What is pharmacogenomics? – Genetics Home Reference – NIH

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Pharmacogenomics is the study of how genes affect a persons response to drugs. This relatively new field combines pharmacology (the science of drugs) and genomics (the study of genes and their functions) to develop effective, safe medications and doses that will be tailored to a persons genetic makeup.

Many drugs that are currently available are one size fits all, but they don't work the same way for everyone. It can be difficult to predict who will benefit from a medication, who will not respond at all, and who will experience negative side effects (called adverse drug reactions). Adverse drug reactions are a significant cause of hospitalizations and deaths in the United States. With the knowledge gained from the Human Genome Project, researchers are learning how inherited differences in genes affect the bodys response to medications. These genetic differences will be used to predict whether a medication will be effective for a particular person and to help prevent adverse drug reactions.

The field of pharmacogenomics is still in its infancy. Its use is currently quite limited, but new approaches are under study in clinical trials. In the future, pharmacogenomics will allow the development of tailored drugs to treat a wide range of health problems, including cardiovascular disease, Alzheimer disease, cancer, HIV/AIDS, and asthma.

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What is pharmacogenomics? - Genetics Home Reference - NIH

MediMap genomics test – precision medicine at Inova …

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Go to Inova Translational Medicine Institute

Pharmacogenomics, also called PGx, combines the science of how medications work (pharmacology) with the science of how genetic differences can influence health (genomics).Inova is pleased to offer the MediMap PGx test to adults and children, as well asto newbornsdelivered atInova Womens Hospital.

MediMap is part of the standard package of services offered to all babies born at Inova Womens Hospital located at Inova Fairfax Medical Campus, and it is therefore performed at no additional cost. Inova is the only health system in the U.S. that provides this optional pharmacogenomics test to newborns as part of our standard package of care. More info about MediMap for newborns

Inova is pleased to announce that we will be offering theMediMap test to adults and children in the near future.More info about MediMap for adults and children

Until recently, most medicines have been developed and prescribed to patients in a one size fits all approach. PGx testing informs your physician about your, or your childs, genetic makeup to help determine which medications to use or the amount prescribed. PGx testing may also reduce side-effects.

MediMap is a one-time genetic test that may indicate how a person will respond to some prescription medications. The test helps guide healthcare providers to better medication choices and doses for their patients. MediMap testing provides information to more effectively manage illnesses and improve their health.

Cant find what you are looking for? Please call us at 1-844-GENOME-4U (1-844-436-6634) or email us at geneinfo@inova.org.

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PHG Foundation – Interactive Tutorial: Pharmacogenomics …

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Pharmacogenetics refers to the study of genetic influences on an individuals response to drugs. In pharmacogenetics, the analysis of a specific gene, or group of genes, may be used to predict responses to a specific drug or class of drugs.

Pharmacogenomics refers collectively to all the genes that influence drug responses, and how genome-wide analysis may be used to identify such genes in the search for novel drug targets and/or key determinants of drug reactions.

The effects of a specific dose of a specific drug will differ between individual recipients. A drug that is effective in one person may have no discernible therapeutic effect in another, whilst a third might show a partial response; in some, there may be undesirable side-effects.

There are multiple contributory factors to such variation in drug response, such as gender, age, body mass, diet, the presence of other drugs or of particular disease states and exposure to certain chemicals or toxins, such as cigarette smoke. In addition to these, genetic factors also influence drug response.

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Pharmacogenomics – ncpanet.org

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General Description, Overview, and Opportunities

Pharmacogenomics has increasingly become an area of interest to clinicians because of the potential to tailor pharmacotherapy based on genetic variations in patients. Pharmacogenomics is one of the key aspects of personalized medicine, focusing on how an individual's DNA affects the way they respond to medications. All individuals have different genetic make-up so they respond differently to the same medication. Based on this insight, pharmacogenomics allows customized treatment for a wide range of health problems including; cardiovascular disease, Alzheimer's disease, cancer, HIV/AIDS, and asthma. Often, drug choice and dosage require experimentation (trial and error) in order to find the best treatment option. With pharmacogenomics testing, the need for this experimentation is decreased. As a result, the process becomes faster and more cost-effective and the possibility of adverse events caused by the wrong drug choice or dosage is significantly reduced.

One avenue for implementing pharmacogenomic is through medication therapy management (MTM), where pharmacists assess and evaluate a patient's complete medication therapy regimen. By gathering key pieces of information, e.g. which medications and supplements a patient is currently taking, pharmacists can assess current treatment and suggest alternative therapies.

As medication experts and POC service providers, pharmacists can educate physicians and patients and perform the actual sample collection to be utilized for genetic testing. The broad application of pharmacogenomics to personalized medicine will improve patient outcomes and lower healthcare costs.

Test Features

Pharmacies require a lab partner to provide clinically relevant data and interpret results for physicians. Most tests screens all well-established pharmacogenomics genes in a single, cost-effective test. Results are delivered quickly via intuitive, clinically relevant, medically actionable report. The data provides lifetime utility of data, thereby decreasing the need for future testing.

Community pharmacists routinely perform point of care services and can assist patients by:

Performing a buccal swab in minutes

Send the collected DNA to the lab

Interpret results and discuss with physicians

Contact the patient to explain the results and any changes in therapy

Companies

Pharmacist Resources and Training

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Pharmacogenomics - ncpanet.org

Internships Internship Search and Intern Jobs …

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Pharmacogenetics – Wikipedia

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Pharmacogenetics is the study of inherited genetic differences in drug metabolic pathways which can affect individual responses to drugs, both in terms of therapeutic effect as well as adverse effects.[1] The term pharmacogenetics is often used interchangeably with the term pharmacogenomics which also investigates the role of acquired and inherited genetic differences in relation to drug response and drug behavior through a systematic examination of genes, gene products, and inter- and intra-individual variation in gene expression and function.[2]

In oncology, pharmacogenetics historically is the study of germline mutations (e.g., single-nucleotide polymorphisms affecting genes coding for liver enzymes responsible for drug deposition and pharmacokinetics), whereas pharmacogenomics refers to somatic mutations in tumoral DNA leading to alteration in drug response (e.g., KRAS mutations in patients treated with anti-Her1 biologics).[3]

