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September 2006 Posts
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Minnesota Gene Pool Blog

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September 18, 2006

What are the ethical issues, needs and priorities regarding genomics in public health education?

Question: What do we know about what public health workers think are priorities in ethics related to using genomics in research and practice? What are public health workers being taught during their training to deal with these questions? This question came to me when I read this press release report on a recent study on what medical residents believe what ethical and professional issues are important. I will look into this further and post more on this as I find it. If you have any ideas, opinions or facts regarding this question, feel free to post them in the comments section or e-mail me.

A lesson in medical ethics: medical residents and faculty pinpoint priorities in ethics education

September 12, 2006 ANN ARBOR, MI – It sounds like a scene from Grey’s Anatomy: “I had to tell them that their dad had cancer, something that would change their life, and they would remember me telling them the news and how I said it and if I connected…but I felt like I couldn’t find the right words.?

So reports a resident when asked about training needs in ethics and professionalism.
There is no shortage of opinions on what physicians in training need to learn in ethics and professionalism; what has been lacking is data. In an article published in the most recent edition of The American Journal of Bioethics, researchers asked residents, faculty, ethic committee members and practicing physicians what residents need to learn to practice medicine ethically.

The authors identified several categories of needs:

Issues about individual ethics or actions, for example honesty in keeping medical records
Interprofessional relations, for example disagreements between residents and faculty
Issues related to individual patients, including how to break bad news (as in the opening example)

Issues arising from the work environment, for example working when sleep-deprived
Issues related to teaching and learning, for instance tension between efficiency and the responsibility to train future physicians

Issues arising due to external forces, such as insurance coverage and malpractice litigation.
“Commonly, a small group of educators decides what topics to cover for residency training in graduate medical education, or it is assumed they will learn by being around proper role models. This study asked residents what issues they confront, and faculty, practicing physicians and other in-the-know professionals what they think residents should learn,? says author Susan Dorr Goold, M.D., MHSA, MA, director of U-M’s Bioethics Program and an associate professor of medicine and health management and policy. “For ethics training to be useful, and used, it needs to be relevant to medical practice. This study is one of the few that collected data about what people think is relevant.?

Residents reported many of the same priorities in ethics and professional training as did faculty, practicing physicians, and other professionals. Still, there were differences. For example, practicing physicians, with their real-world experience, called for more training in the ethics of resource allocation for patients: should patients be just told how their doctor is going to treat their condition, or should patients be presented with alternatives that might be more expensive, or not covered by insurance? Residents raised concerns about conflicts between their need to learn and providing patients with the best care, and wondered how to handle situations in which they feel a supervising physician acts improperly.

Besides obtaining an overview of needs in ethics and professionalism education, the authors specifically looked for topics and issues common to many specialties.

“All residency programs are required to teach in this area,? says Goold “and some of the topics cross specialty boundaries. Learning about confidentiality, or how to obtain consent, is important for internists, surgeons, family practitioners, neurologists – just about every specialty. Why not develop and use the same tools to teach all of them instead of reinventing the wheel in each department??

Goold and coauthor David Stern, M.D., Ph.D., a U-M associate professor of internal medicine and medical education, did just that at the University of Michigan, developing curricula in several topics that can be used across the institution. The study took place in 1999, prior to the launch of the Accreditation Council of Graduate Medical Ethics outcomes-based requirements for residency education, and portions of the curriculum have been emulated at many other institutions.

Written by Mary Beth Reilly


September 16, 2006

DHHS makes push for combining genetic data and electronic health records

The Department of Health and Human Services has put together a team of experts working to integrate genomics into clinical information systems in an effort to better prevent, diagnose and treat disease using information on a patient's genetic makeup. HHS secretary Mike Leavitt said the genomics soon should play a much larger role in medicine and now is the time to begin incorporating genetic information in electronic health records.

Source: Government Health IT and The U.S. Department of Health and Human Services.

NICHD unveils its new, more user-friendly web portal

The National Institute of Child Health and Human Development of the National Institutes of Health has re-designed its web portal to make information on child health and development more easily accessible. Information on health and human development, research projects funded by the agency and funding / grant proposal information and services for children with special needs is contained on the site.

