Rebekah Eliason for redOrbit.com Your Universe Online

A new study from Duke reveals that the genetic trait responsible for predisposing some people to strong stress reactions may also cause the risk of heart attack or death to rise by 38 percent.

This discovery provides a new biological explanation for why some people are inclined towards cardiovascular disease. Since in these cases the disease is linked to stress, the findings suggest that behavior modification and drug therapies targeting stress reduction may lower heart attack related disability and deaths.

Redford B. Williams Jr., M.D., director of the Behavioral Medicine Research Center at Duke University School of Medicine and senior author of the paper, said, Weve heard a lot about personalized medicine in cancer, but in cardiovascular disease we are not nearly as far along in finding the genetic variants that identify people at higher risk. Here we have a paradigm for the move toward personalized medicine in cardiovascular disease.

Building on previous work at Duke and elsewhere, Williams and his colleagues were able to identify a variation in a DNA sequence known as single nucleotide polymorphism (SNP). In this sequence variation, one letter from the genetic code is swapped with another causing a change in the genes function. Specifically the team focused on the SNP occurring on the gene responsible for making a serotonin receptor that causes a hyperactive reaction to stress.

Last year, a study was published reporting that men with the genetic variation were found to contain twice as much cortisol in their blood after exposure to stress than men without the variant. Commonly known as the stress hormone, cortisol is designed to support the bodys biological response to stressful situations that cause negative emotions. This vital hormone is produced in the adrenal glands.

Beverly H. Brummett, PhD, associate professor of Psychiatry and Behavioral Sciences at Duke and lead author of the paper, said, It is known that cortisol has effects on the bodys metabolism, on inflammation and various other biological functions, that could play a role in increasing the risk of cardiovascular disease. It has been shown that high cortisol levels are predictive of increased heart disease risk. So we wanted to examine this more closely.

Several years of data from heart catheterization patients at Duke was formed into a large database used by researchers to run a genetic analysis of over 6,100 white participants. Of those studied, two-thirds were men and one-third was women. Approximately 13 percent of the group was found to possess the genetic variation for the overactive stress response.

Those found to carry the genetic variation corresponded with patients who had the highest rates of heart attacks and deaths when evaluating the median follow-up time of six years. Even when taking into account age, obesity, smoking history, other illnesses and the severity of their heartdisease, the studied genetic trait was found to be associated with a 38 percent increased risk of heart attack and death.

This finding requires independent replication and evaluation in a more diverse population, said Peter Kaufmann, Ph.D., deputy branch chief of the Clinical Applications and Prevention Branch at the NIHs National, Heart, Lung, and Blood Institute (NHLBI). This research may one day help to identify patients who should be candidates for more intensive disease prevention and treatment strategies.

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Stress Gene Linked To Higher Risk Of Heart Attack And Death

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Researchers at the University of California, San Diego School of Medicine, with colleagues in The Netherlands and United Kingdom, have produced the first map detailing the network of genetic interactions underlying the cellular response to ultraviolet (UV) radiation.

The researchers say their study establishes a new method and resource for exploring in greater detail how cells are damaged by UV radiation and how they repair themselves. UV damage is one route to malignancy, especially in skin cancer, and understanding the underlying repair pathways will better help scientists to understand what goes wrong in such cancers.

The findings will be published in the December 26, 2013 issue of Cell Reports.

Principal investigator Trey Ideker, PhD, division chief of genetics in the UC San Diego School of Medicine and a professor in the UC San Diego Departments of Medicine and Bioengineering, and colleagues mapped 89 UV-induced functional interactions among 62 protein complexes. The interactions were culled from a larger measurement of more than 45,000 double mutants, the deletion of two separate genes, before and after different doses of UV radiation.

Specifically, they identified interactive links to the cell's chromatin structure remodeling (RSC) complex, a grouping of protein subunits that remodel chromatin the combination of DNA and proteins that make up a cell's nucleus during cell mitosis or division. "We show that RSC is recruited to places on genes or DNA sequences where UV damage has occurred and that it helps facilitate efficient repair by promoting nucleosome remodeling," said Ideker.

The process of repairing DNA damage caused by UV radiation and other sources, such as chemicals and other mutagens, is both simple and complicated. DNA-distorting lesions are detected by a cellular mechanism called the nucleotide excision repair (NER) pathway. The lesion is excised; the gap filled with new genetic material copied from an intact DNA strand by special enzymes; and the remaining nick sealed by another specialized enzyme.

However, NER does not work in isolation; rather it coordinates with other biological mechanisms, including RSC.

"DNA isn't free-floating in the cell, but is packaged into a tight structure called chromatin, which is DNA wound around proteins," said Rohith Srivas, PhD, a former research scientist in Ideker's lab and the study's first author. "In order for repair factors to fix DNA damage, they need access to naked DNA. This is where chromatin remodelers come in: In theory, they can be recruited to the DNA, open it up and allow repair factors to do their job."

Rohith said that other scientists have previously identified complexes that perform this role following UV damage. "Our results are novel because they show RSC is connected to both UV damage pathways: transcription coupled repair - which acts on parts of DNA being expressed - and global genome repair, which acts everywhere. All previous remodelers were linked only to global genome repair."

The scientists noted that the degree of genetic rewiring correlates with the dose of UV. Reparative interactions were observed at distinct low or high doses of UV, but not both. While genetic interactions at higher doses is not surprising, the authors said, the findings suggest low-dose UV radiation prompts specific interactions as well.

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How cells remodel after exposure to UV radiation

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When Janet Rowley was accepted into the University of Chicago's medical school in 1944, the quota for women was already filled three in a class of 65.

So she had to wait a year.

Dr. Rowley made up for that early setback by becoming an internationally known scientist whose research in the 1970s redefined cancer as a genetic disease and led to a paradigm shift in how it is studied and treated.

An advisor to presidents and recipient of her nation's highest honors, Rowley achieved breakthroughs that prolonged the lives of countless cancer patients. She died Tuesday at age 88 at her home in the Chicago suburb of Hyde Park from complications of ovarian cancer.

"She was a pioneer in the field because, at that time, there was a big divide between what people thought caused cancer," said Dr. Funmi Olopade, director of the Center for Clinical Cancer Genetics at the University of Chicago. "She was able to show that genetic changes were defining specific types of cancers, and it was these genetic abnormalities that were really the trigger to explaining why cancer behaved the way it behaved."

