NEWARK, Calif., Sept. 27, 2012 (GLOBE NEWSWIRE) -- StemCells, Inc. (STEM) today announced that the first patient with an incomplete spinal cord injury has been enrolled in the Company's Phase I/II clinical trial in chronic spinal cord injury and transplanted with the Company's proprietary HuCNS-SC(R) neural stem cells. The patient, a Canadian man who suffered a thoracic spinal cord injury from a sports-related accident, was administered the cells yesterday at Balgrist University Hospital, University of Zurich, a world leading medical center for spinal cord injury and rehabilitation. This is the first patient in the second cohort of the trial, which will be comprised of four patients who retain some sensory function below the level of trauma and are therefore considered to have an incomplete injury.

"This is an important milestone for StemCells and the spinal cord injury community as it is the first time anyone has ever transplanted neural stem cells into a patient with an incomplete injury," said Stephen Huhn, MD, FACS, FAAP, Vice President and Head of the CNS Program at StemCells, Inc. "Given the encouraging interim data from the most severely injured patient cohort that we reported earlier this month, testing patients with less severe injury should afford us an even better opportunity to continue to test safety and to detect and assess clinical changes. Unlike the patients in the first cohort, patients with incomplete injuries have retained a degree of spinal cord function that might be even further augmented by transplantation with neural stem cells."

Earlier this month, the Company reported that interim six-month data from the first patient cohort in the Phase I/II clinical trial continued to demonstrate a favorable safety profile, and showed considerable gains in sensory function in two of the three patients compared to pre-transplant baselines. Patients in the first cohort all suffered a complete injury to their spinal cord, leaving them with no neurological function below the level of injury. Following transplantation with HuCNS-SC cells, there were no abnormal clinical, electrophysiological or radiological responses to the cells, and all the patients were neurologically stable through the first six months after transplantation. Changes in sensitivity to touch, heat and electrical stimuli were observed in well-defined and consistent areas below the level of injury in two of the patients, while the third patient remained stable. Importantly, the changes in sensory function were confirmed objectively by measures of electrical impulse transmission across the site of injury, each of which correlated with the clinical examination.

About the Spinal Cord Injury Clinical Trial

The Phase I/II clinical trial of StemCells, Inc.'s HuCNS-SC(R) purified human adult neural stem cells is designed to assess both safety and preliminary efficacy. Twelve patients with thoracic (chest-level) neurological injuries at the T2-T11 level are planned for enrollment, and their injuries must have occurred within three to twelve months prior to transplantation of the cells. In addition to assessing safety, the trial will assess preliminary efficacy based on defined clinical endpoints, such as changes in sensation, motor function and bowel/bladder function. The Company has dosed the first patient cohort, all of whom have injuries classified as AIS A according to the American Spinal Injury Association Impairment Scale (AIS). In AIS A injuries, there is no neurological function below the injury level. The second cohort will be patients classified as AIS B, in which there is some preservation of sensory or motor function below the injury level. The third cohort will be patients classified as AIS C, in which there is some preservation of both sensory and motor function.

All patients will receive HuCNS-SC cells through direct transplantation into the spinal cord and will be temporarily immunosuppressed. Patients will be evaluated regularly in the post-transplant period in order to monitor and assess the safety of the HuCNS-SC cells, the surgery and the immunosuppression, as well as to measure any recovery of neurological function below the injury site. The Company intends to follow the effects of this therapy long-term, and each of the patients will be invited to enroll into a separate four year observational study after completing the Phase I/II study.

The trial is being conducted at Balgrist University Hospital, University of Zurich, a world leading medical center for spinal cord injury and rehabilitation, and is open for enrollment to patients in Europe, Canada and the United States. Enrollment for the second cohort is now underway. If you believe you may qualify and are interested in participating in the study, please contact the study nurse either by phone at +41 44 386 39 01 or by email at stemcells.pz@balgrist.ch.

Additional information about the Company's spinal cord injury program can be found on the StemCells, Inc. website at http://www.stemcellsinc.com/Therapeutic-Programs/Clinical-Trials.htm and at http://www.stemcellsinc.com/Therapeutic-Programs/Spinal-Cord-Injury.htm, including video interviews with Company executives and independent collaborators.

About Balgrist University Hospital

Balgrist University Hospital, University of Zurich is recognized worldwide as a highly specialized center of excellence providing examination, treatment and rehabilitation opportunities to patients with serious musculoskeletal conditions. The clinic owes its leading international reputation to its unique combination of specialized medical services. The hospital's carefully-balanced, interdisciplinary network brings together under one roof medical specialties including orthopedics, paraplegiology, radiology, anesthesiology, rheumatology, and physical medicine. More information about Balgrist University Hospital is available at http://www.balgrist.ch.

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StemCells, Inc. Achieves Spinal Cord Injury Milestone With First Neural Stem Cell Transplant Into Patient With Sensory ...