The NICHD sponsors research on development, before and after birth; maternal, child, and family health; reproductive biology and population issues; and medical rehabilitation. For more information, visit the Institute’s Web site at

Source: The National Institutes of Health at

The Wide, Wild World of Genetic Testing

An article in the Tuesday, September 12, 2006 issue of the New York Times (free registration required) looks at the wild and largely unregulated world of direct-to-consumer genetic testing. Andrew Pollack details the history, companies, products and practices of this growing phenomenon. These tests promise to provide information relevant for all sorts of quasi-medical and non-medical concerns. As correspondent Andrew Pollack writes:

With a few mouse clicks, consumers can order tests that promise to tell them if they are at risk for particular diseases, to trace their ancestry back to the time of Genghis Khan, to help choose which antidepressant would be best for them, to identify the sex of their fetus as few as five weeks into pregnancy and to give advice on diet or exercise.

The trend to offer genetic tests directly to consumers is growing by leaps and bounds as the number of associations between specific forms of genes that vary between individuals are reported in the scientific literature.

Although vigorously opposed by most mainstream scientists, health care providers, policy makers, and public health officials, the process for accessing these tests online or in retail stores is completely legal. The burden of determining the value of and interpreting the test results is borne completely by the consumer and it is definitely true that in this arena, the "buyer must beware" if considering purchasing these products.

Test Helps Identify Patients with Breast Cancer Who Will Likely Benefit from Chemotherapy, and Those Who Won’t

September 15, 2006 -- CHICAGO -- A test that measures the amounts of two members of the same protein family - one of which appears to act as an oncogene, and the other as a tumor suppressor - helps identify patients with breast cancer who will likely benefit from chemotherapy and those who won’t, according to researchers.

The test, known as OncoPlan™, is already commercially available, and studies have shown that it can predict the aggressiveness of the patient’s tumor and the relative risk of disease recurrence following surgery in breast, colon and gastric cancers. Now, researchers in the U.S. and Canada have studied whether it also can help identify breast cancer patients who would benefit most from chemotherapy.

Results were presented at the first meeting on Molecular Diagnostics in Cancer Therapeutic Development, organized by the American Association for Cancer Research.

OncoPlan measures two forms of Shc protein, which are known to drive the formation of protein complexes involved in signal transduction pathways and have been found to be involved in many of the pathways important to development of aggressive cancer. These two forms have a “push pull? relationship with each other: tyrosine-phosphorylated (PY)-Shc helps drive these dangerous cell pathways, but p66 Shc, after initial stimulation, works to inhibit the very growth pathway the other Shc proteins promote.

"This may be one mechanism whereby normal cells prevent runaway growth," said the study's lead author, A. Raymond Frackelton, Jr., Ph.D., a Brown University associate professor, staff scientist at Roger Williams Medical Center and Vice President of Research at Catalyst Oncology, which is marketing OncoPlan. "Perhaps more importantly, aggressive cancer cells must endure oxidative stress—stress that in normal cells triggers p66 Shc to cause cellular suicide," he said. "Tumor cells, then, may have both growth and survival advantages if p66 Shc levels are low."

Chemotherapy-mediated killing of tumor cells, however, does not require p66 Shc, Frackelton said, suggesting that patients whose tumor cells have low p66 Shc might respond well to chemotherapy. To test this idea, the researchers looked at the Shc proteins in tumors from 2,380 women from British Columbia who were diagnosed with invasive breast cancer, 717 of whom received chemotherapy as part of their initial treatment.

They found that, indeed, patients who had low levels of p66 Shc and did not receive chemotherapy had very poor outcomes. If similar patients received chemotherapy, however, their chances of relapsing and dying from their disease were reduced by two-fold or more, said Frackelton. Conversely, women with high levels of p66 Shc had a much higher likelihood of surviving their disease, but appeared to derive no benefit from chemotherapy, he said.

Possible additional associations between PY-Shc and chemotherapy benefit has not yet been fully explored, Frackelton said. “But even at this point, the results are very exciting because, with further validation in clinical trials, OncoPlan, which is already being used to predict disease aggressiveness, will help to ensure that individual patients receive the most beneficial therapies,? he said.

This work was supported in part by a grant from the Susan G. Komen Breast Cancer Foundation

Sources: The American Association for Cancer Research and Catalyst Oncology.

Study Finds Distinct Genetic Profiles For Northern, Southern Europeans

Results promise to improve genetic studies of human disease.