Rowley graduated from medical school in 1948 at age 23. The next day she married fellow medical student Donald Rowley, who became a professor of pathology at the university. For many years while raising four sons, Rowley worked three days a week, including at a Chicago clinic for children with Down syndrome, a genetic disorder caused by an extra chromosome.

Her interest in chromosomes continued in the 1960s, when she traveled to Oxford University to learn new ways to analyze them.

Back home, a University of Chicago colleague gave Rowley some laboratory space, a microscope and a salary of $5,000 a year and encouraged her to study the chromosomes of leukemia patients.

Rowley's pivotal discovery came during one of her "off days" in 1972, while poring through images of chromosomes that she had spread out on the family dinner table.

At the time, scientists were befuddled by the relationship between genes and cancer, unsure why patients with a particular leukemia displayed one abnormally short chromosome a threadlike structure that carries genetic information.

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Janet Rowley dies at 88; scientist pinpointed genetic cause of leukemia

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How to solve genetics problems using Binominal Expansion Formula
Binomial Expansion Assume that a couple plans to have five children. In this case, it is somewhat tedious to outline and then calculate all the possible comb...

By: GeneticsLessons

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How to solve genetics problems using Binominal Expansion Formula - Video

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IV International Symposium of Genetics and Breeding - 5/7
Session: Genomic selection for beef cattle Dr Matt Kelly - University of Queensland.

By: GenMelhor UFV

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IV International Symposium of Genetics and Breeding - 5/7 - Video

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What Makes Us Who We Are? The Promise (and Perils) of Behavioral Genetics
Sponsored by the Poynter Fellowship in Journalism and Franke Program in Science and the Humanities. Why are some of us happier than othersor sadder, tougher...

By: YaleUniversity

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GENE THERAPY PROF WAGIH P3

By: Asmaa Alhazmi

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GENE THERAPY PROF WAGIH P3 - Video

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GENE THERAPY PROF WAGIH P2

By: Asmaa Alhazmi

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GENE THERAPY PROF WAGIH P2 - Video

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PUBLIC RELEASE DATE:

18-Dec-2013

Contact: Robert Miranda cogcomm@aol.com Cell Transplantation Center of Excellence for Aging and Brain Repair

Putnam Valley, NY. (Dec. 18, 2013) Multiple sclerosis (MS), an inflammatory autoimmune disease affecting more than one million people worldwide, is caused by an immune reaction to myelin proteins, the proteins that help form the myelin insulating substance around nerves. Demyelination and MS are a consequence of this immune reaction. Bone marrow mesenchymal stem cells (MSCs) have been considered as an important source for cell therapy for autoimmune diseases such as MS because of their immunosuppressive properties.

Now, a research team in Brazil has compared MSCs isolated from MS patients and from healthy donors to determine if the MSCs from MS patients are normal or defective. The study will be published in a future issue of Cell Transplantation but is currently freely available on-line as an unedited early e-pub at: http://www.ingentaconnect.com/content/cog/ct/pre-prints/content-ct1131.

"The ability of MSCs to modulate the immune response suggests a possible role of these cells in tolerance induction in patients with autoimmune diseases, and also supports the rationale for MSC application in the treatment of MS," said study corresponding author Dr. Gislane Lelis Vilela de Oliveira of the Center for Cell-Based Research at the University of Sao Paulo. "We found that MS patient-derived MSCs present higher senescence, or biological aging, and decreased expression of important immune system markers as well as a different transcriptional profile when compared to their healthy counterparts."

The researchers suggested that further clinical studies should be conducted using transplanted allogenic (other-donated) MSCs derived from healthy donors to determine if the MSCs have a therapeutic effect over transplanted autologous (self-donated) MSCs from patients.

"Several reports have shown that bone marrow-derived MSCs are able to modulate innate and adaptive immunity cell responses and induce tolerance, thus supporting the rationale for their application in treating autoimmune diseases, " said the researchers.

They also noted that studies have shown that transplanted MSCs migrate to demyelinated areas as well as induce generation and expansion of regulatory T cells, important in immunity.

"We found that the transcriptional profile of patient MSCs after transplantation was closer to that of their pre-transplant MSC samples than those from their healthy counterparts, suggesting that treatment with patient self-donated MSCs does not reverse the alterations we observed in MSCs from MS patients," they concluded.

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Preferable treatment for MS found in allogenic bone marrow stem cells

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Regenerative Medicine: Mayo Clinic and Collaborators Develop New Tool for Transplanting Stem Cells
Mayo Clinic researchers and colleagues in Belgium have developed a specialized catheter for transplanting stem cells into the beating heart. The novel device...

By: Mayo Clinic

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In a typical stem cell transplant for cancer very high doses of chemo are used, often along with radiation therapy, to try to destroy all the cancer cells. This treatment also kills the stem cells in the bone marrow. Soon after treatment, stem cells are given to replace those that were destroyed. These stem cells are given into a vein, much like a blood transfusion. Over time they settle in the bone marrow and begin to grow and make healthy blood cells. This process is called engraftment.

There are 3 basic types of transplants. They are named based on who gives the stem cells.

These stem cells come from you alone. In this type of transplant, your stem cells are taken before you get cancer treatment that destroys them. Your stem cells are removed, or harvested, from either your bone marrow or your blood and then frozen. To find out more about that process, please see the section Whats it like to donate stem cells? After you get high doses of chemo and/or radiation the stem cells are thawed and given back to you.

One advantage of autologous stem cell transplant is that you are getting your own cells back. When you donate your own stem cells you dont have to worry about the graft attacking your body (graft-versus-host disease) or about getting a new infection from another person. But there can still be graft failure, and autologous transplants cant produce the graft-versus-cancer" effect.

This kind of transplant is mainly used to treat certain leukemias, lymphomas, and multiple myeloma. Its sometimes used for other cancers, like testicular cancer and neuroblastoma, and certain cancers in children. Doctors are looking at how autologous transplants might be used to treat other diseases, too, like systemic sclerosis, multiple sclerosis, Crohn disease, and systemic lupus erythematosis.

