Gene Therapy Research

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Epigenetics explains rheumatism? Genes and their regulatory 'tags' conspire to promote rheumatoid arthritis

January 21st, 2013

Jan. 20, 2013 In one of the first genome-wide studies to hunt for both genes and their regulatory "tags" in patients suffering from a common disease, researchers have found a clear role for the tags in mediating genetic risk for rheumatoid arthritis (RA), an immune disorder that afflicts an estimated 1.5 million American adults. By teasing apart the tagging events that result from RA from those that help cause it, the scientists say they were able to spot tagged DNA sequences that may be important for the development of RA. And they suspect their experimental method can be applied to predict similar risk factors for other common, noninfectious diseases, like type II diabetes and heart ailments.

In a report published in Nature Biotechnology Jan. 20, the researchers at Johns Hopkins and the Karolinska Institutet say their study bridges the gap between whole-genome genetic sequencing and diseases that have no single or direct genetic cause. Most genetic changes associated with disease do not occur in protein-coding regions of DNA, but in their regulatory regions, explains Andrew Feinberg, M.D., M.P.H., a Gilman scholar, professor of molecular medicine and director of the Center for Epigenetics at the Johns Hopkins University School of Medicine's Institute for Basic Biomedical Sciences. "Our study analyzed both and shows how genetics and epigenetics can work together to cause disease," he says.

Rheumatoid arthritis is a debilitating disease that causes inflammation, stiffness, pain and disfigurement in joints, especially the small joints of the hands and feet. It is thought to be an autoimmune disease, meaning that the body's immune system attacks its own tissues, an assault led primarily by white blood cells. According to Feinberg, several DNA mutations are known to confer risk for RA, but there seem to be additional factors that suppress or enhance that risk. One probable factor involves chemical "tags" that attach to DNA sequences, part of a so-called epigenetic system that helps regulate when and how DNA sequences are "read," how they're used to create proteins and how they affect the onset or progress of disease.

To complicate matters, Feinberg notes, the attachment of the tags to particular DNA sequences can itself be regulated by genes. "The details of what causes a particular sequence to be tagged are unclear, but it seems that some tagging events depend on certain DNA sequences. In other words, those tagging events are under genetic control," he says. Other tagging events, however, seem to depend on cellular processes and environmental changes, some of which could be the result, rather than the cause, of disease.

To tease apart these two types of tagging events, the researchers catalogued DNA sequences and their tagging patterns in the white blood cells of more than 300 people with and without one form of RA.

The team then began filtering out the tags that did not appear to affect RA risk. For example, if tags were seen on the same DNA sequence in those with and without RA, it was assumed that the tags at those sites were irrelevant to the cause or development of the disease. Then, from among the RA-relevant tags, they narrowed in on tags whose placement seemed to be dependent on DNA sequence. Finally, they made sure that the DNA sequences identified were themselves more prevalent in patients with RA. In this way, they created a list of DNA sequences associated with altered DNA tagging patterns, both of which were associated with RA.

Ultimately, the team identified 10 DNA sites that were tagged differently in RA patients and whose tagging seemed to affect risk for RA. Nine of the 10 sites were within a region of the genome known to play an important role in autoimmune diseases, while the 10th was on a gene that had never before been associated with the disease. "Since RA is a disease in which the body's immune system turns on itself, current treatments often involve suppressing the entire immune system, which can have serious side effects," Feinberg says. "The results of this study may allow clinicians to instead directly target the culpable genes and/or their tags."

"Our method allows us to predict which tagging sites are most important in the development of a disease. In this study, we looked for tagging sites under genetic control, but similar tags can be triggered by environmental exposures, like smoking, so there are many applications for this type of work," says Yun Liu, Ph.D., a lead researcher on the project.

The study also may shed light on how evolution works, explains Feinberg. "It seems that natural selection might not simply be selecting for an individual's current fitness level but also for the adaptability of future generations given an unknown future. We think that certain genetic sequences may be biologically beneficial and conserved over time because they increase the amount of variation found in tagging patterns, giving individuals a greater chance of adapting to environmental changes."