September 14, 2006 -- (SACRAMENTO, Calif.) — An international team of scientists led by researchers at UC Davis Health System has found that, with respect to genetics, modern Europeans fall into two groups: a Northern group and a Southern, or Mediterranean one.

The findings, published in the Sept. 14 edition of Public Library of Science Genetics, are important because they provide a method for scientists to take into account European ancestry when looking for genes involved in diseases.

"Until now, little has been known about the distribution of genetic variation in European populations and how much that distribution matters in terms of doing genetic studies," said Michael Seldin, chair of the Rowe Program in Genetics at UC Davis Health System. "Now we will be able to control for these differences in European populations in our efforts to find genes that cause common diseases."

Seldin, who is also a professor of biochemistry and professor of medicine at UC Davis, worked with his colleagues to compare genetic data for 928 individuals. They looked at 5,700 single nucleotide polymorphisms, called SNPs or "snips." SNPs are changes in which a single base in the DNA differs from the usual base at that position. Millions of SNP's have been cataloged in the human genome. Some SNPs cause diseases, like the one responsible for sickle cell anemia. Other SNPs are normal variations in the genome. People who share ancestry will have many SNPs in common.

Seldin and his group set out to discover which SNPs among Europeans could account for shared common ancestry. "We saw a clustering of individuals that come from either southern Europe or derived from populations that left southern Europe, or the Mediterranean, in the last 2,000 years," Seldin said. This allowed the group to identify a set of 400 informative SNP markers that scientists could now use to control for European ancestry when conducting genetic studies of disease, response to drug treatment, or side effects from therapy.

In addition to future medical applications, the data are also of interest to anthropologists who study historical human migrations. The Southern grouping included individuals from Greece, Italy, Portugal and Spain, as well as Ashkenazi and Sephardic Jews. The Northern group included people with English, Irish, German, Swedish and Ukranian ancestry. These groups correspond to those historically divided by the Pyrenees and Alps mountain ranges.

With respect to population genetics, previous studies have shown that SNPs correlate broadly with continental ancestry, dividing modern humans into four large groups: Asia, Africa, Oceana, America and continental Europe. The new study gives scientists the evidence they need to further subdivide people with European ancestry into the Northern and Southern groups when looking for SNPs that may be involved in disease.

To prove this point, the researchers analyzed two sets of data. They looked at SNPs associated with rheumatoid arthritis and found that, when they corrected for ancestry, several of the genes that were previously believed to be good candidates for being involved in the disease were no longer candidates at all. They also corrected for ancestry in a data set looking at lactose intolerance.

"When we did not control for differences in population structure, we got a lot of false associations," Seldin explained.

Seldin and his colleagues will soon be expanding the current European study by looking at 500,000 SNPs. They also have plans for similar studies of other continental populations and for further defining different subpopulations. Seldin said studies of other continents and ethnic groups are necessary if science is to get the most out of the advances made by the Human Genome Project.

"The ultimate aim of these studies is to be able to better define subgroups and use this information to eliminate false associations, giving us a better chance of finding true associations for disease genes," Seldin said.

Other members of the research team include: Russell Shigeta from UC Davis Health System; Pablo Villoslada at the University of Navarra, Pamplone, Spain; Carlo Selmi at the San Paolo School of Medicine at the University of Milan; Jaakko Tuomilehto at the National Public Health Institute in Helsinki, Finland; Gabriel Silva at the Obras Sociales del Hermano Pedro in Antigua, Guatemala; John W. Belmont at Baylor College of Medicine; Lars Klareskog at Karolinska University Hospital in Stockholm, Sweden; and Peter K. Gregersen at the Feinstein Institute for Medical Research in Manhassett, New York.

This work was supported by grants from the National Institutes of Health.


The Intersection of Biotechnology and Pharmacogenomics: Health Policy Implications

The Intersection Of Biotechnology And Pharmacogenomics: Health Policy Implications
Kathryn A. Phillips

Abstract: Increasing knowledge of the genetic basis of disease is changing the landscape of health care. Two critical aspects are growth in biotechnology and growth in personalized health care, particularly targeting medicines based on genetic information (pharmacogenomics). This paper provides an overview of the health policy implications of the integration of biotechnology and pharmacogenomics. I examine four factors that determine whether relevant technologies will be successfully adopted, using case studies for illustration. Key policy challenges include determining the appropriate role of policy in (1) providing incentives to develop socially beneficial interventions and (2) facilitating development of the evidence base.