Much of current clinical interest is at the level of pharmacogenetics, involving variation in genes involved in drug metabolism with a particular emphasis on improving drug safety. The wider use of pharmacogenetic testing is viewed by many as an outstanding opportunity to improve prescribing safety and efficacy. Driving this trend are the 106,000 deaths and 2.2 Million serious events caused by adverse drug reactions in the US each year.[4][unreliable medical source?] As such ADRs are responsible for 5-7% of hospital admissions in the US and Europe, lead to the withdrawal of 4% of new medicines, and cost society an amount equal to the costs of drug treatment.[5]

Comparisons of the list of drugs most commonly implicated in adverse drug reactions with the list of metabolizing enzymes with known polymorphisms found that drugs commonly involved in adverse drug reactions were also those that were metabolized by enzymes with known polymorphisms (see Phillips, 2001).

Scientists and doctors are using this new technology for a variety of things, one being improving the efficacy of drugs. In psychology, we can predict quite accurately which anti-depressant a patient will best respond to by simply looking into their genetic code.[citation needed][dubious discuss] This is a huge step from the previous practice of adjusting and experimenting with different medications to get the best response. Antidepressants also have a large percentage of unresponsive patients and poor prediction rate of ADRs (adverse drug reactions). In depressed patients, 30% are not helped by antidepressants. In psychopharmacological therapy, a patient must be on a drug for 2 weeks before the effects can be fully examined and evaluated. For a patient in that 30%, this could mean months of trying medications to find an antidote to their pain. Any assistance in predicting a patients drug reaction to psychopharmacological therapy should be taken advantage of. Pharmacogenetics is a very useful and important tool in predicting which drugs will be effective in various patients.[6] The drug Plavix blocks platelet reception and is the second best selling prescription drug in the world, however, it is known to warrant different responses among patients.[7]GWAS studies have linked the gene CYP2C19 to those who cannot normally metabolize Plavix. Plavix is given to patients after receiving a stent in the coronary artery to prevent clotting.

Stent clots almost always result in heart attack or sudden death, fortunately it only occurs in 1 or 2% of the population. That 1 or 2% are those with the CYP2C19 SNP.[8] This finding has been applied in at least two hospitals, Scripps and Vanderbilt University, where patients who are candidates for heart stents are screened for the CYP2C19 variants.[9]

Another newfound use of pharmacogenetics involves the use of Vitamin E. The Technion Israel Institute of Technology observed that vitamin E can be used to in certain genotypes to lower the risk of cardiovascular disease in patients with diabetes, but in the same patients with another genotype, vitamin E can raise the risk of cardiovascular disease. A study was carried out, showing vitamin E is able to increase the function of HDL in those with the genotype haptoglobin 2-2 who suffer from diabetes. HDL is a lipoprotein that removes cholesterol from the blood and is associated with a reduced risk of atherosclerosis and heart disease. However, if you have the misfortune to possess the genotype haptoglobin 2-1, the study shows that this same treatment can drastically decrease your HDL function and cause cardiovascular disease.[10]

Pharmacogenetics is a rising concern in clinical oncology, because the therapeutic window of most anticancer drugs is narrow and patients with impaired ability to detoxify drugs will undergo life-threatening toxicities. In particular, genetic deregulations affecting genes coding for DPD, UGT1A1, TPMT, CDA and CYP2D6 are now considered as critical issues for patients treated with 5-FU/capecitabine, irinotecan, mercaptopurine/azathioprine, gemcitabine/capecitabine/AraC and tamoxifen, respectively. The decision to use pharmacogenetic techniques is influenced by the relative costs of genotyping technologies and the cost of providing a treatment to a patient with an incompatible genotype. When available, phenotype-based approaches proved their usefulness while being cost-effective.[11]

In the search for informative correlates of psychotropic drug response, pharmacogenetics has several advantages:[12]

The first observations of genetic variation in drug response date from the 1950s, involving the muscle relaxant suxamethonium chloride, and drugs metabolized by N-acetyltransferase. One in 3500 Caucasians has less efficient variant of the enzyme (butyrylcholinesterase) that metabolizes suxamethonium chloride.[13] As a consequence, the drugs effect is prolonged, with slower recovery from surgical paralysis. Variation in the N-acetyltransferase gene divides people into "slow acetylators" and "fast acetylators", with very different half-lives and blood concentrations of such important drugs as isoniazid (antituberculosis) and procainamide (antiarrhythmic). As part of the inborn system for clearing the body of xenobiotics, the cytochrome P450 oxidases (CYPs) are heavily involved in drug metabolism, and genetic variations in CYPs affect large populations. One member of the CYP superfamily, CYP2D6, now has over 75 known allelic variations, some of which lead to no activity, and some to enhanced activity. An estimated 29% of people in parts of East Africa may have multiple copies of the gene, and will therefore not be adequately treated with standard doses of drugs such as the painkiller codeine (which is activated by the enzyme). The first study using Genome-wide association studies (GWAS) linked age-related macular degeneration (AMD) with a SNP located on chromosome 1 that increased ones risk of AMD. AMD is the most common cause of blindness, affecting more than seven million Americans. Until this study in 2005, we only knew about the inflammation of the retinal tissue causing AMD, not the genes responsible.[9]