A possible disadvantage of an autologous transplant is that cancer cells may be picked up along with the stem cells and then put back into your body later. Another disadvantage is that your immune system is still the same as before when your stem cells engraft. The cancer cells were able to grow despite your immune cells before, and may be able to do so again.

To prevent this, doctors may give you anti-cancer drugs or treat your stem cells in other ways to reduce the number of cancer cells that may be present. Some centers treat the stem cells to try to remove any cancer cells before they are given back to the patient. This is sometimes called purging. It isnt clear that this really helps, as it has not yet been proven to reduce the risk of cancer coming back (recurrence).

A possible downside of purging is that some normal stem cells can be lost during this process, causing the patient to take longer to begin making normal blood cells, and have unsafe levels of white blood cells or platelets for a longer time. This could increase the risk of infections or bleeding problems.

One popular method now is to give the stem cells without treating them. Then, after transplant, the patient gets a medicine to get rid of cancer cells that may be in the body. This is called in vivo purging. Rituximab (Rituxan), a monoclonal antibody drug, may be used for this in certain lymphomas and leukemias, and other drugs are being tested. The need to remove cancer cells from transplants or transplant patients and the best way to do it is being researched.

Doing 2 autologous transplants in a row is known as a tandem transplant or a double autologous transplant. In this type of transplant, the patient gets 2 courses of high-dose chemo, each followed by a transplant of their own stem cells. All of the stem cells needed are collected before the first high-dose chemo treatment, and half of them are used for each transplant. Most often both courses of chemo are given within 6 months, with the second one given after the patient recovers from the first one.

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Types of stem cell transplants for treating cancer

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Durham, NC (PRWEB) December 18, 2013

A new study released today in STEM CELLS Translational Medicine demonstrates that the therapeutic value of stem cells collected from fat declines when the cells come from older patients.

This could restrict the effectiveness of autologous cell therapy using fat, or adipose-derived mesenchymal stromal cells (ADSCs), and require that we test cell material before use and develop ways to pretreat ADSCs from aged patients to enhance their therapeutic potential, said Anastasia Efimenko, M.D., Ph.D. She and Nina Dzhoyashvili, M.D., were first authors of the study led by Yelena Parfyonova, M.D., D.Sc., at Lomonosov Moscow State University, Moscow.

Cardiovascular disease remains the most common cause of death in most countries. Mesenchymal stromal cells (MSCs), stem cells collected from either bone marrow or adipose tissue, are considered one of the most promising therapeutic agents for regenerating damaged tissue because of their proliferation potential and ability to be coaxed into different cell types. Importantly, they also have the ability to stimulate the growth of new blood vessels, a process known as angiogenesis.

Adipose tissue in particular is considered an ideal source for MSCs because it is largely dispensable and the stem cells are easily accessible in large amounts using a minimally invasive procedure. ADSCs have been used in several clinical trials looking at cell therapy for heart conditions, but most of the studies employed cells taken from relatively healthy young donors rather than sick, older ones the typical patient when it comes to heart disease.

We knew that aging and disease itself may negatively affect MSC activities, Dr. Dzhoyashvili said. So the aim of our study was to investigate how patient age affects the properties of ADSCs, with special emphasis on their ability to stimulate angiogenesis.

The team analyzed age-associated changes in ADSCs collected from patients of different age groups, including some with coronary artery disease and some without. The results showed that ADSCs from the older patients in both groups expressed various age markers, including shorter telomeres, and, thus, confirmed that ADSCs did age. Telomeres, the regions of repetitive DNA at the end of a chromosome, protect it from deterioration.

We showed that ADSCs from older patients both with and without coronary artery disease produced significantly less amounts of angiogenesis-stimulating factors compared with the younger patients in the study and their angiogenic capabilities lessened, Dr. Efimenko concluded. The results provide new insight into molecular mechanisms underlying the age-related decline of stem cells therapeutic potential.

These findings are significant because the successful development of cell therapies depends on a thorough understanding of how age may affect the regenerative potential of autologous cells, said Anthony Atala, M.D., editor of STEM CELLS Translational Medicine and director of the Wake Forest Institute for Regenerative Medicine.

###

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Study Shows Therapeutic Potential of Fat-derived Stem Cells Declines As Donor’s Age Rises

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PUBLIC RELEASE DATE:

18-Dec-2013

Contact: Kevin Punsky punsky.kevin@mayo.edu 904-953-2299 Mayo Clinic

JACKSONVILLE, Fla. -- Abba Zubair, M.D., Ph.D, believes that cells grown in the International Space Station (ISS) could help patients recover from a stroke, and that it may even be possible to generate human tissues and organs in space. He just needs a chance to demonstrate the possibility.

He now has it. The Center for the Advancement of Science in Space (CASIS), a nonprofit organization that promotes research aboard the ISS, has awarded Dr. Zubair a $300,000 grant to send human stem cells into space to see if they grow more rapidly than stem cells grown on Earth.

Dr. Zubair, medical and scientific director of the Cell Therapy Laboratory at Mayo Clinic in Florida, says the experiment will be the first one Mayo Clinic has conducted in space and the first to use these human stem cells, which are found in bone marrow.

"On Earth, we face many challenges in trying to grow enough stem cells to treat patients," he says. "It now takes a month to generate enough cells for a few patients. A clinical-grade laboratory in space could provide the answer we all have been seeking for regenerative medicine."

He specifically wants to expand the population of stem cells that will induce regeneration of neurons and blood vessels in patients who have suffered a hemorrhagic stroke, the kind of stroke which is caused by blood clot. Dr. Zubair already grows such cells in his Mayo Clinic laboratory using a large tissue culture and several incubators -- but only at a snail's pace.

Experiments on Earth using microgravity have shown that stem cells -- the master cells that produce all organ and tissue cell types -- will grow faster, compared to conventionally grown cells.

"If you have a ready supply of these cells, you can treat almost any condition, and can theoretically regenerate entire organs using a scaffold," Dr. Zubair says. "Additionally, they don't need to come from individual patients -- anyone can use them without rejection."

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Mayo Clinic researcher to grow human cells in space to test treatment for stroke

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Newswise Researchers at UCLAs Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research have discovered a mechanism in adult stem cells by which the cells suppress their ability to initiate cancer during their dormant phase, an understanding that could be exploited for better cancer prevention strategies. The study was led by Andrew White, post-doctoral fellow, and William Lowry, associate professor of molecular, cell and developmental biology in the life sciences and the Maria Rowena Ross Term Chair in Cell Biology.

