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anti-Rat (Rattus) DPYD Antikörper:
anti-Mouse (Murine) DPYD Antikörper:
anti-Human DPYD Antikörper:
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Human Monoclonal DPYD Primary Antibody für IF, ELISA - ABIN560640
Kuilenburg, Meijer, Tanck, Dobritzsch, Zoetekouw, Dekkers, Roelofsen, Meinsma, Wymenga, Kulik, Büchel, Hennekam, Largiadèr: Phenotypic and clinical implications of variants in the dihydropyrimidine dehydrogenase gene. in Biochimica et biophysica acta 2016
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.
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 (zeige EGFR Antikörper) cascade and Sp1 (zeige PSG1 Antikörper) and DPD expressions in EGFR (zeige EGFR Antikörper) mutant non-small-cell lung cancer cell lines. EGF (zeige EGF Antikörper)-induced Sp1 (zeige PSG1 Antikörper) 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 (zeige TYMS Antikörper) deficiency was an independent risk factor for shorter progression-free survival.
ERCC1 (zeige ERCC1 Antikörper)-SNP in combination with mRNA ERCC1 (zeige ERCC1 Antikörper), DPYD, and ERBB2 (zeige ERBB2 Antikörper) 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.
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