One of the earliest tests for a genetic variation resulting in a clinically important consequence was on the enzyme thiopurine methyltransferase (TPMT). TPMT metabolizes 6-mercaptopurine and azathioprine, two thiopurine drugs used in a range of indications, from childhood leukemia to autoimmune diseases. In people with a deficiency in TPMT activity, thiopurine metabolism must proceed by other pathways, one of which leads to the active thiopurine metabolite that is toxic to the bone marrow at high concentrations. Deficiency of TPMT affects a small proportion of people, though seriously. One in 300 people have two variant alleles and lack TPMT activity; these people need only 6-10% of the standard dose of the drug, and, if treated with the full dose, are at risk of severe bone marrow suppression. For them, genotype predicts clinical outcome, a prerequisite for an effective pharmacogenetic test. In 85-90% of affected people, this deficiency results from one of three common variant alleles.[14] Around 10% of people are heterozygous - they carry one variant allele - and produce a reduced quantity of functional enzyme. Overall, they are at greater risk of adverse effects, although as individuals their genotype is not necessarily predictive of their clinical outcome, which makes the interpretation of a clinical test difficult. Recent research suggests that patients who are heterozygous may have a better response to treatment, which raises whether people who have two wild-type alleles could tolerate a higher therapeutic dose.[15] The US Food and Drug Administration (FDA) have recently deliberated the inclusion of a recommendation for testing for TPMT deficiency to the prescribing information for 6-mercaptopurine and azathioprine. The information previously carried the warning that inherited deficiency of the enzyme could increase the risk of severe bone marrow suppression. It now carries the recommendation that people who develop bone marrow suppression while receiving 6-mercaptopurine or azathioprine be tested for TPMT deficiency.[citation needed]

A polymorphism near a human interferon gene is predictive of the effectiveness of an artificial interferon treatment for Hepatitis C. For genotype 1 hepatitis C treated with Pegylated interferon-alpha-2a or Pegylated interferon-alpha-2b (brand names Pegasys or PEG-Intron) combined with ribavirin, it has been shown that genetic polymorphisms near the human IL28B gene, encoding interferon lambda 3, are associated with significant differences in response to the treatment.[16] Genotype 1 hepatitis C patients carrying certain genetic variant alleles near the IL28B gene are more probable to achieve sustained virological response after the treatment than others, and demonstrated that the same genetic variants are also associated with the natural clearance of the genotype 1 hepatitis C virus.[17]

Despite the many successes, most drugs are not tested using GWAS. However, it is estimated that over 25% of common medication have some type of genetic information that could be used in the medical field.[18] If the use of personalized medicine is widely adopted and used, it will make medical trials more efficient. This will lower the costs that come about due to adverse drug side effects and prescription of drugs that have been proven ineffective in certain genotypes. It is very costly when a clinical trial is put to a stop by licensing authorities because of the small population who experiences adverse drug reactions. With the new push for pharmacogenetics, it is possible to develop and license a drug specifically intended for those who are the small population genetically at risk for adverse side effects. [19]

The ability to test and analyze an individuals DNA to determine if the body can break down certain drugs through the biochemical pathways has application in all fields of medicine. Pharmacogenetics gives those in the health care industry a potential solution to help prevent the significant amount of deaths that occur each year due to drug reactions and side effects. The companies or laboratories that perform this testing can do so acrossed all categories or drugs whether it be for high blood pressure, gastrointestinal, urological, psychotropic or anti-anxiety drugs. Results can be presented showing which drugs the body is capable of breaking down normally versus the drugs the body cannot break down normally. This test only needs to be done once and can provide valuable information such as a summary of an individuals genetic polymorphisms, which could help in a situation such as being a patient in the emergency room.[20]

As the cost per genetic test decreases, the development of personalized drug therapies will increase.[21] Technology now allows for genetic analysis of hundreds of target genes involved in medication metabolism and response in less than 24 hours for under $1,000. This a huge step towards bringing pharmacogenetic technology into everyday medical decisions. Likewise, companies like deCODE genetics, Navigenics and 23andMe offer genome scans. The companies use the same genotyping chips that are used in GWAS studies and provide customers with a write-up of individual risk for various traits and diseases and testing for 500,000 known SNPs. Costs range from $995 to $2500 and include updates with new data from studies as they become available. The more expensive packages even included a telephone session with a genetics counselor to discuss the results.[9]

Pharmacogenetics has become a controversial issue in the area of bioethics. It's a new topic to the medical field, as well as the public. This new technique will have a huge impact on society, influencing the treatment of both common and rare diseases. As a new topic in the medical field the ethics behind it are still not clear. However, ethical issues and their possible solutions are already being addressed.

There are three main ethical issues that have risen from pharmacogenetics. First, would there be a type equity at both drug development and the accessibility to tests.[22] The concern of accessibility to the test is whether it is going to be available directly to patients via the internet, or over the counter. The second concern regards the confidentiality of storage and usage of genetic information.[23] Thirdly, would patients have the control over being tested.

One concern that has risen is the ethical decision health providers must take with respect to educating the patient of the risks and benefits of medicine developed by this new technology. Pharmacogenetics is a new process that may increase the benefits of medicine while decreasing the risk. However clinicians have been unsuccessful in educating patients regarding the concept of benefits over risk. The Nuffield Council reported that patients and health professionals have adequate information about pharmacogenetics tests and medicine.[23] Health care providers will also encounter an ethical decision in deciding to tell their patients that only certain individuals will benefit from the new medicine due to their genetic make-up.[22] Another ethical concern is that patients who have not taken the test be able to have access to this type of medicine. If access is given by the doctor the medicine could negatively impact the patient's health. The ethical issues behind pharmacogenetics tests, as well as medicine, are still a concern and policies will need to be implemented in the future.

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Pharmacogenetics - Wikipedia

Vanderbilt Pharmacogenomics

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Welcome

Clinicians and patients recognize that not every person responds to drugs in the same way. Some drugs carry a risk of adverse reactions that often seem to occur by chance. Even drugs that are well-tolerated may be highly effective at low doses in some patients, and minimally effective at high doses in others.

The Human Genome Project has established the initial sequence of all human DNA. In doing so, the Genome Project enabled study of how variations among patient genomes affects why disease develops in some patients and not in others. Pharmacogenetics is the study of how individual DNA variations affect drug responses, and the term pharmacogenomics is often used to describe how many variations in an individual patient, or in large groups of patients, affect the outcome of drug therapy.

Vanderbilt University is a center of excellence in the study of mechanisms underlying individual variability in response to drug therapy. This work reaches from basic science to clinical medicine, and includes studies of metabolism and transport of many drugs, as well as, specific studies of drug therapies in diverse clinical settings such as arrhythmias, hypertension, autonomic dysfunction, psychiatric disease, cancer, HIV infection, and recovery from anesthesia.

