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• W2145432007 abstract "The inf luence of genetic variants on drug response is becoming increasingly better understood. In particular, genetic variants in drugmetabolizing enzymes and drug transporters and also mutations of the tumor genome (e.g., in tyrosine kinase signaling pathways) have been extensively characterized in vitro and in vivo. Whereas the consideration of genomic biomarkers is crucial in modern oncologic approaches, so far for non-oncologic diseases, only a few drugrelated genetic biomarkers can be translated into clinical practice. Clear pharmacokinetic consequences have been derived (e.g., for genetic variants in drug-metabolizing enzymes), leading to complete or severe loss of function as in the cases of phase I enzymes, such as CYP2D6, or the phase II enzyme TPMT [1]. In addition, specific HLA alleles have been convincingly demonstrated to be associated with severe adverse drug reactions (e.g., HLA-B*1502 in abacavir exposure) [2]. The majority of genes influencing pharmacokinetics and pharmacodynamics, however, consist of frequent variants leading to no or only modest changes in drug response, and pharmacogenetic data derived from various different in vitro and in vivo studies have not always been reproducible or are sometimes even contradictory. It is possible that the consequences of genetic traits are partly overexposed by the effects of transcriptional and posttranscriptional gene regulation through induction (e.g., by PXR, GCR or cytokines). Obviously, genetic traits – which are often considered to be static variants – are only one, and sometimes only a small piece in the puzzle of complex pharmacokinetic/pharmacodynamic modeling. In recent years, there has been a rapid increase in knowledge regarding genes that are essentially regulated by epigenetics through activation and silencing by DNA methylation and/or histone acetylation and miRNA-related post-transcriptional processes. These general mechanisms are key players in gene expression. Accordingly, administration of drugs inhibiting DNA methylation, such as 5-azacytidine or the anticonvulsant valproate, may increase ADME gene (related to drug absorption, distribution, metabolism and excretion) expression through activation of its promoters. Moreover, DNA methylation or histone acetylation may change under disease conditions." @default.
• W2145432007 created "2016-06-24" @default.
• W2145432007 creator A5059195101 @default.
• W2145432007 date "2013-11-01" @default.
• W2145432007 modified "2023-09-26" @default.
• W2145432007 title "Overlapping effects of genetic variation and epigenetics on drug response: challenges of pharmacoepigenomics" @default.
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• W2145432007 doi "https://doi.org/10.2217/pgs.13.194" @default.
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