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Pharmacogenomics (a portmanteau of pharmacology and genomics) is the study of the role of genetics in drug response. It deals with the influence of acquired and inherited genetic variation on drug response in patients by correlating gene expression or single-nucleotide polymorphisms with drug absorption, distribution, metabolism and elimination, as well as drug receptor target effects.〔(【引用サイトリンク】 url=https://pharmacy.unc.edu/research/centers/cpit/ )〕 The term pharmacogenomics is often used interchangeably with pharmacogenetics. Although both terms relate to drug response based on genetic influences, pharmacogenetics focuses on single drug-gene interactions, while pharmacogenomics encompasses a more genome-wide association approach, incorporating genomics and epigenetics while dealing with the effects of multiple genes on drug response. Pharmacogenomics aims to develop rational means to optimize drug therapy, with respect to the patients' genotype, to ensure maximum efficacy with minimal adverse effects. Through the utilization of pharmacogenomics, it is hoped that drug treatments can deviate from what is dubbed as the "one-dose-fits-all" approach. It attempts to eliminate the trial-and-error method of prescribing, allowing physicians to take into consideration their patient’s genes, the functionality of these genes, and how this may affect the efficacy of the patient’s current and/or future treatments (and where applicable, provide an explanation for the failure of past treatments).〔 Such approaches promise the advent of "personalized medicine"; in which drugs and drug combinations are optimized for each individual's unique genetic makeup. Whether used to explain a patient’s response or lack thereof to a treatment, or act as a predictive tool, it hopes to achieve better treatment outcomes, greater efficacy, minimization of the occurrence of drug toxicities and adverse drug reactions (ADRs). For patients who have lack of therapeutic response to a treatment, alternative therapies can be prescribed that would best suit their requirements. In order to provide pharmacogenomic-based recommendations for a given drug, two possible types of input can be used: genotyping or exome or whole genome sequencing. Sequencing provides many more data points, including detection of mutations that prematurely terminate the synthesized protein (early stop codon).〔 == History == Pharmacogenomics was first recognized by Pythagoras around 510 BC when he made a connection between the dangers of fava bean ingestion with hemolytic anemia and oxidative stress. Interestingly, this identification was later validated and attributed to deficiency of G6PD in the 1950s and called favism.〔 Although the first official publication dates back to 1961, circa 1950s marked the unofficial beginnings of this science. Reports of prolonged paralysis and fatal reactions linked to genetic variants in patients who lacked butyryl-cholinesterase (‘pseudocholinesterase’) following administration of succinylcholine injection during anesthesia were first reported in 1956.〔 The term pharmacogenetic was first coined in 1959 by Friedrich Vogel of Heidelberg, Germany (although some papers suggest it was 1957). In the late 1960s, twin studies supported the inference of genetic involvement in drug metabolism, with identical twins sharing remarkable similarities to drug response compared to fraternity twins. The term pharmacogenomics first began appearing around the 1990s. The first FDA approval of a pharmacogenetic test was in 2005〔(Realities and Expectations of Pharmacogenomics and Personalized Medicine: Impact of Translating Genetic Knowledge into Clinical Practice. 2010 )〕 (for alleles in CYP2D6 and CYP2C19). 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「Pharmacogenomics」の詳細全文を読む スポンサード リンク
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