Health Affairs, 25, no. 5 (2006): 1271-1280

Kathryn A. Phillips ( is a professor of health economics and health services research at the School of Pharmacy, Institute for Health Policy Studies, and Comprehensive Cancer Center at the University of California, San Francisco.

September 10, 2006

Closing In On Lethal Heart Rhythm In Young Athletes

- New findings at Hopkins should improve screening and prevention

September 7, 2006 -- Johns Hopkins experts on the genetics of a potentially lethal heart rhythm defect that runs in families and targets young athletes report they have greatly narrowed the hunt for the specific genetic mutations that contribute to the problem.

Their new findings, described in the July issue of the American Journal of Human Genetics, should increase the accuracy of tests to identify those at risk for arrhythmogenic right ventricular dysplasia (ARVD), which is among the top causes of sudden cardiac death in the young and fit.

In February, the same team linked one-third of ARVD cases in their large database of patients to a dozen abnormal changes in a gene called plakophilin-2 (PKP2), which makes proteins involved in heart cell stickiness.

In the new study, confirming experiments elsewhere, the Hopkins team found four mutations in another sticky protein gene, Desmoglein-2 (DSG2), in five of 33 patients tested.

“This gene is highly expressed in the heart, where muscle tissue expands and contracts with the heartbeat,? says senior study author and cardiac geneticist Daniel P. Judge, M.D. “Our results confirm that altered genes in the desmosomal cellular complex are responsible for ARVD. And now that we know the genetic roots of this disease, we can also create better blood tests for their proteins to predict who is at risk for developing this condition.?

ARVD is characterized by weakness in the desmosome, or cell-to-cell binding structure. The inherited condition leads to the buildup of excess fatty and scar tissue in the heart’s right ventricle, causing irregular beats and – unless diagnosed and treated with drugs or implanted defibrillators – triggering a fatal heart rhythm disturbance.

Judge, an assistant professor at The Johns Hopkins University School of Medicine and its Heart Institute, says DSG2 mutations appear to account for at least 10 percent and possibly more of the estimated 25,000 deaths each year from ARVD.

“We expect a test for DSG2 mutations to be available to those with a family history of the condition before the end of the year,? he says. The same Hopkins team developed a blood test to screen for PKP2 mutations. That test became available in May and is currently the only one available for detecting those at greater risk of the disease.

More than 400 people have been screened at Hopkins so far and of these, two-thirds have had serious enough forms of the condition to warrant implantation of a defibrillator, an electrical device that corrects any disturbances in the heart’s rhythm.

The Hopkins researchers identified the DSG2 mutation through genetic analysis of blood taken from 60 men and women already diagnosed with ARVD. All were part of a patient database created at Hopkins in 1998. The researchers focused on cell-adhesion proteins because they had already been linked to Naxos syndrome, which produced symptoms in the right ventricle similar to those documented in ARVD.

When scientists excluded their ARVD patients with PKP2 mutations, they were left with 33 who had no known genetic explanation for their condition. Additional testing revealed the four mutations in DSG2.

“We knew right away that we had found something very significant,? says lead author Mark Awad, B.A., a medical and predoctoral sciences student at Hopkins. “The mutations were confined to a highly functional part of the gene and were highly conserved, meaning that evolution had not drastically changed the genetic sequence over time – the gene was kept the way it was because it was important to the heart’s normal function.?

According to Awad, not everyone with a genetic mutation develops ARVD. He adds that further analysis of the condition’s genetic roots will help researchers to calculate the precise increased risk from each mutation for developing symptoms and dying. Previous research by the Hopkins team showed that familial ARVD generally strikes after puberty and its symptoms – dizziness, fatigue and fainting after exercise – may appear up to 15 years before diagnosis.

Funding for this study was provided by the Bogle Foundation, the Campanella family, the Wilmerding Endowments, the National Institutes of Health, the Donald W. Reynolds Foundation and the W.W. Smith Charitable Trust.