Other authors of the report include Martin J. Aryee, M. Daniele Fallin, Arni Runarsson and Margaret Taub of the Johns Hopkins University School of Medicine; and Leonid Padyukov, Espen Hesselberg, Lovisa Reinius, Nathalie Acevedo, Marcus Ronninger, Lementy Shchetynsky, Annika Scheynius, Juha Kere, Lars Alfredsson, Lars Klareskog and Tomas J. Ekstrm of the Karolinska Institutet, Sweden.

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Philanthropist gives Princess Margaret hospital $50-million to fight cancer

January 21st, 2013

In what is being billed as the largest private donation for cancer research in Canadian history, Princess Margaret Hospital announced a $50-million gift on Monday.

The money will support personalized medicine, a burgeoning field in which doctors use patients genetic information to diagnose disease and deliver customized treatments.

This gift literally is a game changer for cancer research, said Paul Alofs, president and CEO of Princess Margaret Cancer Foundation.

The $50-million donation, which has been pledged over 10 years, is from philanthropists Emmanuelle Gattuso and her husband, broadcast tycoon Allan Slaight. Ms. Gattuso is a breast cancer survivor who was treated at Princess Margaret in Toronto.

We believe that personalized cancer medicine will revolutionize the way that cancer patients are treated, Ms. Gattuso, 65, told a crowd of staff and journalists in the hospitals atrium.

The money will be used to hire more cancer specialists and support their research, said Benjamin Neel, the hospitals research director.

Their unprecedented $50-million donation will enable us to create a superfund to provide the necessary long-term sustainable funding to attract, support and retain the best and brightest scientists in the world, he said.

Princess Margaret Hospital is developing a model of personalized cancer medicine that focuses on earlier detection, more precise diagnosis, targeted treatment and better support for patients.

In 2009, Ms. Gattuso and Mr. Slaight donated $22-million to Princess Margaret to create a rapid diagnostic centre for breast cancer, which provides diagnoses and treatment plans in one day.

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Genetic basis of high-risk childhood cancer points to possible new drug treatment strategy

January 21st, 2013

Public release date: 20-Jan-2013 [ | E-mail | Share ]

Contact: Carrie Strehlau media@stjude.org 901-595-2295 St. Jude Children's Research Hospital

(MEMPHIS, Tenn. January 20, 2013) Research led by St. Jude Children's Research Hospital scientists has identified a possible lead in treatment of two childhood leukemia subtypes known for their dramatic loss of chromosomes and poor treatment outcomes.

The findings also provide the first evidence of the genetic basis for this high-risk leukemia, which is known as hypodiploid acute lymphoblastic leukemia (ALL). Normal human cells have 46 chromosomes, half from each parent, but hypodiploid ALL is characterized by fewer than 44 chromosomes. Chromosomes are highly condensed pieces of DNA, the molecule that carries the inherited instructions for assembling and sustaining a person. The research appears in the January 20 advance online edition of the scientific journal Nature Genetics.

The study, the largest ever focused on hypodiploid ALL, confirmed that this tumor has distinct subtypes distinguished by the number of chromosomes lost and the submicroscopic genetic alterations they harbor. Researchers found evidence suggesting more than one-third of patients with a subtype known as low hypodiploid ALL have Li-Fraumeni syndrome. Families with Li-Fraumeni syndrome harbor inherited mutations in the TP53 tumor suppressor gene and have a high risk of a range of cancers. Hypodiploid ALL had not previously been recognized as a common manifestation of Li-Fraumeni syndrome.

Researchers reported that the major hypodiploid subtypes are both sensitive to a family of compounds that block the proliferation of cancer cells. The compounds include drugs already used to treat other cancers. The subtypes are low hypodiploid ALL, characterized by 32 to 39 chromosomes, and near haploid ALL, which has 24 to 31 chromosomes.