Research Centers with a special focus on pharmacogenetics and pharmacogenomics include the Division of Clinical Pharmacology, the Vanderbilt-Ingram Cancer Center, the Center for Molecular Neuroscience, the Vanderbilt-Meharry Center for AIDS Research, the Division of Genetic Medicine, the General Clinical Research Center, the Center for Human Genetics Research, and the Center for Genetics and Health Policy. Studies of arrhythmia therapies are supported by Vanderbilt's participation in the NIH-sponsored Pharmacogenetics Research Network.

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Genomics|Update|Non Communicable Diseases

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FDA: The steps were taking to push precision medicine forward, by Meghana Keshavan, Med City News, September 23, 2015

Dr. Henry T. Lynch Symposium: Advances in hereditary cancer summary by G, I have Lynch Syndrome, September 22, 2015

Who knows what it means, Genome Web, September 21, 2015 [by subscription only]

87-year-old Creighton University doctor finds motivation in tracking cancer families, by Rick Ruggles, Omaha.com, September 20, 2015

Genomics will redraw the rare disease map: The "Rarity Catch-22", CVID, Primary Immune and Rare Disease Blog, September 19, 2015

NIH moves forward on genetic database while hoping for funding, iHealthBeat, September 18, 2015

Enthusiasm for personalized cancer drugs runs ahead of the science, by Asher Mullard, Nature News, September 17, 2015

For some children with cancer, genomic information may help guide treatment decisions, Cancer Currents Blog, NCI, September 17, 2015

Is fish oil good for you? Depends on your DNA, by Elizabeth Pennisi, Science News, September 17, 2015

Cure for sickle cell in adults validated, Science Daily, September 16, 2015

Pres. Obama's precision medicine initiative, the human genome project, and your individualized genetic data, by Samantha Olson, Medical Daily, September 16, 2015

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Genomics|Update|Non Communicable Diseases

Pharmacogenomics – PubMed Central (PMC)

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BMJ. 1999 Nov 13; 319(7220): 1286.

Departments of Biopharmaceutical Sciences and Pharmaceutical Chemistry, University of California, San Francisco, CA94143-0446, USA

We all differ in our response to drug treatmentoccasionally with dramatic effects. The era of one drug fits all patients is about to give way to individualised therapy matching the patient's unique genetic make up with an optimally effective drug.1 Pharmacogenetics and pharmacogenomics are the emerging disciplines that are leading the way towards individualised medicine.2,3 Initially, researchers focused their attention on pharmacogeneticsvariations in single candidate genes responsible for variable drug response. Subsequently, studies involving the entire human genome broadened the scope of investigation, giving rise to pharmacogenomics as one of the hottest fields in biotechnology today.

Response to drug treatment can vary greatly between patients; genetic factors have a major role in treatment outcome

Pharmacogenetics and pharmacogenomics are emerging disciplines that focus on genetic determinants of drug response at the levels of single genes or the entire human genome respectively

Technologies involving gene chip arrays can determine thousands of variations in DNA sequences for individual patients; most variants are single nucleotide polymorphisms

Pharmacogenomics aims at establishing a signature of DNA sequence variants that are characteristic of individual patients to assess disease susceptibility and select the optimal drug treatment

This approach has the potential to revolutionise prevention and treatment of diseases

Unexpected drug reactions have been noted for some time, but the systematic study of hereditary origins began only in the 1950s. A few patients developed prolonged respiratory muscular paralysis after being given succinylcholine (suxamethonium), a short acting muscle relaxant widely used in surgery and electroshock treatment. In the 1970s, a trial with the antihypertensive agent debrisoquine resulted in a precipitous drop of blood pressure and collapse in nearly 10% of volunteers. Furthermore, isoniazid therapy for tuberculosis caused peripheral neuropathies in patients who were sensitive to the neurotoxic effects of the drug. Ground breaking genetic and biochemical studies by Werner Kalow and others showed that these adverse effects result from polymorphisms in genes encoding the drug metabolising enzymes serum cholinesterase,4 cytochrome P-450,5 and N-acetyltransferase.6 These observations laid the foundation for pharmacogenetics.

Today, many examples of genetic variability in drug response and toxicity are known (table). In a few cases, genetic tests are beginning to find their way into clinical practice. In cancer chemotherapy with tioguanine, severe toxicity or even death can result if a patient is unable to inactivate the drug. Functional assays of thiopurine methyltransferase in red blood cells or genotyping can identify those patients who are at risk and must be given a much lower dose of tioguanine.7,8 This is particularly critical for the 1 in 300 patients who is homozygous for null alleles (non-functional) of the gene encoding thiopurine methyltransferase which converts the drug to its inactive methylated form. Therefore, genotyping or functional analysis has become standard practice in major cancer treatment centres such as the Mayo Clinic in Rochester, Minneapolis, and St Jude Children's Research Hospital in Memphis, Tennessee.

The large family of cytochrome P-450 genes has been most intensely studied because it contains the main drug metabolising enzymes encoded by numerous genes.2 Among the cytochrome P-450 subtypes, CYP2D6 and CYP2C19 play a critical part in determining the response to several drugs. This is particularly important for lipophilic drugssuch as drugs that act on the central nervous system and penetrate the lipophilic blood-brain barrierbecause renal excretion is minimal and cytochrome P-450 metabolism provides the only means of effective drug elimination. Thus, homozygous carriers of CYP2D6 null alleles and cannot readily degrade and excrete many drugs, including debrisoquine, metoprolol, nortriptyline, and propafenone.9 These patients are termed poor metabolisers for CYP2D6 selective drugs. Because of this they are exquisitely sensitive to these drugs. The incidence of poor metabolisers varies greatly among ethnic groups, ranging from 1% in Japanese people to 15% in Nigerians. Similarly, patients with defective CYP2C19 subtypes are highly sensitive to methoin (mephenytoin), hexobarbital (hexobarbitone), and other drugs selectively metabolised by this P-450 isoform.