In addition to Judge and Awad, other researchers involved in this study, conducted solely at Hopkins, were Darshan Dalal, M.D., Ph.D., Eunpi Cho; Nuria Amat-Alarcon, M.S.; Cynthia James, Ph.D.; Crystal Tichnell, M.G.C, Sc.M.; April Tucker, M.G.C.; Stuart Russell, M.D.; David Bluemke, M.D., Ph.D.; Harry Dietz, M.D.; and Hugh Calkins, M.D. Calkins receives research support from device manufacturers Guidant, Medtronic and St. Jude. The terms of these arrangements are being managed by The Johns Hopkins University in accordance with its conflict of interest policies.


Source: HealthOrbit Headline News from September 9, 2006

Focusing in on Cancer's Complexity

“Scientists who have seen these data have told us that it keeps them up all night thinking.?
Bert Vogelstein

September 08, 2006 -- In the first large-scale screen of genetic changes in cancer cells, researchers have found that a typical breast or colorectal tumor results from mutations in about 90 genes, with different sets of mutations producing the same type of cancer.

But the many different genetic routes to malignancy share common features that point toward new means of cancer prevention, diagnosis, and treatment.

Previous genetic studies of cancer have concentrated on specific genes or on chromosomal regions. In the September 8, 2006, issue of Science, Howard Hughes Medical Institute (HHMI) investigators Bert Vogelstein at Johns Hopkins University and Sanford D. Markowitz at Case Western Reserve University School of Medicine, together with a team of researchers from The Kimmel Cancer Center at Johns Hopkins and other institutions, report on a radically new way of identifying genes involved in cancer.

They screened the most well-annotated human genes, a total of more than 13,000 genes that all major genomic centers agree encode proteins. They first looked for mutations in 22 cancerous breast and colorectal tumors. From that list, 191 genes appeared to be particularly important. “Scientists who have seen these data have told us that it keeps them up all night thinking,? said Vogelstein. “It will hopefully open up a large number of opportunities in many areas of cancer research.?

The team found far more mutated genes in tumor cells than they had expected. The average breast or colorectal cancer cell was predicted to have an average of 90 mutations that alter protein structure. However, not all 90 were likely to contribute equally to the development of cancers. Through subsequent validation studies, the researchers identified an average of 11 genes in each cancer that were most likely to be directly responsible for its biologic properties. Extrapolating to the total number of genes in the human genome, an average of about 17 genes are expected to have critical involvement in the development of each cancer.

The researchers also were surprised by the heterogeneity of the cancers. Different genes were mutated in cancers of the same type, and the genes contributing to breast cancer were different from those mutated in colorectal cancers. “It presents a whole new view of the neoplastic process,? said Vogelstein, “and explains the heterogeneity that clinicians have long noted to exist among cancer patients.?

Despite the complexity of the results, a closer examination of the data has started to reveal an underlying order. Many of the genes that are mutated are involved in pathways thought to be important in cancer, such as cell adhesion, movement, and signaling. Each of these pathways relies on multiple genes, and flaws in any of the genes in a pathway may have similar consequences.

“By taking a systems biology approach to connect these genes, we suspect that the complexity will be less than it appears at first sight,? said Vogelstein. “The same 10 or 20 pathways may be altered in every cancer, though the particular mutated genes in these pathways will be different. The picture will become much clearer as the function of these genes and the ways they interact are better worked out.?

This kind of study could not have been done a few years ago, said Tobias Sjöblom, an HHMI research associate in Vogelstein's lab, who is the lead author of the Science article. But the availability of the human genome sequence and improvements in sequencing and bioinformatics technologies have made it possible to examine the genome of cancer cells in a comprehensive and unbiased manner, he said.

Still, a massive amount of work was involved. “It was a straightforward process once all the mechanistic details had been worked out and the bioinformatic infrastructure was in place,? said Sjöblom, “but very laborious.? The research team formulated 135,483 sets of DNA primers for the polymerase chain reactions needed to sequence the tumor cell genes. They then looked at 11 tumors for each type of cancer, along with two normal samples as a control. The result was almost a half billion letters of DNA sequence that had to be screened for suspicious mutations.
Successive rounds of computer analysis focused attention on smaller and smaller subsets of nucleotides. “The hard work was to remove all the junk so that you were left with the true mutations,? Sjöblom said. In the final stages, visual inspection of the sequences was required to confirm each mutation. According to Vogelstein, “the eye is better than a computer for some types of pattern recognition.?