The study was published online ahead of print in Nature Cell Biology on December 15, 2013.

Hair follicle stem cells (HFSC), the tissue-specific adult stem cells that generate the hair follicles, are also the cells of origin for cutaneous squamous cell carcinoma (SCC), a common skin cancer. These HFSCs cycle between periods of activation, during which they can grow, and quiescence, when they remain dormant.

Using mouse models, White and Lowry applied known cancer-causing genes (oncogenes) to HFSCs and found that during cell quiescence, the cells could not be made to initiate SCC. Once the HFSC were in their active period, they began growing cancer.

We found that this tumor suppression via adult stem cell quiescence was mediated by Pten, a gene important in regulating the cells response to signaling pathways, White said, therefore, stem cell quiescence is a novel form of tumor suppression in hair follicle stem cells, and Pten must be present for the suppression to work.

Understanding cancer suppression through quiescence could better inform preventative strategies in patients susceptible to SCC, such as organ transplant patients, or those taking the drug vemurafenib for melanoma, another type of skin cancer. This study also may reveal parallels between SCC and other cancers in which stem cells have a quiescent phase. This research was supported by the California Institute of Regenerative Medicine (CIRM), University of California Cancer Research Coordinating Committee (CRCC) and National institutes of Health (NIH).

The stem cell center was launched in 2005 with a UCLA commitment of $20 million over five years. A $20 million gift from the Eli and Edythe Broad Foundation in 2007 resulted in the renaming of the center. With more than 200 members, the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research is committed to a multi-disciplinary, integrated collaboration of scientific, academic and medical disciplines for the purpose of understanding adult and human embryonic stem cells. The center supports innovation, excellence and the highest ethical standards focused on stem cell research with the intent of facilitating basic scientific inquiry directed towards future clinical applications to treat disease. The center is a collaboration of the David Geffen School of Medicine, UCLAs Jonsson Comprehensive Cancer Center, the Henry Samueli School of Engineering and Applied Science and the UCLA College of Letters and Science. To learn more about the center, visit our web site at http://www.stemcell.ucla.edu.

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Adult Stem Cells Found to Suppress Cancer While Dormant

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Gypenosides pre-treatment protects the brain against cerebral ischemia and increases neural stem cells/progenitors in the subventricular zone.

Gypenosides pre-treatment protects the brain against cerebral ischemia and increases neural stem cells/progenitors in the subventricular zone.

Int J Dev Neurosci. 2013 Dec 12;

Authors: Wang XJ, Sun T, Kong L, Shang ZH, Yang KQ, Zhang QY, Jing FM, Dong L, Xu XF, Liu JX, Xin H, Chen ZY

Abstract Gypenosides (GPs) have been reported to have neuroprotective effects in addition to other bioactivities. The protective activity of GPs during stroke and their effects on neural stem cells (NSCs) in the ischemic brain have not been fully elucidated. Here, we test the effects of GPs during stroke and on the NSCs within the subventricular zone (SVZ) of middle cerebral artery occlusion (MCAO) rats. Our results show that pre-treatment with GPs can reduce infarct volume and improve motor function following MCAO. Pre-treatment with GPs significantly increased the number of BrdU-positive cells in the ipsilateral and contralateral SVZ of MCAO rats. The proliferating cells in both sides of the SVZ were glial fibrillary acidic protein (GFAP)/nestin-positive type B cells and Doublecortin (DCX)/nestin-positive type A cells. Our data indicate that GPs have neuroprotective effects during stroke which might be mediated through the enhancement of neurogenesis within the SVZ. These findings provide new evidence for a potential therapy involving GPs for the treatment of stroke.

PMID: 24334222 [PubMed - as supplied by publisher]

Cell based therapies for ischemic stroke: from basic science to bedside.

Prog Neurobiol. 2013 Dec 12;

Authors: Liu X, Ye R, Yan T, Yu SP, Wei L, Xu G, Fan X, Jiang Y, Stetler RA, Chen J

Abstract Cell therapy is emerging as a viable therapy to restore neurological function after stroke. Many types of stem/progenitor cells from different sources have been explored for their feasibility and efficacy for the treatment of stroke. Transplanted cells not only have the potential to replace the lost circuitry, but also produce growth and trophic factors, or stimulate the release of such factors from host brain cells, thereby enhancing endogenous brain repair processes. Although stem/progenitor cells have shown a promising role in ischemic stroke in experimental studies as well as initial clinical pilot studies, cellular therapy is still at an early stage in humans. Many critical issues need to be addressed including the therapeutic time window, cell type selection, delivery route, and in vivo monitoring of their migration pattern. This review attempts to provide a comprehensive synopsis of preclinical evidence and clinical experience of various donor cell types, their restorative mechanisms, delivery routes, imaging strategies, future prospects and challenges for translating cell therapies as a neurorestorative regimen in clinical applications.

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Stroke and Stem Cell Therapy

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Shutdowns, lethal viruses, typhoons and meteorites much of this years science news seemed to come straight from the set of a Hollywood disaster movie. But there were plenty of feel-good moments, too. Space exploration hit a new high, cash poured in to investigate that most cryptic of human organs, the brain, and huge leaps were made in stem-cell therapies and the treatment of HIV. Here, captured in soundbites, statistics and summaries, is everything you need to know about the science that mattered in 2013.

LUX: Carlos H. Faham

The Large Underground Xenon dark-matter experiment, deep in a mine in South Dakota.

One of the years most important cosmological results was an experimental no-show. The Large Underground Xenon (LUX, pictured) experiment at Sanford Underground Research Facility in Lead, South Dakota 370 kilograms of liquid xenon almost 1.5kilometres down in a gold mine did not see any particles of elusive dark matter flying through Earth. But it put the tightest constraints yet on the mass of dark-matter particles, and their propensity to interact with visible matter. Theoretical physicist Matthew Strassler at Rutgers University in Piscataway, New Jersey, says a consensus is forming that hints of dark matter seen by earlier experiments in the past three years were probably just statistical fluctuations.

