Genetic tests that can help predict and refine a patient's response to drug therapy may be the first big thing in personalized medicine. But the vast majority of physicians don't know how to use them, a new survey finds.
Individual genetic variations can affect how a patient will respond to many antidepressants, pain medications, cardiovascular medicines and certain drugs that treat cancers and gastrointestinal ailments. In all, roughly one in four American patients take medications whose effectiveness could be tweaked or predicted by a pharmacogenetic test. And purveyors of genomic testing services and devices are rushing to provide tests for them all.
A survey of more than 10,000 U.S. physicians undertaken by the American Medical Assn. and the pharmacy benefits manager Medco Healthcare Solutions Inc. found that just more than one in four had had any type of education in the use of genetic testing to guide medication decisions. And only 1 in 10 felt he or she had the necessary training and knowledge to put pharmacogenetic testing to good use in treating patients. Some 13% had ordered or recommended a genetic test for a patient in the last six months. But twice that many said they would do so in the next six months.
Genes that regulate liver enzymes can have a particularly powerful influence on a patient's response to a medication. Scientists believe that one such enzyme may be responsible for governing the way patients respond to some 30% of all drugs used today. In oncology, a test can help predict if breast cancer patients will respond to the drug tamoxifen. And cancer drugs in the development pipeline are expected overwhelmingly to be administered with the guidance of genetic tests. Genetic tests also can help reduce unwanted side effects; the blood thinner warfarin, for instance, can cause blood clots or serious bleeds in some patients with an identified genetic variance, and physicians are increasingly testing those on a blood-thinning regimen in an effort reduce such risks.
"It's clear there's wide acceptance" on physicians' part for the role that genetic testing can play in guiding medication decisions, said Dr. Robert Epstein, Medco's chief medical officer, who briefed physicians and researchers on the survey at the annual meeting of the American Society for Human Genetics on Thursday. But the AMA and other groups must step up efforts to educate physicians in the use of these tests, added Epstein. "With the number of new drugs coming to market with a companion diagnostic, it's paramount that this education takes place."
Showing posts with label Genetics. Show all posts
Showing posts with label Genetics. Show all posts
Friday, October 23, 2009
Thursday, October 8, 2009
IBM using nanotech to read DNA
Scientists at IBM are using a combination of nanotechnology and microchips to map out personal genetic code -- a development that could significantly improve the process of diagnosing and treating diseases.
Merging biology with computer technology, researchers at IBM are working on a project that aims to make it easier to decode human DNA, and thus help scientists discover and test new medicines and medical techniques. And, IBM says, a faster and less expensive way to obtain genetic information would help doctors better understand their patients' predisposition to diseases.
The ultimate goal of IBM's project is to create process that could read, or sequence, a person's genome at a cost of $100 to $1,000. In comparison, the first sequencing ever done by the Human Genome Project cost $3 billion, according to IBM.
"The technologies that make reading DNA fast, cheap and widely available have the potential to revolutionize bio-medical research and herald an era of personalized medicine," said IBM research scientist Gustavo Stolovitzky, in a statement today. "Ultimately, it could improve the quality of medical care by identifying patients who will gain the greatest benefit from a particular medicine and those who are most at risk of adverse reaction."
IBM reported today that its researchers have drilled nano-sized holes, or nanopores, into microchips. When DNA strands are passed through the holes, the chips can sequence the genes.
Researchers said one of their challenges has been to figure out how to control the speed of the DNA strand's movement through the tiny nanopore. It needs to move slowly through the hole in order for sensors in the chip to be able to read the sequencing.
IBM reported that its scientists used a multi-layer nanostructure to surround the nanopore. The structure creates an electrical field inside the nanopore, which traps the DNA strand and should allow scientists to have minute control over the speed at which the strand moves through the hole.
Combining DNA with nanotechnology is an idea that's been getting some traction.
Just two months ago, IBM announced that it was using a combination of DNA molecules and nanotechnology to create tiny circuits that could form the basis of smaller, more powerful and energy-efficient computer chips that also are easier and cheaper to manufacture.
The DNA molecules would serve as scaffolding on which carbon nanotubes could assemble themselves into precise patterns. IBM said the process could help chip manufacturers move from 45-nanometer processor technology to 22nm or smaller.