"This study is a good example of the important insights that can be gained by studying the largest possible number of patients in as much detail as possible. This approach led us to key insights about these leukemia subtypes that we would otherwise have missed," said the study's senior and corresponding author, Charles Mullighan, MBBS(Hons), MSc, M.D., an associate member of the St. Jude Pathology Department. Mullighan is a Pew Scholar in Biomedical Sciences.

January 21st, 2013

Genome and Clinic in the Care of Renal Cell Carcinoma - by W. Kimryn Rathmell, MD, PhD
Uniting the Genome and Clinic to Advance the Science and Care of Renal Cell Carcinoma Lecture by W. Kimryn Rathmell, MD, PhD Associate Professor of Medicine and Genetics, UNC School of Medicine

By: TheOncologistJournal

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Genome and Clinic in the Care of Renal Cell Carcinoma - by W. Kimryn Rathmell, MD, PhD - Video

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BCA Represents Independent Blood Centers at Phacilitate Cell & Gene Therapy Forum

January 21st, 2013

Blood Centers of America, Inc. continues to drive market diversification into the cell therapy and regenerative medicine sectors.

West Warwick, RI (PRWEB) January 21, 2013

BCA will be hosting one-on-one meetings with senior executives of leading cell therapy and cell-based immunotherapy companies, participating in sessions and high-profile networking events, and showcasing BCA member capabilities in the event's 3-day tradeshow.

"Participating in what is often described as one of the leading cell therapy industry conferences of the year is a great way to launch our 2013 initiative to raise the profile of BCA in the cell therapy industry and engage in one-on-one discussions about what BCA has to offer companies in the cell therapy sector," stated BCA's newly appointed CEO, Bill Block.

"BCA is a network of centers geographically dispersed throughout North America with considerable experience in collecting, processing and distributing regulatory-compliant, clinical-grade biologial materials", continued Block. "We are keen to engage cell therapy leadership in a discussion about how we can leverage BCA member infastructure and capabilities in the development and processing of cell therapy products and their safe and cost-effective delivery to patients."

About BCA

BCA is a member-owned organization comprised of 37 independent blood centers geographically dispersed throughout the North America, providing more than 46% of the U.S. blood supply. Along with their core business of providing a substantial portion of U.S. blood supply, BCA members provide a myriad of other services in cell therapies, blood management, therapeutic apheresis, tissue and cord blood banking, etc.

BCA provides thousands of units of biological materials annually to life science researchers, clinicians, therapeutic companies, or companies doing medical device, diagnostic or therapeutic development work.

BCA assists cell therapy companies with securing reliable and compliant sources for the cells used in their therapeutic products and/or pre-clinical research. Where a client need exceeds the capacity of a single center, BCA can assist with putting in place a multi-center supply agreement around cell collections, processing, storage or other handling.

In 2012, BCA generated over $6 million in custom products and services to cell therapy companies including patient-donor collections for autologous cell therapies in clinical trial and commercial distribution.

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Study Sheds Light on the Complexity of Gene Therapy for Congenital Blindness

January 21st, 2013

New Discoveries Provide a Path to a More Complete Cure with Gene Therapy Treatment

Newswise PHILADELPHIA - Independent clinical trials, including one conducted at the Scheie Eye Institute at the Perelman School of Medicine, have reported safety and efficacy for Leber congenital amaurosis (LCA), a congenital form of blindness caused by mutations in a gene (RPE65) required for recycling vitamin A in the retina. Inherited retinal degenerative diseases were previously considered untreatable and incurable. There were early improvements in vision observed in the trials, but a key question about the long-term efficacy of gene therapy for curing the retinal degeneration in LCA has remained unanswered. Now, new research from the Scheie Eye Institute, published this week in the Proceedings of the National Academy of Sciences, finds that gene therapy for LCA shows enduring improvement in vision but also advancing degeneration of affected retinal cells, both in LCA patients and animal models of the same condition.

