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DPD gene

Raida, M., Schwabe, W., Hausler, P., et al. (2001) Prevalence of a common fwint mutation in the dihydropyrimidine dehydrogenase (DPD) gene within the 5 -splice donor site of intron 14 in patients with severe 5-fluorouracil (5-FU)-related toxicity compared with controls. Clin. Cancer Res. 7, 2832-2839. [Pg.73]

Jiang H, Lu J, Ji J. Circadian rhythm of dihydrouracil/uracil ratios in biological fluids a potential biomarker for dihydropyrimidine dehydrogenase levels. Br J Pharmacol 2004 141 616-623. van Kuilenburg AB, Haasjes J, Riehel DJ et al. Clinieal implieations of dihydropyrimidine dehydrogenase (DPD) defleieney in patients with severe 5-fluorouraeil-assoeiated toxicity identification of new mutations in the DPD gene. Clin Cancer Res 2000 6 4705 712. [Pg.259]

Sato K, Kitajima Y, Miyoshi A et al. Deficient expression of the DPD gene is caused by epigenetic modification in biliary tract cancer cells, and induces high sensitivity to 5-FU treatment. Int J Oncol... [Pg.262]

Another reason for the variation in 5-FU-related toxicity may be the detection of mutations in the DPYD gene. Most patients with 5-FU-related toxicity have multiple mutations in the DPYD gene. Flowever, only a few patients with a low DPD phenotype have a molecular basis for reduced activity. Although novel DPYD variants have been identified in studies, the DPYD mutations now described do not entirely explain polymorphic DPD activity and toxic response to 5-FU. [Pg.66]

These data emphasize the complex nature of the molecular mechanisms controlling polymorphic DPD activity in vivo. The clinical utility for genetic polymorphism testing to date is not optimal because of its low sensitivity and unknown specificity (28). Overall, it can be remarked that the splice site mutation IVS14+1G>A causes severe, even lethal, 5-FU-related toxicity. Unfortunately, the roles of other polymorphisms in the DPYD gene in the severe 5-FU-related toxicity are not clarified. [Pg.66]

Expression of selected elements of the 5-FU metabolic pathway is predictive of response to 5-FU based chemotherapy regimens. High levels of TS, TP, and DPD are independent predictors of decreased response vice versa, lower levels of TS, TP, and DPD correlate with higher sensitivity to 5-FU. High expression levels of one of these genes, even in the presence of down-regulation of the other two, has an adverse effect on response to 5-FU. [Pg.167]

DPD Impairment Implication of DPYD Gene Polymorphism and Genetic Down-Regulation Catch Me If You Can Determining DPD Status in Cancer Patients Perspectives References... [Pg.249]

The evidence for the role of DPD deficiency in capecitabine-induced toxicities has been demonstrated by some recent clinical reports (20, 29, 38), and has been finally confirmed by the first report of a toxic-death in a patient with DPYD gene polymorphism and severe enzyme deficiency treated in a capecitabine-containing protocol (28). Overall, numerous clinical reports have shown a link between the level of enzyme deficiency and the severity/lethality of the observed toxicities upon fiuoropyrimidines administration (35,39), thus warranting the need for early detection of patients at risk. [Pg.253]

DPD IMPAIRMENT IMPLICATION OF DPYD GENE POLYMORPHISM AND GENETIC DOWN-REGULATION... [Pg.253]

Genetic mutations are a major cause of DPD impairment (24,58). Polymorphism of the DPYD gene has been well characterized as an autosomal recessive disease, with 0.5% and 3%-5% of the Caucasian population being subsequently affected by total and partial deficiencies, respectively (7,59,60). Thymine uraciluria is a condition caused by inherited total DPD deficiency that can be either associated with neurological disorders or be asymptomatic (61,62,63). [Pg.253]


See other pages where DPD gene is mentioned: [Pg.291]    [Pg.305]    [Pg.73]    [Pg.163]    [Pg.163]    [Pg.257]    [Pg.80]    [Pg.2417]    [Pg.857]    [Pg.291]    [Pg.305]    [Pg.73]    [Pg.163]    [Pg.163]    [Pg.257]    [Pg.80]    [Pg.2417]    [Pg.857]    [Pg.283]    [Pg.63]    [Pg.66]    [Pg.73]    [Pg.274]    [Pg.281]    [Pg.404]    [Pg.153]    [Pg.250]    [Pg.255]    [Pg.255]    [Pg.255]    [Pg.255]    [Pg.256]    [Pg.265]    [Pg.630]    [Pg.233]    [Pg.2398]   
See also in sourсe #XX -- [ Pg.291 ]




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