PlancK: ESA/Planck Collaboration

Whatever dark matter is, it makes up around 84% of the Universes total matter, according to observations, released in March, of the Universes cosmic microwave background (CMB) by the European Space Agencys Planck satellite. Plancks image (pictured) also strongly supports the hypothesis of inflation, in which the Universe is thought to have expanded rapidly after the Big Bang. A better probe of inflation might be provided through its predicted influence on how the polarization of CMB photons varies across the sky (B-mode polarization). That subtle signal has not been measured yet, but astronomers hopes were raised by news of the first sighting of a related polarization signal, by the South Pole Telescope, in July. And another Antarctic telescope the underground IceCube observatory confirmed this year that the high-energy neutrinos it has detected come from far away in the cosmos, hinting at a new world of neutrino astronomy.

Jae C. Hong/AP

US workers came out in force against the shutdown.

The slow decline of US federal support for research and development spending is already down 16.3% since 2010 reached a new nadir in October, when political brinkmanship led the government to shut down for 16 days. Grant money stopped flowing; work halted at major telescopes, US Antarctic bases and most federal laboratories; and key databases maintained by the government went offline. Many government researchers were declared non-essential and barred by law from visiting their offices and laboratories, or even checking their official e-mail accounts. Since the shutdowns end, grant backlogs and missed deadlines have scrambled agency workloads.

Away from the deadlock in the United States, the European Union negotiated a path to a 201420 research budget of almost 80billion (US$110billion), a 27% rise in real terms over the previous 200713 period. And funding in South Korea, China, Germany and Japan continued to increase (the United Kingdom and France saw little change). But Japans largesse came with the clear understanding that its science investment would bring fast commercial pay-offs. Along similar lines, US Republican politicians are calling for the National Science Foundation to justify every grant it awards as being in the national interest.

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365 days: 2013 in review

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Dec. 17, 2013 A systematic survey of the scientific literature shows that stem cell therapy can have a statistically significant impact on animal models of spinal cord injury, and points the way for future studies.

Spinal cord injuries are mostly caused by trauma, often incurred in road traffic or sporting incidents, often with devastating and irreversible consequences, and unfortunately having a relatively high prevalence (250,000 patients in the USA; 80% of cases are male). High-profile campaigners like the late actor Christopher Reeve, himself a victim of sports-related spinal cord injury, have placed high hopes in stem cell transplantation. But how likely is it to work?

This question is addressed in a paper published 17th December in the open access journal PLOS Biology by Ana Antonic, David Howells and colleagues from the Florey Institute and the University of Melbourne, Australia, and Malcolm MacLeod and colleagues from the University of Edinburgh, UK.

Stem cell therapy aims to use special regenerative cells (stem cells) to repopulate areas of damage that result from spinal cord injuries, with the hope of improving the ability to move ("motor outcomes") and to feel ("sensory outcomes") beyond the site of the injury. Many studies have been performed that involve animal models of spinal cord injury (mostly rats and mice), but these are limited in scale by financial, practical and ethical considerations. These limitations hamper each individual study's statistical power to detect the true effects of the stem cell implantation.

This new study gets round this problem by conducting a "meta-analysis" -- a sophisticated and systematic cumulative statistical reappraisal of many previous laboratory experiments. In this case the authors assessed 156 published studies that examined the effects of stem cell treatment for experimental spinal injury in a total of about 6000 animals.

Overall, they found that stem cell treatment results in an average improvement of about 25% over the post-injury performance in both sensory and motor outcomes, though the results can vary widely between animals. For sensory outcomes the degree of improvement tended to increase with the number of cells introduced -- scientists are often reassured by this sort of "dose response," as it suggests a real underlying biologically plausible effect.

The authors went on to use their analysis to explore the effects of bias (whether the experimenters knew which animals were treated and which untreated), the way that the stem cells were cultured, the way that the spinal injury was generated, and the way that outcomes were measured. In each case, important lessons were learned that should help inform and refine the design of future animal studies. The meta-analysis also revealed some surprises that should provoke further investigation -- there was little evidence of any beneficial sensory effects in female animals, for example, and it didn't seem to matter whether immunosuppressive drugs were administered or not.

The authors conclude: "Extensive recent preclinical literature suggests that stem cell-based therapies may offer promise; however the impact of compromised internal validity and publication bias means that efficacy is likely to be somewhat lower than reported here."

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Will stem cell therapy help cure spinal cord injury?

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Novartis AG (NOVN) has a promising therapy for cancer. Its just not sure how to get it to patients easily.

The treatment is so potent that it cleared malignant cells in about 90 percent of patients facing almost certain death from the most common form of cancer in children.

The approach involves taking T cells, part of the bodys immune system, from the blood and engineering them to identify proteins on cancer cells. When returned to the patients bloodstream, the revamped T cells seek and destroy cancer cells. Its so specific that a single mistake can mean death for a patient, and so turbo-charged that Novartis plans to set up a network of hospitals versed in treating the spiking fever, chills and flu-like symptoms that may come as side effects.

The question is really if this is the right way to go at immunotherapy, a burgeoning field of medicine that empowers the immune system to fight diseases such as cancer, Michael Leuchten, an analyst at Barclays Plc in London, said in an interview.

Cancer cells can use proteins on their surfaces as biological cloaks of invisibility to elude detection by the immune-system cells policing the body. Immunotherapies include checkpoint agents, drugs that strip away such disguises and expose cancer cells to attack; products such as Dendreon Corp. (DNDN)s Provenge, which combines a patients immune cells with vaccine components in an infusion; and so-called biconjugated antibodies that help immune cells anchor themselves to cancerous ones.

The total market may amount to a $35 billion watershed for cancer drugs, according to Andrew Baum, a pharmaceutical analyst for Citigroup Inc. in London. Baum sees Roche Holding AG (ROG) and Bristol-Myers Squibb Co. (BMS), based in New York, as the fields leaders. Roche -- like Novartis, based in Basel, Switzerland -- is developing an infused immunotherapy which blocks a protein that prevents the immune system from attacking cancer cells. Bristol-Myers sells the drug Yervoy, which helps the immune system fight melanoma.

Unlike those therapies, Novartiss CTL019 isnt as easy to produce and transport. For the researchers and the company, the results are worth the effort. If they find a way to deliver the treatment to the masses, CTL019, also known as CART-19, has the potential to generate $10 billion a year if approved to treat multiple forms of cancer, according to Baum.