LCA disease from RPE65 mutations has two-components: a biochemical blockade leading to impaired vision, and a progressive loss of the light-sensing photoreceptor cells throughout life of the affected patient. The authors of the new study explain that until now gene therapy has been optimistically assumed, but not proven, to solve both disease components at the same time.

We all hoped that the gene injections cured both components re-establishing the cycle of vision and also preventing further loss of cells to the second disease component said Artur V. Cideciyan, PhD, lead author and co-investigator of an LCA clinical trial at Penn.

Yet, when the otherwise invisible cell layers of the retina were measured by optical imaging in clinical trial participants serially over many years, the rate of cell loss was the same in treated and untreated regions. In other words, gene therapy improved vision but did not slow or halt the progression of cell loss, commented Cideciyan.

These unexpected observations should help to advance the current treatment by making it better and longer lasting, commented co-author Samuel G. Jacobson, MD, PhD, principal investigator of the clinical trial. Slowing cell loss in different retinal degenerations has been a major research direction long before the current gene therapy trials. Now, the two directions must converge to ensure the longevity of the beneficial visual effects in this form of LCA.

In a continuation of the longstanding collaboration between the Scheie investigators and the Section of Ophthalmology at Penn School of Veterinary Medicine headed by co-authors Gustavo D. Aguirre, VMD, PhD, and William A. Beltran, DVM, PhD, studies were performed to test whether the clinical results were also present in the canine model of this LCA at disease stages equivalent to those in human patients.

Our gene treatment in this canine model provided the groundwork for the clinical trials of patients, and now we added data to confirm the fact that retinal degeneration does continue despite improved vision said Aguirre. The next step is to perform the relevant experiments to ask what intervention will stop the degeneration if added to the gene therapy.

These new findings contribute to greater clarity in understanding the natural history and complexity of the RPE65 form of LCA and provide a firm foundation for future investigations, said Joan M. OBrien MD, professor and chair of the Department of Ophthalmology and director of the Scheie Eye Institute.

Co-authors, in addition to the Penn researchers include, William W. Hauswirth, PhD, professor of Ophthalmology, at the University of Florida, Gainesville.

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Mrs. Lemons Ag Bio Commercial – Video

January 20th, 2013

Mrs. Lemons Ag Bio Commercial
Video about the cons of Genetic Engineering

By: Elias Guzman

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Mrs. Lemons Ag Bio Commercial - Video

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DM’s Guide: Spyro the Dragon – Beast Makers (HD) – Video

January 20th, 2013

DM #39;s Guide: Spyro the Dragon - Beast Makers (HD)
The Beast Makers dragons live in a kingdom covered with swamps and teeming with life. They create it, making all the different species that live in the Dragon Realms. The Beastmasters are quiet dragons who like to keep themselves to themselves. Gnasty Gnorc has filled the place up with some pretty bizarre Gnorcic creations of his own, and they all seem to have very large mouths... genetic engineering the Gnasty way.

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DM's Guide: Spyro the Dragon - Beast Makers (HD) - Video

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UN biotechnology institute seeks govt takeover

January 20th, 2013

Kalyan Ray New Delhi, Jan 18, 2013, DHNS

Primary fund source dried up due to the economic crisis in Europe

A United Nations institute on biotechnology research has approached the Indian government for take over as its primary fund source has dried up due to the economic crisis in Europe.

International Centre for Genetic Engineering and Biotechnology started as a UN Industrial Development Organisation project in 1987 and later became a full fledged UN centre in Delhi since 1994 with the objective of translating western biotechnology research into products for the developing world. An autonomous inter-governmental organisation with 61 member states, ICGEB now has three separate institutes in Delhi, Trieste and Cape Town.

In June 2012, the Italian government, which provided two-thirds of funding to the Indian component, decided to quit the Delhi centre triggering a financial crisis for the institute, which discovered malaria vaccine and dengue diagnostic kit among other research accomplishments in the last 15 years.

