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To date, different mutations have been reported that result in a complete deficiency, including: two deletions (295¨C298delTCAT and 1897delC), one splice-site mutation (IVS14+IG>A), four missense mutations (85T>C, 703C>T, 2657G>A, and 2983 G>T), a deletion of two nucleotides (1039¨C1040delTG), and the point mutations P86L, S201R, S492L, D949V and H978R [13]. The 85T>C mutation might be a common polymorphism, although functional analysis of a recombinantly expressed human protein carrying the 85T>C mutation showed no significant residual mutant enzyme activity [10,14]. An in-depth discussion of the clinical import of DPD can be found in a number of review articles, and two examples are provided in Refs. [37,38], which discuss the role of DPD in cancer therapy with 5FU |
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