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By Barbara Puffer, Conn. Health I-Team Writer

The American Civil Liberties Union (ACLU) this week asked the U.S. Supreme Court to invalidate patents for two genes used to test for hereditary breast and ovarian cancer held by a Utah Company.

The lawsuit against Myriad Genetics of Utah which holds the patents on genes called BRCA1 and BRCA 2 charges that the patents are illegal and restrict both scientific research and patients access to medical care. In the 15 years that Myriad had held the patent, the cost for the test has more than doubled to about $3,340 -- and plaintiffs say that the cost is too expensive for some women.

The ACLU and the Public Patent Foundation filed the lawsuit against Myriad in 2009 on behalf of 20 plaintiffs including Ellen Matloff of New Haven, a research scientist in genetics at the Yale School of Medicine and director of Cancer Genetic Counseling at the Yale Cancer Center.

The suit also raises broad legal and ethical questions under the First Amendment about whether genes are products of nature or commercial commodities.

Myriad has previously stated: Since a landmark US Supreme Court decision in 1980, the US Patent and Trademark Office has granted tens of thousands of genetic and genetic related patents which cover a large number of life-saving pharmaceutical and diagnostic productsMyriad strongly believes that its patents are valid and enforceable and will be upheld by the courts.

For women who have had breast or ovarian cancer before the age of 50, and/or have immediate family members who had had one of these cancers, the BRCA1 and BRCA2 genetic test could be a lifesaver. Precautions can be taken by those who discover they have the mutation. The testing also detects familial risk in men. Yet many uninsured and underinsured candidates are finding Myriads monopoly testing costs out of reach, the lawsuit says.

Connecticut has the second highest incidence of female breast cancer in the nation with 2,920 new breast cancer cases diagnosed in 2008and ranks 35th in the nation for breast cancer mortality. The U.S Preventive Services Task Force estimates that 2 percent of all women which would include about 2,700 of the uninsured women in Connecticutare likely candidates for the BRAC Analysis test.

Sandra Park, staff attorney with the ACLU Womens Rights Project, said, We are asking the Supreme Court to rule in favor of women who are counting on access to the best possible medical care and research. No single company should be able to stop the brightest scientific minds from advancing what we know about two genes that are connected to devastating diseases.

In July 2011, the U.S. Court of Appeals upheld the patents. The appeals court decision was appealed to the U.S. Supreme Court and in March, the high court issued an order directing the appeals court to reconsider its initial decision in light of a related patent case decided by the court a year earlier. In August, by a 2-to-1 vote, the appeals court ruled Myriad could hold the patents.

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Breast cancer gene patent suit heads back to U.S. Supreme Court

Recommendation and review posted by Bethany Smith

Public release date: 27-Sep-2012 [ | E-mail | Share ]

Contact: Paula Faria pfaria@wakehealth.edu 336-716-1279 Wake Forest Baptist Medical Center

WINSTON-SALEM, N.C. Sept., 26, 2012 Fewer than 100 people in the world are known to be affected by a movement disorder called rapid-onset dystonia-parkinsonism (RDP), but its symptoms are life-changing. Seemingly normal young people are suddenly and dramatically unable to control movement of their arms or legs and have trouble speaking or swallowing. A normal life is nearly impossible.

RDP is caused by a genetic mutation (ATP1A3) that often runs in families. Now Wake Forest Baptist Medical Center researchers believe that same genetic predisposition might also be associated with psychiatric problems, such as anxiety, mood disorders and substance abuse/dependence.

Allison Brashear, M.D., chair of neurology at Wake Forest Baptist, and the lead investigator in this $2.5 million, four-year study funded by the National Institute of Neurological Disorders and Stroke (NINDS), said this is one of the few studies to look at this rare condition that has no known treatment. "RDP often occurs suddenly after a stressful episode, such as running a marathon or childbirth," said Brashear. "Patients become severely disabled over hours to days and do not recover."

Brashear and nine other Wake Forest Baptist scientists, as well as colleagues from Harvard Medical School and Mount Sinai School of Medicine, enrolled 56 individuals for this study. Twenty-three of the RDP patients were related, three RDP patients were unrelated.

Of the 29 participants with the genetic mutation, 26 had dystonia symptoms and three were carriers, but without the motor symptoms; the remaining 27 participants without the mutation, were enrolled as the control group.

Following standard physical examination and behavioral assessment, Brashear's team found that individuals with the mutation but without the motor symptoms did not report any history of psychiatric disorder, while those with dystonia symptoms reported anxiety (48 percent; control 41percent), mood (50 percent; control 22 percent), psychotic (19 percent; control 0 percent) and substance abuse/dependence (38 percent; control 27 percent).

Researchers concluded that ATP1A3 mutations cause a wide spectrum of motor and nonmotor symptoms and that psychotic symptoms tended to develop before or simultaneous to the beginning of motor dysfunction. Further, the team believes the findings suggest psychiatric disorders may be another expression of the genetic mutation. Brashear said there are also clinical implications as a result of this study and suggested that those who deal with patients with psychosis, particularly in families with a history of dystonia-parkinsonism, consider the genetic mutation as a possible contributor to the mental illness.

