Pharmacogenomics - Scope and Future

Khushbu, Certainly drug development and testing benefits from pharmacogenomics mainly in economic way (cost).
For example,SNP screenings will benefit drug development and testing because pharmaceutical companies could exclude from clinical trials those people whose pharmacogenomic screening would show that the drug being tested would be harmful or ineffective for them. Excluding these people will increase the chance that a drug will show itself useful to a particular population group and will thus increase the chance that the same drug will make it into the marketplace. Pre-screening clinical trial subjects should also allow the clinical trials to be smaller, faster, and therefore less expensive; therefore, the consumer could benefit in reduced drug costs. Finally, the ability to assess an individual's reaction to a drug before it is prescribed will increase a physician's confidence in prescribing the drug and the patient's confidence in taking the drug, which in turn should encourage the development of new drugs tested in a like manner.
Coming to future, it certainly gives cost effective drugs (lower cost) and safer,efficacy and accurate drugs.
links: http://www.ncbi.nlm.nih.gov/

Bhawna, can you ask the question clearly, am unable to understand your question that, "pharmacogenomics is linked with modified nucleic acid" but actually it is the study of genitic variation with response to the drug action and you also wrote "they are responsible for causing dangerous reactions in the body" here they means "modified nucleic acid or pharmacogenomics or drugs" ?
Also please specify the dangerous reactions you mentioned.
Hoping your question again so that i can clarify your doubts. Thank you

Good evening sir,
sir before talking about the kits, i would like to say about techniques used for identifying the genetic polymorhisms, A preferred technique involves Restriction Enzyme Digestion (RED) and is based upon the fact that polymorphisms can lead to the production of different sized DNA fragments following treatment with a restriction enzyme (because of the introduction or deletion of a restriction site by the mutation causing the polymorphism). These fragments may be visualised on gels and the polymorphism or mutant identified based upon the number and size (i.e. distance moved on the gel) of the fragments from a DNA sample derived from a subject.
Preferably the DNA comprising the Zf9 gene and/or regulatory elements thereof is amplified prior to detection of the polymorphism This amplification is preferably by means of the polymerase chain reaction (PCR). For instance a preferred method according to the invention known as the PCR-restriction fragment length polymorphism method (PCR-RFLP) involves PCR amplification of DNA containing the polymorphism prior to RED and subsequent analysis.
Apart this, there are some more techniques used and coming to kits, The commercially available kits include: Cy5™ Thermo Sequenase™ dye terminator kit—Amersham Pharmacia Biotech.
Preferably the kit comprises of:1) PCR primers for amplifying genetic polymorphisms.
2) Control DNA samples of known genotype for each polymorphism.
3) A suitable restriction enzyme for generating fragments of the DNA sample.
4) A data card outlining linkage between a particular polymorphism and a disease.
5) Protocols for PCR amplification, restriction enzyme digestion of PCR products and agarose gel electrophoresis of DNA fragments.
6) Relevant buffers.
7) Suitable reaction vessels, centrifuge tubes.
Not all cases physicians using these for individualizing dosage regimen but in few cases for example: polymorphisms in the uridine diphosphoglucuronosyl transferase 1A1 (UGT 1A1) gene: the TATA box polymorphism and UGT 1A1 G71R and Y486D mutations in the coding sequence, the main mutations characterizing Gilbert’s syndrome, as predictors of severe toxic event occurrence after irinotecan (CPT-11) administration. Therefore, we set up a rapid, sensitive, and reliable technique in routine practice to detect before CPT-11 treatment, the at-risk patients.
The method we set up is suitable for the detection of UGT 1A1polymorphism in routine practice before irinotecan treatment. It could help to detect the patients homozygous or heterozygous for Gilbert’s syndrome, at-risk of CPT 11-induced toxicity, and thus could help to individualize the dose to optimize efficacy and limit toxicity.
links include:
http://www.freepatentsonline.com/
http://clincancerres.aacrjournals.org/content/
linkinghub.elsevier.com/
http://www.genetic-future.com/

Richa rajan, Pharmacogenomics in India is in developing stage and requires lot of funds and looking future for personalized medicine. It is a new field and has good scope, as it is very essential to know what kind of toxicity and efficacy a drug has on the human body. The subject will focus on the effect of drugs on an individual basis as every individual has a different kind of metabolism. Though we have the required instruments and equipment in the Biotechnology and Microbiology departments, we need some streamlining equipment before a great future and success of this field in India.
At present many colleges are trying to include pharmacogenomics as a academic course, for example MSU (university) has decided to introdue as a PG course. MSU has received the seed money from the Centre under the 11th Five-Year Plan to start the course in Pharmacogenomics and Clinical Research.
Also many biotechnology scientists are recieving funds to study on pharmacogenomics.