The Italian government requested (to ICGEB) that from 2014 all the components (Delhi, Trieste and Cape Town) be funded by the host governments exclusively while the contribution of member states will go to the extramural program that includes fellowships, courses and grants to all the member countries, ICGEB director general Francisco Baralle told Deccan Herald.

The cash-strapped institute with a sprawling campus in south Delhi has now approached the department of biotechnology under the central government with a request of taking charge of the institute.

This, in fact, will possibly be one of the first tasks cut out for the new DBT secretary K Vijayraghavan currently director of National Centre for Biological Sciences in Bangalore who is scheduled to take up his new assignment in the last week of January, sources said.

Vijayraghans predecessor in the DBT, M K Bhan, decided to set up a five-member panel to review technical and administrative issues involved in central governments taking over of an UN organisation. But the panels terms of reference are yet to be framed and is expected only after the new DBT secretary assume his charge.

While Indias contribution in ICGEB currently hovered around Rs 10 crore, it might go up to Rs 30 crore if DBT took over it as a national institute, said ICGEB director V S Chauhan.

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"Adventurous Female Human" Needed to Give Birth to Neandertal

January 20th, 2013

Many Germans are afraid of genetic engineering, according to Spiegel Online, the online offshoot of the German news magazine Der Spiegel, and Harvard's George Church doesn't do much to alleviate those fears.

In an online excerpt of a Q&A published in this week's Der Spiegel, Church talks about recreating Neandertals, engineering humans to live to 120, making people resistant to viruses, and exchanging DNA with other species.

"Like no one else, molecular biologist George Church represents a guild that is prepared to try out anything that can be done, unconditionally," Spiegel Online writes.

According to the site, Church is currently developing technology in his lab that can be used to make human cells similar to those of Neandertals. Eventually, an "adventurous female human" needs to be found as a surrogate mother for the first Neandertal baby, Church is cited as saying, and, from many individuals, "a kind of Neandertal culture" could arise that could gain "political significance."

Church doesn't understand "why many people should be so profoundly upset by these kinds of technologies," since the concept of biological species is currently changing anyway. Up until now, the notion has been that people cannot exchange DNA with other biological species. "But this barrier will fall," he says.

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Vulnerabilities in security of personal genetic information

January 20th, 2013

Jan. 17, 2013 Using only a computer, an Internet connection, and publicly accessible online resources, a team of Whitehead Institute researchers has been able to identify nearly 50 individuals who had submitted personal genetic material as participants in genomic studies.

Intent on conducting an exercise in "vulnerability research" -- a common practice in the field of information security -- the team took a multi-step approach to prove that under certain circumstances, the full names and identities of genomic research participants can be determined, even when their genetic information is held in databases in de-identified form.

"This is an important result that points out the potential for breaches of privacy in genomics studies," says Whitehead Fellow Yaniv Erlich, who led the research team. A description of the group's work is published in this week's Science magazine.

Erlich and colleagues began by analyzing unique genetic markers known as short tandem repeats on the Y chromosomes (Y-STRs) of men whose genetic material was collected by the Center for the Study of Human Polymorphisms (CEPH) and whose genomes were sequenced and made publicly available as part of the 1000 Genomes Project. Because the Y chromosome is transmitted from father to son, as are family surnames, there is a strong correlation between surnames and the DNA on the Y chromosome.

Recognizing this correlation, genealogists and genetic genealogy companies have established publicly accessible databases that house Y-STR data by surname. In a process known as "surname inference," the Erlich team was able to discover the family names of the men by submitting their Y-STRs to these databases. With surnames in hand, the team queried other information sources, including Internet record search engines, obituaries, genealogical websites, and public demographic data from the National Institute of General Medical Sciences (NIGMS) Human Genetic Cell Repository at New Jersey's Coriell Institute, to identify nearly 50 men and women in the United States who were CEPH participants.