CART-19 gives us a huge move into immunotherapy, a first-mover advantage, Chief Executive Officer Joe Jimenez said during a conference this year.

Nineteen out of 22 children who had exhausted all drug treatment and bone-marrow transplant options for acute lymphoblastic leukemia went into remission after receiving the therapy, also known as CART-19, according to data presented this month at the American Society of Hematology meeting in New Orleans. Five patients later relapsed, including one whose new tumor cells produced a protein that enabled them to elude the souped-up T cells.

In chronic lymphocytic leukemia, a much larger market, the therapy provoked a response in 47 percent of patients, with half of those patients experiencing a complete remission.

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Novartis Needs Special Delivery for Potent Cell Therapy

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Genetic genealogy is the application of genetics to traditional genealogy. Genetic genealogy involves the use of genealogical DNA testing to determine the level and type of the genetic relationship between individuals. This application of genetics became popular with family historians in the first decade of the 21st century, as tests became affordable. The tests have been promoted by amateur groups, such as surname study groups, or regional genealogical groups, as well as research projects such as the genographic project. As of 2013 hundreds of thousands of people had been tested. As this field has developed, the aims of practitioners broadened, with many seeking knowledge of their ancestry beyond the recent centuries for which traditional pedigrees can be constructed.

The investigation of surnames in genetics can be said to go back to George Darwin, a son of Charles Darwin. In 1875, George Darwin used surnames to estimate the frequency of first-cousin marriages and calculated the expected incidence of marriage between people of the same surname (isonymy). He arrived at a figure between 2.25% and 4.5% for cousin-marriage in the population of Great Britain, higher among the upper classes and lower among the general rural population.[1]

Origin of peoples in a context of DNA genealogy is an assignment of each of them to a particular tribe or its branch (lineage) initiated in a genealogical sense by a particular ancestor who had a base (ancestral) haplotype. This also includes an estimation of a time span between the common ancestor and its current descendants. If information obtained this way can be presented in a historical context and supported, even arguably, by other independent archeological, linguistic, historical, ethnographic, anthropological and other related considerations, this can be called a success.[2] Just in the last 20 years scientists began to use Y-Chromosome markers and Mt-Chromosome markers, to provide evidence of common ancestry between individuals with a tradition of common ancestry. Two notable studies showed common heritage between men from Cohen Jewish lineages.[3]

One famous study examined the lineage of descendants of Thomas Jeffersons paternal line and male lineage descendants of the freed slave, Sally Hemmings.[4]

Bryan Sykes, a molecular biologist at Oxford University tested the new methodology in general surname research. His study of the Sykes surname obtained results by looking at four STR markers on the male chromosome. It pointed the way to genetics becoming a valuable assistant in the service of genealogy and history.[5]

The first company to provide direct-to-consumer genetic DNA testing was the now defunct GeneTree. However, it did not offer multi-generational genealogy tests. In fall 2001, GeneTree sold its assets to Salt Lake City-based Sorenson Molecular Genealogy Foundation (SMGF) which originated in 1999.[6] While in operation, SMGF provided free Y-Chromosome and mitochondrial DNA tests to thousands.[7] Later, GeneTree returned to genetic testing for genealogy in conjunction with the Sorenson parent company and eventually was part of the assets acquired in the Ancestry.com buyout of SMGF.[8]

In 2000, Family Tree DNA, founded by Bennett Greenspan and Max Blankfeld, was the first company dedicated to direct-to-consumer testing for genealogy research. They initially offered eleven marker Y-Chromosome STR tests and HVR1 mitochondrial DNA tests. They originally tested in partnership with the University of Arizona.[9][10][11][12][13][14][15]

The publication of Sykes The Seven Daughters of Eve in 2001, which described the seven major haplogroups of European ancestors, helped push personal ancestry testing through DNA tests into wide public notice. With the growing availability and affordability of genealogical DNA testing, genetic genealogy as a field grew rapidly. By 2003, the field of DNA testing of surnames was declared officially to have arrived in an article by Jobling and Tyler-Smith in Nature Reviews Genetics.[16] The number of firms offering tests, and the number of consumers ordering them, rose dramatically.[17]

The original Genographic Project was a five-year research study launched in 2005 by the National Geographic Society and IBM, in partnership with the University of Arizona and Family Tree DNA. Its goals were primarily anthropological. The project announced that by April 2010 it had sold more than 350,000 of its public participation testing kits, which test the general public for either twelve STR markers on the Y-Chromosome or mutations on the HVR1 region of the mtDNA.[18]

In 2007, annual sales of genetic genealogical tests for all companies, including the laboratories that support them, were estimated to be in the area of $60 million (2006).[7]

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Genetic genealogy - Wikipedia, the free encyclopedia

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Tomorrows oranges might just have a little spinach in them. To battle the spread of a disease called citrus greeningwhich starves trees of nutrients and causes oranges to become green, misshapen, and bitter, and to fall prematurelyTropicana (PEP) supplier Southern Gardens Citrus has been funding research to engineer an orange plant that resists greening through a spinach gene. Field trials are showing promise, according to a recent update from Food Safety News.

The Department of Agriculture last week said orange output in Florida for the 12 months that started Oct. 1 will be 121 million boxes, the lowest since 1990, reported Bloomberg News. The decrease pushed up orange juice futures prices in New York.

Citrus greening, a disease spread by a small insect called a psyllid, has plagued Floridas crop for about a decade and now threatens other citrus fruits such as oranges, lemons, and grapefruits in South Carolina, Georgia, Louisiana, Texas, and California. Greening has already cost Florida more than $4 billion in lost economic output and thousands of jobs since 2005, economists at the University of Florida estimate.

Having achieved little success with a search for an immune tree, unleashing psyllid predators like wasps and spraying large amounts of pesticides, growers are increasingly seeking a cure by engineering new, disease-resistant trees.