The principal molecular defect in poor metabolisers is a single base pair mutation (AG) in exon 5 of CYP2C19.10 Gene chips designed to test for polymorphisms of the main subtypes of cytochrome P-450 are now commercially available, but not yet in general clinical use. Cytochrome P-450 polymorphisms also affect the inactivation or, in some cases, activation or toxification of xenobiotics, and thus affect an individual's susceptibility to environmental toxins. This is studied in a field of research called toxicogenetics. Launched recently by the US National Institute of Environmental Health Sciences, the environmental genome project aims at understanding genetic factors in individual responses to the environment and parallels the study of genetic variability in drug response.11

As a scientific discipline, pharmacogenetics has made steady progress, but the human genome project has shattered any complacency as it has revealed profound gaps in our knowledge. By broadening the search for genetic polymorphisms that determine drug responses, the new field of pharmacogenomics begins to supersede the candidate gene approach typical of earlier pharmacogenetic studies. Initially hailed by pharmaceutical biotechnology as the latest trend in biotechnology, pharmacogenomics is now taken seriously everywhere. While genomic techniques serve to identify new gene targets for drug research, and some might refer to this as pharmacogenomics, the broader consensus is that pharmacogenomics deals specifically with genetic variability in drug response. The distinction between pharmacogenetics and pharmacogenomics remains blurred, but here are some of the new ideas typical of pharmacogenomics.

Each drug is likely to interact in the body with numerous proteins, such as carrier proteins, transporters, metabolising enzymes, and multiple types of receptors.1 These proteins determine the absorption, distribution, excretion, targeting to the site of action, and pharmacological response of drugs. As a result, multiple polymorphisms in many genes could affect the drug response, requiring a genome-wide search for the responsible genes. We now know that that there are thousands of receptor genes in the human genome, many of which are closely related to each other because they have evolved by gene duplications. Therefore, we must anticipate that a drug rarely binds just to a single receptor but rather interacts promiscuously with several receptor types. Chlorpromazine, for example, is known to engage several dopaminergic, adrenergic, and serotonergic receptors. As a result, polymorphisms in multiple genes can affect the drug response.

Polymorphisms are generally defined as variations of DNA sequence that are present in more than 1% of the population. Most polymorphisms are single nucleotide polymorphisms (referred to as snips). As the human genome contains three billion nucleotides, and variations between individuals occur in 1/300 base pairs, around 10 million single nucleotide polymorphisms probably exist. Only 1% of these may have any functional consequence at all, and thus individuals differ from each other genetically by roughly 100000 polymorphic sites, providing for near infinite variety. As only a small fraction of these single nucleotide polymorphisms will prove relevant to drug response, our goal will be to identify the most important variants.

Novel technology in the form of microarray chips enables us to scan the entire human genome for relevant polymorphisms.12,13 We can determine simultaneously many thousands of polymorphisms in a patient. At present, these single nucleotide polymorphisms are selected merely as markers evenly distributed throughout the genome, in the hope that functionally relevant polymorphisms can be associated with specific markers by virtue of their proximity on the chromosome. Such genome-wide association studies are already being used in the discovery of susceptibility genes for diseases such as asthma and prostate cancer, but they are equally suitable for determining the genes involved in drug response. Genome-wide scanning can identify these genes even if we do not know the mechanisms by which the drug acts in the body. The French genomics company, Genset, currently uses gene chips with 60000 single nucleotide polymorphism markerssufficient for a complete genomic scanapplied to clinical drug trials in partnership with major pharmaceutical companies. Expanding the number of single nucleotide polymorphisms and selecting functionally relevant single nucleotide polymorphisms in coding or promoter/enhancer regions of genes is quite feasible with current technology and would greatly enhance the power of genome-wide scanning. Herein lies the main incentive for the current rush in the pharmaceutical industry to patent single nucleotide polymorphism markers. It might also be possible to salvage useful experimental drugs that would have failed with standard clinical trials, because of an unacceptable incidence of toxicity in a poorly defined patient population. Stratifying patient populations in relation to genetic criteria emerges as a major challenge to the pharmaceutical industry. Undoubtedly, the insights expected to emerge from such an approach are staggering, but they cannot be gauged accurately at present.

Microarrays can further serve to determine the expression pattern of genes in a target tissue. This shows the mechanisms of drug action in a genomic context. It can also clarify interindividual differences in drug response that are downstream of immediate drug effects in the body by shear force of the massive amount of information emanating from chip technology. Analysing the entire transcriptional programme of a tissuefor example, fibroblasts in response to serum stimulation14provides unprecedented details of a complex system and leads to new insights in pathophysiology and biological drug response. Tissue transcript profiling is especially appropriate in cancers because mRNA can be extracted from biopsy specimens or surgical samples. Altered gene expression in the tumour can serve as a guide for selecting effective drug therapy or avoiding unnecessary exposure to toxic but ineffective drugsfor example, the overexpression of drug resistance genes encoding transporters (table).

These advances are the harbinger of profound changes in treatment. What then do we expect to gain from pharmacogenomics? In the near future, genotyping can help avert severe drug toxicity that is genetically determined but occurs only rarely. Alternatively, drugs may be designed a priori so that they are not subject to extreme variations that result from a few well defined polymorphisms. Drug structures under development are already being selected so that they do not interact with cytochrome P-450 subtype CYP2D6 to avoid unwarranted toxicity in people who metabolise this poorly.

Looking further ahead, and on a much broader scale, we could improve drug efficacy by distinguishing between people who respond well to a drug and those who respond poorly. Often, an effective drug response is found in a few patients treated, while most benefit little or not at all. Much could be gained if we could select the optimal drug for the individual patient before treatment begins. Perhaps a gene chip that establishes a single nucleotide polymorphism signature involving multiple genes relevant to therapeutic outcome for each individual will be developed. This signature could offer insights into an individual's susceptibility to disease and responsiveness to drugs, enabling optimal drug selection by genetic criteria. For example, cure rates with combined surgical and drug treatment of advanced colorectal carcinoma range from 20% to 40%, while the remainder of the patients experience little gain or even severe toxicity from chemotherapy. If we could predict which patients respond best to a particular drugor better, which drug will yield optimal effects for a given patientmuch will be gained. The success of this approach will depend critically on the selection of single nucleotide polymorphisms tested by the gene chip. Single nucleotide polymorphisms must be informative and many must be tested to scan the entire genome. This task is by no means complete and constitutes a major goal of those companies which are focusing on genomics.

