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Clinical Chemistry 49: 707-708, 2003; 10.1373/49.4.707
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(Clinical Chemistry. 2003;49:707-708.)
© 2003 American Association for Clinical Chemistry, Inc.

Letters to the Editor

Detection of a Novel 1905C->T Mutation within the Dihydropyrimidine Dehydrogenase Gene and Potential for Misclassification with the Exon 14-skipping Mutation

Andreas Lazar1,a, Soenke Jan Weissenborn2, Dirk Gründemann1, Reinhard Berkels1, Uwe Fuhr1, Herbert Pfister2 and Edgar Schömig1

1 Department of Pharmacology and
2 Institute of Virology, University of Cologne, Gleueler Strasse 24, 50931 Cologne, Germany

aAuthor for correspondence. Fax 49-221-478-5022; e-mail andreas.lazar@medizin.uni-koeln.de.

The first 20% of the full text of this article appears below.


To the Editor:

Dihydropyrimidine dehydrogenase (DPYD) is the initial and rate-limiting enzyme in the metabolism of the chemotherapeutic drug 5-fluorouracil (5-FU), thus affecting its pharmacokinetics, efficacy, and toxicity (1). Application of 5-FU is restricted by a narrow therapeutic index because of severe toxicity of WHO grades III–IV (2). Polymorphisms within the DPYD gene have been reported, with deficiency in enzyme activity leading to severe 5-FU-related toxicity in cancer patients (3). The so-called exon 14-skipping mutation at the 5'-splice donor site of exon 14 (1905 + 1G->A) has been detected in ~25% of affected patients (4). To identify patients at increased risk for severe 5-FU-induced toxicity, many medical centers routinely screen for the exon 14-skipping mutation before . . . [Full Text of this Article]






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