Previous studies have contemplated the possibility of genetic identification by matching the DNA of a single person, assuming the person's DNA were cataloged in two separate databases. This work, however, exploits data between distant paternally-related individuals. As a result, the team notes that the posting of genetic data from a single individual can reveal deep genealogical ties and lead to the identification of a distantly-related person who may have no acquaintance with the person who released that genetic data.

"We show that if, for example, your Uncle Dave submitted his DNA to a genetic genealogy database, you could be identified," says Melissa Gymrek, a member of the Erlich lab and first author of the Science paper. "In fact, even your fourth cousin Patrick, whom you've never met, could identify you if his DNA is in the database, as long as he is paternally related to you."

Aware of the sensitivity of his work, Erlich emphasizes that he has no intention of revealing the names of those identified, nor does he wish to see public sharing of genetic information curtailed.

"Our aim is to better illuminate the current status of identifiability of genetic data," he says. "More knowledge empowers participants to weigh the risks and benefits and make more informed decisions when considering whether to share their own data. We also hope that this study will eventually result in better security algorithms, better policy guidelines, and better legislation to help mitigate some of the risks described."

To that end, Erlich shared his findings with officials at the National Human Genome Research Institute (NHGRI) and NIGMS prior to publication. In response, NIGMS and NHGRI moved certain demographic information from the publicly-accessible portion the NIGMS cell repository to help reduce the risk of future breaches. In the same issue of Science in which the Erlich study appears, Judith H. Greenberg and Eric D. Green, the Directors of NIGMS and NHGRI, and colleagues author a perspective on this latest research in which they advocate for an examination of approaches to balance research participants' privacy rights with the societal benefits to be realized from the sharing of biomedical research data.

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How are middle-aged women affected by burnout?

January 20th, 2013

Public release date: 17-Jan-2013 [ | E-mail | Share ]

Contact: Vicki Cohn vcohn@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, January 17, 2013Emotional exhaustion and physical and cognitive fatigue are signs of burnout, often caused by prolonged exposure to stress. Burnout can cause negative health effects including poor sleep, depression, anxiety, and cardiovascular and immune disorders. The findings of a 9-year study of burnout in middle-aged working women are reported in an article in Journal of Women's Health, a peer-reviewed publication from Mary Ann Liebert, Inc., publishers. The article is available free on the Journal of Women's Health website at http://www.liebertpub.com/jwh.

In the article "Development of Burnout in Middle-Aged Working Women: A Longitudinal Study," authors Annika Evolahti, PhD, Daniel Hultell, PhD, and Aila Collins, PhD, Karolinska Institute, Stockholm, Sweden, found that in contrast to previous research findings that showed burnout to be stable over time, they were able to cluster the women in the study into groups characterized by different developmental patterns of burnout. Some middle-aged women had high levels of burnout followed by recovery, whereas others had increasing, decreasing, or stable levels over a 9-year period. The authors explored how these patterns related to changes in work-related and other types of stress in the women's lives and individual personality factors.

"This important study expands our understanding of burnout in working women, in terms of both patterns of development and relation to various stressors and individual factors," says Susan G. Kornstein, MD, Editor-in-Chief of Journal of Women's Health, Executive Director of the Virginia Commonwealth University Institute for Women's Health, Richmond, VA, and President of the Academy of Women's Health.

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About the Journal

Journal of Women's Health, published monthly, is a core multidisciplinary journal dedicated to the diseases and conditions that hold greater risk for or are more prevalent among women, as well as diseases that present differently in women. The Journal covers the latest advances and clinical applications of new diagnostic procedures and therapeutic protocols for the prevention and management of women's healthcare issues. Tables of content and a sample issue may be viewed on the Journal of Women's Health website at http://www.liebertpub.com/jwh. Journal of Women's Health is the Official Journal of the Academy of Women's Health and the Society for Women's Health Research.