There are also formidable obstacles that we are unlikely to overcome in the near future. The dynamic complexity of the human genome, involvement of multiple genes in drug responses, and racial differences in the prevalence of gene variants impede effective genome-wide scanning and progress towards practical clinical applications. Furthermore, the drug response is probably affected by multiple genes, each gene with multiple polymorphisms distributed in the general population. For example, the anticancer drug 5-fluorouracil used in the treatment of colorectal cancer is activated and inactivated by nearly 40 different enzymes. Each of these is currently being scanned for relevant polymorphisms at the biotech company Variagenics. Dihydropyrimidine dehydrogenase is a likely candidate in 5-fluorouracil inactivation (table). However, whether extensive genotyping will provide useful predictors of clinical response remains to be seen.

Racial differences add further confounding factors. Drug response might be predicted from a certain pattern of polymorphisms rather than only a single polymorphism, yet these patterns probably differ between ethnic groups. This could prevent us from making predictions about drug responses across the general patient population, and it emphasises the need to stratify clinical pharmacogenomics studies.

Genomic technologies are still evolving rapidly, at an exponential pace similar to the development of computer technology over the past 20 years. We are not certain where genomic technologies will be 10 years from now.

Ethical issues also need to be resolved. Holding sensitive information on someone's genetic make up raises questions of privacy and security and ethical dilemmas in disease prognosis and treatment choices. After all, polymorphisms relevant to drug response may overlap with disease susceptibility, and divulging such information could jeopardise an individual. On the other hand, legal issues may force the inclusion of pharmacogenomics into clinical practice. Once the genetic component of a severe adverse drug effect is documented, doctors may be obliged to order the genetic test to avoid malpractice litigation.

Pharmacogenomics will have a profound impact on the way drug treatment is conducted. We can include here bioengineered proteins as drugs, or even gene therapy designed to deliver proteins to target tissues. These treatments are also subject to constraints and complexities engendered by individual variability. A case in point is the treatment of breast cancer with trastuzumab (Herceptin; Genentech, USA) a humanised monoclonal antibody against the HER2 receptor. Overexpression of HER2 may occur as a somatic genetic change in breast cancer and other tumours. This correlates with poor clinical prognosis and serves as a marker for effective therapy with trastuzumab, either alone or in combination with chemotherapy.15,16

Whether we will see broad use of gene chips in clinical practice within 10 years is questionable, but the mere knowledge of the principles underlying genetic variability will prove valuable in optimising drug therapy. Pharmacogenomics will lead us towards individualised therapy, but it will also help us understand limitations inherent in treating disease in a broad patient population

Incyte's microarray service allows researchers to analyse differential expression in normal and diseased cells

Examples of inherited or acquired variations in enzymes and receptors that affect the drug response23

Competing interests: None declared.

2. Weber WW. Pharmacogenetics. New York: Oxford University Press; 1997.

13. Sinclair B. Everything's great when it sits on a chip: a bright future for DNA arrays. Scientist. 1999;13:1820.

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CDC authors are indicated in bold

Distinct pathological phenotypes of Creutzfeldt-Jakob disease in recipients of prion-contaminated growth hormone. Cali I, Miller CJ, Parisi JE, Geschwind MD, Gambetti P, Schonberger LB. Acta Neuropathol Commun. 2015 Jun 25;3(1):37.

Bacterial factors associated with lethal outcome of enteropathogenic Escherichia coli infection: genomic case-control studies Donnenberg MS, Hazen TH, Farag TH, Panchalingam S, Antonio M, Hossain A, Mandomando I, Ochieng JB, Ramamurthy T, Tamboura B, Zaidi A, Levine MM, Kotloff K, Rasko DA, Nataro JP. PLoS Negl Trop Dis. 2015 May;9(5):e0003791.

Specificity and Strain-Typing Capabilities of Nanorod Array-Surface Enhanced Raman Spectroscopy for Mycoplasma pneumoniae Detection. Henderson KC, Benitez AJ, Ratliff AE, Crabb DM, Sheppard ES, Winchell JM, Dluhy RA, Waites KB, Atkinson TP, Krause DC. PLoS One. 2015 Jun 29;10(6):e0131831

Identification of influenza A/PR/8/34 donor viruses imparting high hemagglutinin yields to candidate vaccine viruses in eggs Johnson A, Chen LM, Winne E, Santana W, Metcalfe MG, Mateu-Petit G, Ridenour C, Hossain MJ, Villanueva J, Zaki SR, Williams TL, Cox NJ, Barr JR, Donis RO. PLoS One. 2015 ;10(6):e0128982.

A novel botulinum toxin, previously reported as serotype H, has a hybrid structure of known serotypes A and F that is neutralized with serotype A antitoxin Maslanka SE, Luquez C, Dykes JK, Tepp WH, Pier CL, Pellett S, Raphael BH, Kalb SR, Barr JR, Rao A, Johnson EA. J Infect Dis. 2015 Jun 10.

Effects of laser printer-emitted engineered nanoparticles on cytotoxicity, chemokine expression, reactive oxygen species, DNA methylation, and DNA damage: a comprehensive analysis in human small airway epithelial cells, macrophages, and lymphoblasts Pirela SV, Miousse IR, Lu X, Castranova V, Thomas T, Qian Y, Bello D, Kobzik L, Koturbash I, Demokritou P. Environ Health Perspect. 2015 Jun 16.

Pathway-Focused Genetic Evaluation of Immune and Inflammation Related Genes with Chronic Fatigue Syndrome. Rajeevan MS, Dimulescu I, Murray J, Falkenberg VR, Unger ER. Hum Immunol. 2015 Jun 24. pii: S0198-8859(15)00180-9.

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Pharmacogenomic Testing Services | Personalized … – DNA stat

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Welcome to DNA Stat. We specialize in personalized medicine services, specifically in the pain management and pharmacogenomics arena. We take pride in both our research and unsurpassed customer service, providing clients with genetic & pharmacogenomics testing which is the fastest growing field in the medical industry today.