Once the list of mutations was winnowed down, the chromosomal regions containing those mutations were resequenced in the tumors and matched to normal DNA samples to validate each mutation. This process resulted in 1,307 confirmed somatic mutations in 1,149 genes. These genes then were analyzed in 48 additional breast or colorectal tumors, which turned up an additional 365 mutations in 236 of the genes. Altogether, 921 and 751 somatic protein-altering mutations were identified in breast and colorectal cancers, respectively, most of which were changes in single nucleotides.

The researchers then used statistical techniques to identify the changes in a given gene that were more likely to contribute directly to the cancers' properties. This identified 122 genes in breast cancer tumor cells and 71 genes in colorectal cancers, which the researchers called CAN-genes (candidate cancer genes). Surprisingly, only two genes appeared on both lists.

Furthermore, even the types of mutations differed between breast cancer and colorectal cancer. For example, 59 percent of the colorectal cancer mutations went from a C:G base pair to an T:A pair, whereas this was the case for only 35 percent of the breast cancer mutations. “These differences may be due to different kinds of carcinogens, different types of repair mechanisms, or different exposures to endogenous mutagens,? said Vogelstein. “This is a very fertile area of epidemiologists.?

Even within each type of cancer, each tumor had its own distinct collection of mutated genes. No cancer had more than six mutated CAN-genes in common with any other cancer. This finding also was unexpected, “but it's consistent with clinical observations,? said Vogelstein, “because clinicians have observed for years that each cancer behaves in a unique way.?

The complexity of the results may seem discouraging, Vogelstein notes. “If anyone thought cancer was simple, they were wrong,? he said. “On the other hand, once you get the picture in focus, you can start to figure out what's going on.? Many of the genes they identified were not previously known to be involved in cancer, and each gene offers potential insights into the disease. “The first thing we'll probably delve into is diagnostics, as that's been one of the themes of our lab,? Vogelstein said. In particular, they will be looking to find evidence of the mutated genes in blood or other clinical specimens to help identify cancers before they cause symptoms.
Therapeutics based on the newly discovered genes are “a ways off,? in Vogelstein's estimation. But once the key pathways necessary for cancer are identified, researchers can look for ways to reverse the effects of the activated genes, said Vogelstein. "We now have a whole new set of targets to guide drug development."


Source: HealthOrbit Headlines on September 8, 2006

September 9, 2006

Aging as the price for suppressing cancer?

An article in the New York Times reports that a gene known for the suppression of tumor development also is responsible for the shutting down of the ability of stem cells to proliferate. This inhibition of stem cell function may be responsible for lowering the risk for cancer, but also may be related to many of the chronic degenerative conditions that are associated with aging. The finding is reported online by three research groups as advance online publications in Nature.

September 1, 2006

Live Long? Die Young? Answer Isn't Just in the Genes

Gina Kolata's article in the August 31 New York Times reviews what we know about the contributions of nature and nurture to our lifespans. She correctly identifies that genetics plays a role, but that what happens to us in our lives is at least as--and likely is even more important than--the genes we inherit in most cases. This is not a ground-shaking revelation. When you think about this, it isn't a huge stretch to see that genes, behavior and environment all contribute to the vast majority of components that contribute to the human condition, including lifespan. It is probably true that, as in the case of most other traits we possess, we do not exhaust what genetic potential that we inherently possess for a maximal lifespan in most cases. When you consider that genetic potential for longevity does not seem to be what is in short supply for most of us, but that how and where and with whom we spend our lives is more often the deciding factor in how many years we are around around this earth, then it is no great surprise that studies that look at the genetic component of longevity tend to find only very modest genetic contributions.

I really like this quote by Peter Parham when he wrote in the New England Journal of Medicine "The genome is a set of boundary conditions that limits the nature of the organism, not a blueprint that defines it." At first, you might think that this statement just negated everything I just argued in the previous paragraph. However, when you think of limits, think of them in the mathematical sense. What he means is that we can't develop beyond the boundaries that nature (read "genes") has given us, but within some very broad borders, the sky is the limit.

Ten Hot Jobs for 2007

According to MSN and, one of the hot jobs for 2007 will be genetic counseling!

Genetic Screening: Who should have it and when?

I happened upon this video presentation on genetic screening, testing and counseling. It has information on when to refer for genetic counseling and what such a referral entails. Check it out!