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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.
Data suggest that both common and rare DPYD variants may be associated with toxicity to fluoropyrimidine-based chemotherapy in colorectal cancer patients.
Phenotypic and clinical implications of variants in the dihydropyrimidine dehydrogenase gene.
DPYD*2A and MTHFR C677T polymorphisms could explain 5-FU toxicity or clinical outcome in Bangladeshi colorectal patients
This study reports novel and rare genetic variants underlying DPD deficiency in 9 cancer patients presenting with severe fluoropyrimidine-associated toxicity.
TYMS 2R3R polymorphism and the -[IVS]14+1G>A mutation in DPYD was not associated with susceptibility to CRC. However, the 2R/2R and 2R/3R genotypes of TYMS polymorphism could significantly contribute to hematological and gastric toxicity in CRC patients in this sample populatio
Results still showed UGT1A1*6 and UGT1A1*28 to be partially associated with irinotecan-induced toxicity and clinical response. An examination of more UGT1A loci, except for UGT1A1*6 and UGT1A1*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 cascade and Sp1 and DPD expressions in EGFR mutant non-small-cell lung cancer cell lines. EGF-induced Sp1 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 deficiency was an independent risk factor for shorter progression-free survival.
ERCC1-SNP in combination with mRNA ERCC1, DPYD, and ERBB2 from pretherapeutic endoscopic biopsies can predict minor response to chemoradiation, as a basis for individualized therapy of advanced esophageal cancer.
this study was to identify potential risk variants in DPYP gene in an understudied East African population as predictors of severe adverse toxicity to 5-FU
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)
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