The spinach gene produces a protein that attacks the bacteria, according to Erik Mirkov, a Texas A&M University plant pathologist whos leading the study. And no, it does not make the oranges taste like spinach. Mirkov has grafted shoots of the new variety onto existing trees to help them flower faster, thus hastening safety testing of the new pollen on animals including bees and mice and, eventually, government testing of the juice. His work is described in a July New York Times story:

In some rows were the trees with no new gene in them, sick with greening. In others were the 300 juvenile trees with spinach genes, all healthy. In the middle were the trees that carried his immediate hopes: 15 mature Hamlins and Valencias, seven feet tall, onto which had been grafted shoots of Dr. Mirkovs spinach gene trees.

While Southern Gardens testing has been positive, any juice from these trees remains years away. And their success on the market would be challenged by consumer concerns about the effect of genetically modified foods on health (such as provoking allergies) and the environment (like escaping into the wild or harming beneficial insects). As Southern Gardens President Ricke Kress told Food safety News: Proof of success will only come with the public.

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Can Genetically Modifying an Orange With a Spinach Gene Save Florida’s Crop?

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PUBLIC RELEASE DATE:

17-Dec-2013

Contact: Ben Jones B.P.Jones@leeds.ac.uk University of Leeds

A new gene mutation which will help doctors give a more accurate diagnosis of a particular type of brain and muscle disease in children has been discovered for the first time by University of Leeds experts.

Mitochondrial myopathy, as it is known, causes muscle weakness, movement problems and learning difficulties and affects more than 70,000 people in the UK.

For the first time, mutations in a particular gene, MICU1, have been linked to myopathy. The discovery gives a better understanding of the genetic causes of the condition.

Working with colleagues from University College London and Great Ormond Street Hospital, as well as colleagues from the Netherlands and Italy, Dr Eamonn Sheridan's team identified two mutations in the gene using a technique called exome sequencing an alternative to whole genome sequencing.

Mitochondria are the batteries of the body's cells where energy is produced. They are found in large numbers in nerve and muscle cells, which have high energy demands. To function properly, mitochondria need a certain amount of calcium. If calcium levels are either too high or too low, they stop working properly.

MICU1 carries instructions for a protein which is essential for mitochondrial function.

Researchers found that mutations in the MICU1 gene caused less protein to be produced which led to an increase in calcium in the mitochondria. This resulted in damage to the mitochondria and changes in calcium levels in the rest of the cell.

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New gene mutation will help better diagnosis of myopathy

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CTVNews.ca Staff Published Tuesday, December 17, 2013 4:23PM EST Last Updated Tuesday, December 17, 2013 6:29PM EST

Parents of mentally ill adults have long reported that the first signs of mental illness emerged during their childrens teen years. Now researchers say theyve identified what they call the teen gene, which could be the biological trigger for teen-related behavioural problems.

Researchers at the McGill-affiliated Douglas Institute Research Centre say the gene, called DCC, controls dopamine connectivity in the prefrontal cortex during adolescence, and that dysfunction of the gene -- through stress and drug abuse, for example -- can lead to long-term mental health consequences.

The prefrontal cortex, associated with judgment, decision-making and flexibility, is crucial for learning, motivation, and cognitive processes. And because the prefrontal cortex continues to develop into adulthood, the region is highly susceptible to being shaped by life experiences in adolescence.

"Certain psychiatric disorders can be related to alterations in the function of the prefrontal cortex and to changes in the activity of the brain chemical dopamine," said Cecilia Flores, senior author on the study and psychiatry professor at McGill University. "Prefrontal cortex wiring continues to develop into early adulthood, although the mechanisms were, until now, entirely unknown."

The breakthrough discovery, which provides the first clues to a fuller understanding of brain development, could hold promise in combating severe mental illness, the researchers say.

What we are finding is that the function and the amount of DCC that we have during adolescence can determine our vulnerability to certain psychiatric disorders in adulthood, Flores told CTV News.

And whats more, the study suggested that the amount or the levels of the DCC gene during adolescence can be changed (through) life events.

Dr. Hazen Gandy, a child and adolescent psychiatrist at CHEO,notes the work was partially done in mice,which means much more work needs to be done to confirm it plays a role in humans.

It is a piece of the puzzle;I think its hard to say how big a piece it is-- wehave to appreciate that this is research in animal models and we always have to be careful about translating what we find in animal models in terms of how that really translates in human behaviour, Gandy told CTV News. But it is a piece of larger puzzle of understanding human brain development, and I think it speaks to the need for us to really look atfocusing on early detection and working on better ways of intervention in the adolescent population.

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Discovery of 'teen gene' could help combat severe mental illness later in life

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PUBLIC RELEASE DATE:

18-Dec-2013

Contact: Sarah Avery sarah.avery@duke.edu 919-660-1306 Duke University Medical Center

DURHAM, N.C. A genetic trait known to make some people especially sensitive to stress also appears to be responsible for a 38 percent increased risk of heart attack or death in patients with heart disease, scientists at Duke Medicine report.

The finding outlines a new biological explanation for why many people are predisposed to cardiovascular disease and death, and suggests that behavior modification and drug therapies could reduce deaths and disability from heart attacks.

The study appears in the Dec. 18, 2013, issue of the journal PLOS ONE.

"We've heard a lot about personalized medicine in cancer, but in cardiovascular disease we are not nearly as far along in finding the genetic variants that identify people at higher risk," said senior author Redford B. Williams Jr., M.D. director of the Behavioral Medicine Research Center at Duke University School of Medicine. "Here we have a paradigm for the move toward personalized medicine in cardiovascular disease."

Williams and colleagues built on previous work at Duke and elsewhere that identified a variation in a DNA sequence, known as a single nucleotide polymorphism (SNP), where one letter in the genetic code is swapped for another to change the gene's function. The SNP the Duke team focused on occurs on the gene that makes a serotonin receptor, and causes a hyperactive reaction to stress.

In a study published last year, the researchers reported that men with this genetic variant had twice as much cortisol in their blood when exposed to stress, compared to men without the genetic variant. Known as a "stress hormone," cortisol is produced in the adrenal gland to support the body's biological response when reacting to a situation that causes negative emotions.

"It is known that cortisol has effects on the body's metabolism, on inflammation and various other biological functions, that could play a role in increasing the risk of cardiovascular disease," said lead author Beverly H. Brummett, Ph.D., associate professor of Psychiatry and Behavioral Sciences at Duke. "It has been shown that high cortisol levels are predictive of increased heart disease risk. So we wanted to examine this more closely."