And last winter, researchers at MIT found a way to use a combination of nanotechnology and DNA to fight cancerous tumors. The university announced that a group of scientists there had developed sensors made out of carbon nanotubes that were wrapped in DNA. The sensors then were placed inside living cells to determine whether chemotherapy drugs were reaching their targets or attacking healthy cells.
Merging biology with computer technology, researchers at IBM are working on a project that aims to make it easier to decode human DNA, and thus help scientists discover and test new medicines and medical techniques. And, IBM says, a faster and less expensive way to obtain genetic information would help doctors better understand their patients' predisposition to diseases.
The ultimate goal of IBM's project is to create process that could read, or sequence, a person's genome at a cost of $100 to $1,000. In comparison, the first sequencing ever done by the Human Genome Project cost $3 billion, according to IBM.
"The technologies that make reading DNA fast, cheap and widely available have the potential to revolutionize bio-medical research and herald an era of personalized medicine," said IBM research scientist Gustavo Stolovitzky, in a statement today. "Ultimately, it could improve the quality of medical care by identifying patients who will gain the greatest benefit from a particular medicine and those who are most at risk of adverse reaction."
IBM reported today that its researchers have drilled nano-sized holes, or nanopores, into microchips. When DNA strands are passed through the holes, the chips can sequence the genes.
Researchers said one of their challenges has been to figure out how to control the speed of the DNA strand's movement through the tiny nanopore. It needs to move slowly through the hole in order for sensors in the chip to be able to read the sequencing.
IBM reported that its scientists used a multi-layer nanostructure to surround the nanopore. The structure creates an electrical field inside the nanopore, which traps the DNA strand and should allow scientists to have minute control over the speed at which the strand moves through the hole.
Combining DNA with nanotechnology is an idea that's been getting some traction.
Just two months ago, IBM announced that it was using a combination of DNA molecules and nanotechnology to create tiny circuits that could form the basis of smaller, more powerful and energy-efficient computer chips that also are easier and cheaper to manufacture.
The DNA molecules would serve as scaffolding on which carbon nanotubes could assemble themselves into precise patterns. IBM said the process could help chip manufacturers move from 45-nanometer processor technology to 22nm or smaller.
And last winter, researchers at MIT found a way to use a combination of nanotechnology and DNA to fight cancerous tumors. The university announced that a group of scientists there had developed sensors made out of carbon nanotubes that were wrapped in DNA. The sensors then were placed inside living cells to determine whether chemotherapy drugs were reaching their targets or attacking healthy cells.
Thursday, August 27, 2009
Major Genetic Determinant Of Psoriasis
A specific genetic region that has been increasingly identified as the strongest genetic link to psoriasis has an even more significant role in the chronic skin disease than has been suspected, University of Utah medical researchers show in a new study.
n the Aug. 13 issue of PLoS Genetics, researchers in the U School of Medicine's Department of Dermatology confirm that the presence of HLA-Cw*0602, a gene variation or allele on chromosome 6 found to be associated with psoriasis by numerous investigators, is the "major genetic determinant" of psoriasis, but that other nearby genetic variations also play an independent role in contributing to the disease
"The HLA-Cw*0602 gene variation stands alone as a high risk for psoriasis," said Gerald G. Krueger, M.D., professor of dermatology, Benning Presidential Endowed Chair holder, and a co-author on the study. "A major question has been: are there other genetic variations in this region that associate with psoriasis?"
The study reported in PLoS Genetics identifies two other genetic variations on chromosome 6 that also have significant association with psoriasis. People who have all three genetic variations are nearly nine times more at risk for psoriasis.
Psoriasis is a chronic disease that causes red scaly patches on the skin and affects up to 7.5 million people in the United States. About 25 percent of subjects with the disease also develop a painful inflammation of the joints called psoriatic arthritis.
University researchers, led by first author Bing-Jian Feng, Ph.D., postdoctoral fellow, and senior author David E. Goldgar, Ph.D., research professor of dermatology in the U of U School of Medicine, reached their conclusion after an expanded analysis of data from a study published earlier this year by investigators at Utah in collaboration with colleagues from the University of Michigan and Washington University.
That study (Nature Genetics, Jan. 25) used new technology to scan nearly 500,000 genetic variants (single nucleotide polymorphisms or SNPs) in 1,359 people with psoriasis and 1,400 without to find those with the strongest relationship with psoriasis. After identifying 18 SNPs with the highest associations with psoriasis, the researchers expanded the study to include 5,048 people with psoriasis and 5,051 without the disease. From that, they identified four new genetic "hotspots" for psoriasis and confirmed two others that Krueger and colleagues identified in previous studies.