Pain management and pharmacogenomics is vitally important as we progress into the 21st century as it is a realization and acknowledgement that one size does not fit all when it comes to medications. What might work for one individual flawlessly could mean an adverse reaction and a trip to the emergency room for another. Genetic Testing is the tool used to determine the difference before the medication is ingested. In this way, we are spearheading and defining personalized medicine services and enabling people to recover and maintain their illnesses and conditions worry-free. By eliminating the guess work, patients can recover more fully and quicker than ever before.

We know that the medical industry can be daunting to most people. Fortunately, the genetic & pharmacogenomics testing at DNA Stat comes down to a simple Buccal swab of the cheek. No needles involved, no fear, no blood no problem. Within three weeks, the patients doctor will have in his or her hands a Pharm D Report which is the roadmap to prescribing better medications and better treatments for their patient. DNA Stat, the leader in genetic& pharmacogenomics testing, is changing the way the world sees medicine one patient at a time.

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New Genetic Tools Learn Genetics

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Pharmacogenomics

Your Doctor's New Genetic Tools

When physicians are given the tools to evaluate a patient's genetic make-up, they will be able to make more accurate diagnoses, and prescribe more efficient drug therapies with fewer adverse side effects.

Differences between people extend beyond our outer physical features. How individuals respond to drugs for the treatment of cancer or other illnesses differs based on the activity and function of enzymes in the body. This information is available in each individual's genetic profile. Even today, genetics is being integrated into individuals' medical treatment plans.

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APA format: Genetic Science Learning Center (2014, June 22) Your Doctor's New Genetic Tools. Learn.Genetics. Retrieved July 10, 2015, from http://learn.genetics.utah.edu/content/pharma/intro/ MLA format: Genetic Science Learning Center. "Your Doctor's New Genetic Tools." Learn.Genetics 10 July 2015 <http://learn.genetics.utah.edu/content/pharma/intro/> Chicago format: Genetic Science Learning Center, "Your Doctor's New Genetic Tools," Learn.Genetics, 22 June 2014, <http://learn.genetics.utah.edu/content/pharma/intro/> (10 July 2015)

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What is pharmacogenomics? – Genetics Home Reference

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Pharmacogenomics is the study of how genes affect a persons response to drugs. This relatively new field combines pharmacology (the science of drugs) and genomics (the study of genes and their functions) to develop effective, safe medications and doses that will be tailored to a persons genetic makeup.

Many drugs that are currently available are one size fits all, but they dont work the same way for everyone. It can be difficult to predict who will benefit from a medication, who will not respond at all, and who will experience negative side effects (called adverse drug reactions). Adverse drug reactions are a significant cause of hospitalizations and deaths in the United States. With the knowledge gained from the Human Genome Project, researchers are learning how inherited differences in genes affect the bodys response to medications. These genetic differences will be used to predict whether a medication will be effective for a particular person and to help prevent adverse drug reactions.

The field of pharmacogenomics is still in its infancy. Its use is currently quite limited, but new approaches are under study in clinical trials. In the future, pharmacogenomics will allow the development of tailored drugs to treat a wide range of health problems, including cardiovascular disease, Alzheimer disease, cancer, HIV/AIDS, and asthma.

The National Institute of General Medical Sciences offers a list of Frequently Asked Questions about Pharmacogenomics.

A list of Frequently Asked Questions about Pharmacogenomics is also offered by the National Human Genome Research Institute.

Additional information about pharmacogenetics is available from the Centre for Genetics Education as well as Genes In Life.

The Smithsonian National Museum of Natural Historys exhibit Genome: Unlocking Lifes Code discusses the utility of pharmacogenomics.

The Genetic Science Learning Center at the University of Utah offers an interactive introduction to pharmacogenomics. Another interactive tutorial is available from the PHG Foundation.

The American Medical Association explains what pharmacogenomics is and provides a list of practical applications.

The National Genetics and Genomics Education Centre of the National Health Service (UK) provides information about predicting the effects of drugs based on a persons genes.

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Pharmacogenomics – Wikipedia, the free encyclopedia

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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.[1][2][3] 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.[4][5][6]

Pharmacogenomics aims to develop rational means to optimize drug therapy, with respect to the patients' genotype, to ensure maximum efficacy with minimal adverse effects.[7] 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 patients genes, the functionality of these genes, and how this may affect the efficacy of the patients current and/or future treatments (and where applicable, provide an explanation for the failure of past treatments).[4] Such approaches promise the advent of "personalized medicine"; in which drugs and drug combinations are optimized for each individual's unique genetic makeup.[8][9] Whether used to explain a patients 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.[10] Sequencing provides many more data points, including detection of mutations that prematurely terminate the synthesized protein (early stop codon).[10]

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.[11][12] Although the first official publication dates back to 1961,[13] 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.[1][14] 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.[15] The term pharmacogenomics first began appearing around the 1990s.[11]

There are several known genes which are largely responsible for variances in drug metabolism and response. The focus of this article will remain on the genes that are more widely accepted and utilized clinically for brevity.

The most prevalent drug-metabolizing enzymes (DME) are the Cytochrome P450 (CYP) enzymes. The term Cytochrome P450 was coined by Omura and Sato in 1962 to describe the membrane-bound, heme-containing protein characterized by 450nm spectral peak when complexed with carbon monoxide.[16] The human CYP family consists of 57 genes, with 18 families and 44 subfamilies. CYP proteins are conveniently arranged into these families and subfamilies on the basis of similarities identified between the amino acid sequences. Enzymes that share 35-40% identity are assigned to the same family by an Arabic numeral, and those that share 55-70% make up a particular subfamily with a designated letter.[17] For example, CYP2D6 refers to family 2, subfamily D, and gene number 6.

From a clinical perspective, the most commonly tested CYPs include: CYP2D6, CYP2C19, CYP2C9, CYP3A4 and CYP3A5. These genes account for the metabolism of approximately 80-90% of currently available prescription drugs.[18][19] The table below provides a summary for some of the medications that take these pathways.

