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Data suggest that both common and rare DPYD variants may be associated with toxicity to fluoropyrimidine-based chemotherapy in colorectal cancer patients.
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Phenotypic and clinical implications of variants in the dihydropyrimidine dehydrogenase gene.
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DPYD*2A and MTHFR C677T polymorphisms could explain 5-FU toxicity or clinical outcome in Bangladeshi colorectal patients
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This study reports novel and rare genetic variants underlying DPD deficiency in 9 cancer patients presenting with severe fluoropyrimidine-associated toxicity.
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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
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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.
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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.
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Low DPYD expression is associated with colorectal cancer.
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*6 rs1801160 and *2A rs3918290 DPYD variant alleles were significantly associated with time to neutropenia in colon cancer.
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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.
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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.
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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
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Combined expression analyses of hENT1, TS, and DPD may predict long-term outcomes in patients with borderline resectable pancreatic cancer after neoadjuvant chemoradiotherapy
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We demonstrated that real-time DPYD genotyping using TaqMan probes is cost effective in all fluoropyrimidine-based treatments
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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.
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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.
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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
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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.
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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
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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)