Using the data from the Nature Genetics study, Feng, Goldgar, and colleagues employed two statistical methods, imputation and logistic regression analysis, to determine with a much greater degree of accuracy those genes that have the highest association with psoriasis. Using imputation they were able to reliably predict the *0602 status of all subjects in the recent Nature Genetics study. This did two things; first, it increased the confidence that *0602 is the major genetic variation on this chromosome and, second, it permitted them to determine if there was any other associated genetic variation in this region.
Removing the strong effect of *0602 resulted in the identification of two other loci (fixed position on a chromosome) that are independently associated with psoriasis (MICA/HLA-B and c6orf10). These two loci increased the risk for the disease by 1.23 and 1.6 times, respectively. However, when all three genetic variations that Feng, Goldgar, and colleagues report are present, the risk for psoriasis is 8.9 times higher than when none of these is present.
To confirm the results, the researchers examined an independent patient population in China, which corroborated their conclusions.
While *0602 and the associated, but independent, genetic variations reported have a major genetic contribution to psoriasis, many other genes undoubtedly play a role, according to Krueger. The number of DNA sites discovered to have strong associations with psoriasis has more than doubled in the past two years.
n the Aug. 13 issue of PLoS Genetics, researchers in the U School of Medicine's Department of Dermatology confirm that the presence of HLA-Cw*0602, a gene variation or allele on chromosome 6 found to be associated with psoriasis by numerous investigators, is the "major genetic determinant" of psoriasis, but that other nearby genetic variations also play an independent role in contributing to the disease
"The HLA-Cw*0602 gene variation stands alone as a high risk for psoriasis," said Gerald G. Krueger, M.D., professor of dermatology, Benning Presidential Endowed Chair holder, and a co-author on the study. "A major question has been: are there other genetic variations in this region that associate with psoriasis?"
The study reported in PLoS Genetics identifies two other genetic variations on chromosome 6 that also have significant association with psoriasis. People who have all three genetic variations are nearly nine times more at risk for psoriasis.
Psoriasis is a chronic disease that causes red scaly patches on the skin and affects up to 7.5 million people in the United States. About 25 percent of subjects with the disease also develop a painful inflammation of the joints called psoriatic arthritis.
University researchers, led by first author Bing-Jian Feng, Ph.D., postdoctoral fellow, and senior author David E. Goldgar, Ph.D., research professor of dermatology in the U of U School of Medicine, reached their conclusion after an expanded analysis of data from a study published earlier this year by investigators at Utah in collaboration with colleagues from the University of Michigan and Washington University.
That study (Nature Genetics, Jan. 25) used new technology to scan nearly 500,000 genetic variants (single nucleotide polymorphisms or SNPs) in 1,359 people with psoriasis and 1,400 without to find those with the strongest relationship with psoriasis. After identifying 18 SNPs with the highest associations with psoriasis, the researchers expanded the study to include 5,048 people with psoriasis and 5,051 without the disease. From that, they identified four new genetic "hotspots" for psoriasis and confirmed two others that Krueger and colleagues identified in previous studies.
Using the data from the Nature Genetics study, Feng, Goldgar, and colleagues employed two statistical methods, imputation and logistic regression analysis, to determine with a much greater degree of accuracy those genes that have the highest association with psoriasis. Using imputation they were able to reliably predict the *0602 status of all subjects in the recent Nature Genetics study. This did two things; first, it increased the confidence that *0602 is the major genetic variation on this chromosome and, second, it permitted them to determine if there was any other associated genetic variation in this region.
Removing the strong effect of *0602 resulted in the identification of two other loci (fixed position on a chromosome) that are independently associated with psoriasis (MICA/HLA-B and c6orf10). These two loci increased the risk for the disease by 1.23 and 1.6 times, respectively. However, when all three genetic variations that Feng, Goldgar, and colleagues report are present, the risk for psoriasis is 8.9 times higher than when none of these is present.
To confirm the results, the researchers examined an independent patient population in China, which corroborated their conclusions.
While *0602 and the associated, but independent, genetic variations reported have a major genetic contribution to psoriasis, many other genes undoubtedly play a role, according to Krueger. The number of DNA sites discovered to have strong associations with psoriasis has more than doubled in the past two years.
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