Abstract
The term “pharmacogenetics” was coined in 1950s as it became evident that there was an inherited basics for differences in disposition and effects of drugs [1]. In 1990s, the concept of pharmacogenomics was introduced in the literature. In 2001, Pirmohamed [2] reported that pharmacogenetics is dened as the study of genetic variation in drug response, whereas the term pharmacogenomics was a broader term encompassing all genes in the genome that may determine drug response. He considered this distinction arbitrary as both terms are frequently used interchangeably. According to Jose de Leon [3], pharmacogenetics is commonly used in the context of studies that investigate the role of candidate genes, whereas pharmacogenomics is generally used in the exploratory context of genomewide association studies. Roses [4] has made a distinction between the two types of pharmacogenetics: safety pharmacogenetics is aimed at avoiding adverse drug reactions (ADRs), whereas efcacy pharmacogenetics is aimed at predicting response to medications. A drug’s activity is the result of interactions with proteins involved in absorption, distribution, metabolism, elimination, and cellular targets. Genetic variation in any of these proteins can have a signicant effect on drug response. Pharmacogenomics affects many aspects of therapy, including disposition of the drug (pharmacokinetics), efcacy of the drug (pharmacodynamics), dose selection, and adverse events of the drug-whether dose related or not [5,6]. Thus, pharmacogenomics is expected to contribute to personalized medicine [7].
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