Hi, first of all I would like to correct your statement that, how drug is responsible for variation in genes in patient? But actually genes are responsible for variation in drug response. And coming to mode of action it will be specific to a particular individual and particular disease, all that is, it depends on the particular genes. Especially during embryonic condition the response to a drug varies.

Herceptin reduces the risk of death significantly if given to appropriate breast cancer patients after surgery and chemotherapy, a trial has indicated.
While it is not suitable for all patients, up to a quarter of women with breast cancer have the type of disease that it is designed to treat. Earlier trials have shown that it works, as well as raising some doubts about its side-effects.
The new trial, the Herceptin Adjuvant (Hera) study was designed to compare the outcomes for women treated with Herceptin for either one or two years after surgery and chemotherapy with those who had the same initial treatments but were then simply observed.
Herceptin is a targeted drug that is effective in women whose cancers express the protein HER-2. It offers no advantages to other women with different breast cancer types

Hi sirisha, Yes there will be 100% effective treatment through pharmacogenomics because we are treating the specific genes which are responsible for causing disease.
Herceptin have some side effects but mostly in case of simultaneous use of Herceptin therapy and Chemotherapy.
However, not everyone who takes the medication will experience side effects. In fact, most people tolerate it quite well. If side effects do occur, in most cases, they are minor and either require no treatment or are easily treated by you or your healthcare provider.
It is important to discuss potential treatment benefits and risks with doctors and to have realistic expectations of Herceptin therapy before using it.

Mr.Dixon , thanks for your comment and coming to answer part: Pharmacogenomics certainly decrease the cost of development of a drug to a disease because, after finding the causative gene/genes in developing a specific disease, then the specific drug is developed by targeting only that specific gene by having a thorough knowledge on gene and the disease it causing.

Hi Hemangi,thanks for your comments: 1) Techniques used in pharmacogenomics are many, some of them include ( as mentioned )Hap map project, Gene markers, DNA chips, Geno typing, Human genome sequencing and the main objective of these include directly/indirectly give complete information of human genome and helps in identifying the specific gene/genes which results in specific disease. A complete pictorial representation in one of my slides gives you the knowledge of how the genes show a response to a drug (pharmacogenomics).
2) In my reference source i provided the links and others include the books on pharmacogenomics through google ebooks and google scholar.
3) Herceptin for treating breast cancer, Gleevec for treatment of chronic myeloid leukemia (CML), a cancer of white blood cells, and for the treatment of a rare form of stomach cancer called gastrointestinal stromal tumor. Jantoven for treatment/preventing of harmful blood clots as a anticoagulant.Thank you

Sir,
I completly agree that millions of SNPs must be identified and analyzed to determine their involvement in drug response.But according to my statement (specific person specific gene specific disease specific drug is the success of pharmacogenomics) means that a dominant gene is responsible for disease.
On average, people probably carry from 5 to 10 variant or disease genes in their cells. Problems arise when the disease gene is dominant or when the same recessive disease gene is present on both chromosomes in a pair. Problems can also occur when several variant genes interact with each other — or with the environment — to increase susceptibility to diseases.If a person carries the dominant gene for a disease, he or she will usually have the disease and each of the person's children will have a 1 in 2 (50%) chance of inheriting the gene and getting the disease so we can target that disease by targeting that specific dominant gene (sp.gene sp.disease sp.drug).
For example diseases caused by a dominant gene include achondroplasia, Marfan syndrome, and Huntington disease.
You asked that is it economically feasible? Absolutely feasible on condition that, to achieve a great success in pharmacogenomics.
You also asked how extent this can be considered rationale? Through my above explanation i certainly consider it should be taken as rationale.
links :
http://www.nci.nih.gov
http://kidshealth.org