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Stress reaction gene linked to death, heart attacks

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PHILADELPHIA This December marks the 40th anniversary of the Abramson Cancer Center (ACC) of the University of Pennsylvania being designated a Comprehensive Cancer Center by the National Cancer Institute. To celebrate this momentous milestone, over 400 people gathered together early this month for an event recognizing the centers vast achievements in cancer research, patient care, and education during the last four decades.

Leaders from the ACC, including its director Chi V. Dang, MD, PhD, also bestowed Bert Vogelstein, MD, a world-renowned geneticist from The Johns Hopkins University and a University of Pennsylvania alumni, with the inaugural Abramson Award. The award recognizes key achievements made by the world's most innovative contributors in the field of oncology -- those whose work has changed the paradigm of modern cancer research and clinical care.

Dr. Vogelsteins pioneering studies of the genetic causes of human cancer have placed him among the most influential biomedical scientists in the world, and his work has helped provide the conceptual basis for what is now called "personalized medicine. He and his team were the first to map cancer genomes and use genome-wide sequencing to identify the basis of a hereditary form of cancer.

Dr. Vogelstein and his colleagues have demonstrated that colorectal tumors result from the gradual accumulation of genetic alterations in specific oncogenes and tumor suppressor genes. A recent recipient of the inaugural Breakthrough Prize in Life Sciences, his work on colorectal cancers forms the foundation for much of modern cancer research, with profound implications for diagnostic and therapeutic strategies in the future.

The celebratory evening also included remarks from Penn Medicine leaders J. Larry Jameson, MD, PhD, executive vice president of the University of Pennsylvania for the Health System and Dean of the Perelman School of Medicine, and Ralph W. Muller, CEO of the University of Pennsylvania Health System, and Daniel J. Keating, III, Chair of the ACC Director's Leadership Council, who shared his personal cancer journey and the stories of a several remarkable cancer patients and survivors.

Endowed professorships are the highest honor a Perelman School of Medicine faculty member can achieve, and these important posts were highlighted throughout the evening. They are vital to the ACCs mission to stay at the forefront of cancer research and care by attracting and supporting extraordinary minds, allowing them to explore new avenues of discovery treatment, and cures. Click here for a full listing of endowed professors and the generous donors who support them.

Numerous other awards and honors were given to recognize the ACCs most promising investigators, compassionate clinicians, and distinguished teachers. Click here for a full list of honorees.

Click below to watch a video portraying the story of the Abramson Cancer Center over the past 40 years.

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Penn Medicine is one of the world's leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of theRaymond and Ruth Perelman School of Medicine at the University of Pennsylvania(founded in 1765 as the nation's first medical school) and theUniversity of Pennsylvania Health System, which together form a $4.3 billion enterprise.

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Penn Medicine's Abramson Cancer Center Celebrates 40 Years, Bestows Inaugural Abramson Award

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When personal genomics and biotech firm 23andMe was founded in Mountain View, Calif., in 2006, the hype over the genetic tests it offered directly to consumers was immediate and irresistible to many. The company promised that for a nominal fee, it could scan your saliva sample and tell you based on your genetics everything from who your ancestors were to what diseases you may be at risk of developing many years down the road. 23andMe raised more than $100 million in capital from such big-name investors as Google and Genentech. Today, the companys website boasts having close to 500,000 genotyped consumers.

So it was a surprise to some observers when, on November 22, the U.S. Food & Drug Administration (FDA) sent a strongly worded letter to 23andMe CEO Anne Wojcicki demanding that the company stop marketing its test, called Personal Genome Service (PGS), until it secures authorization from the agency. The FDA contends that PGS is a medical device being pitched for the diagnosis and prevention of disease, and therefore it must obtain approval under federal law.

Whenever regulators step in and try to yank a product off the market particularly when the company selling it is already well entrenched it invariably sparks a debate about whether over-regulation will stifle technology innovation. However, some experts believe the real issue at stake in the 23andMe controversy is not innovation, but rather the firms selling strategy. I suspect that a lot of this boils down to the way 23andMe has been marketing itself. It has taken a pretty aggressive stance in saying its services have a medical benefit, notes Reed Pyeritz, professor of medicine and chief of the division of medical genetics at the Perelman School of Medicine at the University of Pennsylvania. That does get the attention of the FDA.

Indeed, as the FDA pointed out in its letter, PGS promised to provide information on 254 health conditions, including heart disease, diabetes and breast cancer. 23andMe offered complete reports along with the test results, with advice on genetic susceptibility, potential response to particular drugs and preventative steps customers might take to protect their health. Most of the intended uses for PGS listed on your website, a list that has grown over time, are medical device uses, the warning letter says.

The understanding of the human genome is still in its infancy, and in most cases, genetic susceptibility to a disease does not translate into a definitive risk of developing that condition. The FDA expressed concern that 23andMes customers would take drastic measures to prevent diseases without fully understanding what their genetic results truly prove about their risks. The worries are well-founded because who knows what individuals will do with information that they interpret themselves? Pyeritz says. Very few genetic tests actually have been studied for clinical utility. Had 23andMe been marketing things more truthfully, I wonder if they would have ever gotten this warning letter from the FDA.

I suspect that a lot of this boils down to the way 23andMe has been marketing itself. It has taken a pretty aggressive stance in saying its services have a medical benefit. Reed Pyeritz

23andMe continues to sell PGS; however, it is only offering ancestry information and raw genetic data without any interpretation, a spokeswoman for the company told Knowledge@Wharton in an e-mail. Our goal is to work with the FDA in a way that clearly demonstrates the benefit to people and the validity of the science that underlies the test, she wrote, adding that the company intends to complete the regulatory review process.

Recreational Genetics

Just how useful are genetic tests marketed directly to consumers? Pyeritz has undertaken a few studies designed to answer that question. One set of studies, done in conjunction with the Coriell Institute for Medical Research in Camden, N.J., set out to determine the demographics of people who seek out direct-to-consumer genetic tests. The researchers discovered that most customers are Caucasian, well educated and economically upscale exactly what they expected for a product that could be considered recreational genetics, Pyeritz says.

Beyond that, we asked them what they intended to do with the information, he notes. The majority said, Were going to give it to our physicians.

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The FDA vs. 23andMe: A Lesson for Health Care Entrepreneurs

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