HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Submit an electronic Letter to the Editor about this paper View responses Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by von Ahsen, N. Articles by Oellerich, M. Search for Related Content PubMed PubMed Citation Articles by von Ahsen, N. Articles by Oellerich, M. Related Collections Molecular Diagnostics and Genetics

Chip-Based Genotyping: Translation of Pharmacogenetic Research to Clinical Practice

Department of Clinical Chemistry, University of Göttingen, Göttingen, Germany

^aAddress correspondence to this author at: Georg-August University, Department Clinical Chemistry, Robert-Koch-Str. 40, 37099 Göttingen, Germany. Fax 49-551-39-8551; e-mail nahsen@gwdg.de.

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

The observation of interindividual differences in drug tolerance is perhaps as old as pharmacotherapy itself. Since the 1950s several monogenetic traits have been described that explain differences in drug response or drug toxicity in population subsets (1). These early discoveries have evolved into our current understanding of pharmacogenetics as a complex trait. Therapy selection guided by gene test, however, has still not made the transition into clinical practice. In the current issue of Clinical Chemistry, Daly et al. (2) present a dedicated single-microarray assay, or gene chip, for comprehensive genotyping of potentially thousands of variants in genes involved in drug metabolism, excretion, and transport.

These expanded capabilities are necessary because of the complexity of drug disposition. Single polymorphisms alone do not adequately predict drug disposition because multiple routes of metabolism or transport may compensate for deficiencies in a single pathway (3). For example, the anticancer drug irinotecan is not only metabolized by UGT1A1 but is also a substrate for transporter molecules coded by ABCB1, ABCC2, ABCG2, and SLCO1B1 (4). Comprehensive genotyping based on gene chips allows large-scale studies on the utility of validated and exploratory biomarkers. The pharmacogenetic gene chip developed by Daly et al. (2) covers the 7 valid genomic biomarkers of drug disposition listed by the US Food . . . [Full Text of this Article]

eLetters: