGT1A1 Proteins) loci, except for UGT1A1 (show UGT1A1 Proteins)*6 and UGT1A1 (show UGT1A1 Proteins)*28, was not helpful to improve the predictive value of irinotecan-based toxicity and efficacy. An examination of DPYD*5 assisted in the prediction of severe diarrhea.
The present study suggests that the SNP rs1801160 and the "IISt" haplotype in the DPYD gene may also have a role in colorectal cancer risk.
Low DPYD expression is associated with colorectal cancer.
*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.
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