Also known as debrisoquine hydroxylase (named after the drug that led to its discovery), CYP2D6 is the most well-known and extensively studied CYP gene.[22] It is a gene of great interest also due to its highly polymorphic nature, and involvement in a high number of medication metabolisms (both as a major and minor pathway). More than 100 CYP2D6 genetic variants have been identified.[21]

Discovered in the early 1980s, CYP2C19 is the second most extensively studied and well understood gene in pharmacogenomics.[20] Over 28 genetic variants have been identified for CYP2C19,[23] of which affects the metabolism of several classes of drugs, such as antidepressants and proton pump inhibitors.[24]

CYP2C9 constitutes the majority of the CYP2C subfamily, representing approximately 20% of the liver content. It is involved in the metabolism of approximately 10% of all drugs, which include medications with narrow therapeutic windows such as warfarin and tolbutamide.[24][25] There are approximately 57 genetic variants associated with CYP2C9.[23]

The CYP3A family is the most abundantly found in the liver, with CYP3A4 accounting for 29% of the liver content.[20] These enzymes also cover between 40-50% of the current prescription drugs, with the CYP3A4 accounting for 40-45% of these medications.[12]CYP3A5 has over 11 genetic variants identified at the time of this publication.[23]

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Pharmacogenomics - Wikipedia, the free encyclopedia

Pharmacogenomics – American Medical Association

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What is pharmacogenomics? Pharmacogenomics is the study of genetic variations that influence individual response to drugs. Knowing whether a patient carries any of these genetic variations can help prescribers individualize drug therapy, decrease the chance for adverse drug events, and increase the effectiveness of drugs.

Pharmacogenomics combines traditional pharmaceutical sciences such as biochemistry with with an understanding of common DNA variations in the human genome. The most common variations in the human genome are called single nucleotide polymorphisms (SNPs). There is estimated to be approximately 11 million SNPs in the human population, with an average of one every 1,300 base pairs. An individual's response to a drug is often linked to these common DNA variations. In a similar manner, susceptibility to certain diseases is also influenced by common DNA variations. Currently, much of the research in the field of pharmacogenomics is focused on genes encoding either metabolic enzymes that can alter a drug's activity or defective structural proteins that result in increased susceptibility to disease.

Anticipated benefits of pharmacogenomics Pharmacogenomicshas the potential toprovide tailored drug therapy based on genetically determined variation in effectiveness and side effects. This will mean:

Practical applications of pharmacogenomics today Following are links to scientific abstracts that discuss practical applications of pharmacogenomics in cancer, depression, cardiovascular disease and drug metabolism:

Economic issues from molecule to marketplace Pharmacogenomics eventually can lead to an overall decrease in the cost of health care because of decreases in:

Additional resources

The Department of Energy (DOE) Human Genome Project Information - pharmacogenomics

International HapMap Project

National Institute of General Medical Science

Listing of federally-sponsored clinical trials in US

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Pharmacogenomics - American Medical Association

FAQ About Pharmacogenomics

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Frequently Asked Questions About Pharmacogenomics

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Pharmacogenomics uses information about a person's genetic makeup, or genome, to choose the drugs and drug doses that are likely to work best for that particular person. This new field combines the science of how drugs work, called pharmacology, with the science of the human genome, called genomics.

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Until recently, drugs have been developed with the idea that each drug works pretty much the same in everybody. But genomic research has changed that "one size fits all" approach and opened the door to more personalized approaches to using and developing drugs.

Depending on your genetic makeup, some drugs may work more or less effectively for you than they do in other people. Likewise, some drugs may produce more or fewer side effects in you than in someone else. In the near future, doctors will be able to routinely use information about your genetic makeup to choose those drugs and drug doses that offer the greatest chance of helping you.

Pharmacogenomics may also help to save you time and money. By using information about your genetic makeup, doctors soon may be able to avoid the trial-and-error approach of giving you various drugs that are not likely to work for you until they find the right one. Using pharmacogenomics, the "best-fit" drug to help you can be chosen from the beginning.

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Doctors are starting to use pharmacogenomic information to prescribe drugs, but such tests are routine for only a few health problems. However, given the field's rapid growth, pharmacogenomics is soon expected to lead to better ways of using drugs to manage heart disease, cancer, asthma, depression and many other common diseases.

One current use of pharmacogenomics involves people infected with the human immunodeficiency virus (HIV). Before prescribing the antiviral drug abacavir (Ziagen), doctors now routinely test HIV-infected patients for a genetic variant that makes them more likely to have a bad reaction to the drug.

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Pharmacogenomics – Learn Genetics

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What is Pharmacogenomics?

Why do people vary in their responses to prescribed medications, both with respect to how well the drug works and in their adverse reactions to it? The answer may lie in our genes. Scientists, doctors, and the pharmaceutical industry are working to customize medical treatments to suit our genetic signatures. The study of how our genetic variations interface with disease risk and responses to drugs is called pharmacogenomics.

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Investigate a pharmacogenetic test that is being used in the clinic today.

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See how tiny variations in a person's DNA can help predict drug response or disease risk.

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Consider how pharmacogenetics might remake the drug development process.

Supported by a Science Education Partnership Award (SEPA) Grant No. R25RR023288 from the National Center for Research Resources, a component of the NIH. The contents provided here are solely the responsibility of the authors and do not necessarily represent the official views of NIH.

APA format: Genetic Science Learning Center (2014, June 22) Pharmacogenomics. Learn.Genetics. Retrieved May 20, 2015, from http://learn.genetics.utah.edu/content/pharma/ MLA format: Genetic Science Learning Center. "Pharmacogenomics." Learn.Genetics 20 May 2015 <http://learn.genetics.utah.edu/content/pharma/> Chicago format: Genetic Science Learning Center, "Pharmacogenomics," Learn.Genetics, 22 June 2014, <http://learn.genetics.utah.edu/content/pharma/> (20 May 2015)

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Optimized Medication Outcomes through Pharmacogenomics Part I: Basic Principles – Video

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Optimized Medication Outcomes through Pharmacogenomics Part I: Basic Principles
The sometimes dramatic variation in a patient #39;s response to medications has long been recognized by physicians. Inter-individual differences in medication efficacy and safety profiles have...

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