About the Academy

Academy of Women's Health (http://www.academyofwomenshealth.org) is an interdisciplinary, international association of physicians, nurses, and other health professionals who work across the broad field of women's health, providing its members with up-to-date advances and options in clinical care that will enable the best outcomes for their women patients. The Academy's focus includes the dissemination of translational research and evidence-based practices for disease prevention, diagnosis, and treatment of women across the lifespan.

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How hackers can unlock your genetic secrets

January 20th, 2013

Christine Cox / NBC News file

Researchers say genetic genealogy databases can be leveraged to unlock more sensitive genetic information.

By Alan Boyle, Science Editor, NBC News

Researchers have shown that it's possible to link your identity to supposedly secret genetic information about your predisposition to diseases, merely by analyzing family-tree databases and other publicly available information.

"It was quite surprising," said Yaniv Erlich, a genetic researcher at the Whitehead Institute for Biomedical Research. "When we got the first family, I was surprised. ... It's as if you opened a box that for a long time was locked."

Erlich led the research team whose work is being published in this week's issue of the journal Science. The team's study already has led to a tightening of security measures for federally sponsored genetic databases.

The security-cracking trick relies on the availability of genetic information linked to surnames in a variety of public family-tree databases. DNA samples from males can be tested to look at dozens of genetic markers on the Y-chromosome that change only rarely from generation to generation. If the markers from two individuals with the same surname are a close match, that's a tip-off that the two are closely related, even if they don't know each other.

Tens of thousands of people (including yours truly) make that information public in hopes that someone else will match up with their results. The genealogical markers aren't linked to disease or other specific traits. But under the right circumstances, they could provide an opening for links with other, more sensitive genetic information.

How the secrets were revealed Erlich and his colleagues conducted a three-step process to see how easy it'd be to use that opening. First, they analyzed anonymous Y-chromosome data from a public database for the 1000 Genomes Project, to come up with the DNA coding for markers that are used for genealogical purposes. Then they compared those markers against entries in the two largest family-tree databases, Ysearch and the Sorenson Molecular Genealogy Foundation.

The researchers said their analysis projected a success rate of 12 percent for recovering the surnames of U.S. Caucasian males. Another 5 percent would theoretically be linked up with the wrong surnames. They said upper- to middle-class Caucasian males were easier to identify, presumably because they're more likely to participate in the family-tree databases.

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Ground breaking research saves animals in hospital

January 20th, 2013

Brad Kelley/The Daily EvergreenDr. Katrina Mealey, Dr. Michael Court, and Taylor Gwinn swabs Harley for DNA at the School of Veterinary Medicine. Several years ago in a lab at WSU, Katrina Mealey discovered a genetic mutation in herding dogs that produces an alarming reaction to medication for parasites.

If you gave it to certain collies, they would go into a coma; but other dogs, it didnt affect them at all, said Mealey, a professor who runs the universitys Veterinary Clinical Pharmacology Laboratory.

Mealey published her findings in 2001, and today, she offers a test for dogs to screen for the genetic mutation.

We have owners and veterinarians from all around the world send a cheek swab that just gives us a little bit of DNA from the dog, and we can tell them whether they should avoid that drug completely or whether they should use a decreased dose, she said. Were basically saving dogs lives every day.

Mealeys work is part of a budding field of research called pharmacogenetics, often colloquially referred to as individualized medicine a subfield of pharmacology that examines how genetic variations among patients produce differing responses to drugs.

While individualized medicine is common in human health care, Mealey is one of only a handful of researchers across the globe focusing on the pharmacogenetics of animals. And now, she is part of a new team at WSU which is the first program ever created to study individualized medicine in animals.

For now, Mealey is one of only two researchers in the program. Her partner, professor Michael Court, came to WSU about four months ago, bringing with him a background in veterinary anesthesiology.

During his time as an anesthesiologist, Court gained firsthand experience observing the effects of anesthesia on dogs.

What amazed me was how different was their response to the anesthesia, he said.

Some dogs recovered much quicker than others, he said. Greyhounds, for instance, exhibited a much longer recovery period when exposed to certain types of anesthesia.

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