###

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Research suggests shared genetic link in psychiatric and movement disorders

Recommendation and review posted by Bethany Smith

Public release date: 26-Sep-2012 [ | E-mail | Share ]

Contact: Kristen Woodward kwoodwar@fhcrc.org 206-667-5095 Fred Hutchinson Cancer Research Center

SEATTLE Uncovering colon cancer's genetic roots is the focus of a new $13 million, four-year, National Cancer Institute-funded project at Fred Hutchinson Cancer Research Center. Ulrike (Riki) Peters, Ph.D., M.P.H., a member of the Hutchinson Center's Public Health Sciences Division, will lead the effort. She and her colleagues will use next-generation sequencing, a technique that captures entire genome sequences, to identify genetic links to colorectal cancer.

"This is an important step, to look at much of the genetic variation across the entire genome. We didn't have the opportunity to study this in the past with the technologies we had before," Peters said. "We are now able to investigate millions of common and rare variants across the genome. Next-generation sequencing is becoming more readily available to look at these variants on a large scale." Colorectal cancer is the third most common and second deadliest cancer in the U.S., killing more than 50,000 every year. About one-third of these cancers can be attributed to heritable factors, meaning genetic mutations play a role in the cancer's development. Some of these genetic variations can also affect a person's susceptibility to environmental risk factors. For example, smoking increases the risk of colorectal cancer, but it's possible that certain genetic factors in combination with smoking could even further increase that risk.

For the past four years, Peters and colleagues have been studying the genes linked to colorectal cancer through the Genetics and Epidemiology of Colorectal Cancer Consortium, a collaboration involving researchers from North America, Australia and Europe who have pooled data from approximately 40,000 study participants, approximately half of whom have colorectal cancer. The Hutchinson Center houses GECCO's coordinating center and Peters is its principal investigator.

Due to the infrastructure the team already has built and the knowledge gained from GECCO, they are well equipped for this next stage of work on heritable risk factors for colorectal cancer.

Peters' new study will use next-generation sequencing to reveal entire genome sequences of a subset of GECCO's samples. Her study is among the first NCI-funded projects to use this technology on such a large sample set.

Peters' past studies have also looked at genetic links to colorectal cancer in these same study participants, but using the traditional means of genotyping allowed her group to identify only the most common variants and only certain types of mutations. Next-generation sequencing will capture more rare variants and many more types of genetic irregularities that could be linked to heritable factors of colorectal cancer.

Identifying rare genetic variants involved in colorectal cancer could ultimately help everyone with or at risk for this disease, Peters said. Knowing which genes play a role in triggering the cancer will lead to a better understanding of how the cancer develops and could ultimately lead to improved drug development.

Peters' and other researchers' work has identified about 20 different common genetic links to colorectal cancer, which explains about 8 to 10 percent of inherited colorectal cancers. "Our new grant will allow us to identify some of the missing heritability that has not been found so far," Peters said.

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Colorectal cancer genetics research gets $13 million boost

Recommendation and review posted by Bethany Smith

ST. FRANCIS, Wis. There was a time when Marquis Daniels thought he would never play again. Now, after recovering from a spinal cord injury he suffered in February 2011 and playing out the rest of last season in a reserve role in Boston, the veteran guard has signed with the Milwaukee Bucks -- likely filling the team's final roster spot for the upcoming season.

Daniels averaged just 3.2 points in 38 games with the Boston Celtics last season, but he played a key role off the bench on defense due to his ability to guard quick point guards and also longer wing players. At a Bucks workout last week, Daniels, 31, said he wants to be known primarily as an unselfish player the kind of player who will play defense and create for his teammates, first and foremost.

But for now, he's just happy to be a professional basketball player at all. After a collision on the court resulted in a bruised spinal cord which was made worse by a preexisting condition making him more susceptible to neck or spinal injuries, Daniels said there were questions about his ability to return to the court.

"Once a couple injuries happened, they were like, 'You can't play no more,'" he said. "I was like, 'I'm fine. I can walk.' My doctor gave me the surgery and said I could play again."

After the surgery, Daniels said he felt some of his skills on the court came easier than they had in the past.

"Actually, I feel so much better now," Daniels said. "I wish I would have known earlier in my career. My strength and my grip and everything is a lot better than it had been in the past."

With a healthy Daniels, the Bucks get a versatile player who can defend multiple positions something their defense desperately needed, considering how small in stature Milwaukee's guards are, collectively. Daniels' spot on the team may make it more difficult for rookie Doron Lamb to get minutes, but for a backcourt desperate for defense, Daniels' signing was indeed necessary.

Daniels' deal is expected to be a one-year contract, but the details of the contract have not yet been released by the Bucks.

Follow Ryan Kartje on Twitter.

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Bucks fill out roster with ex-Celtics swingman

Recommendation and review posted by sam

DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/xwcbjb/applied) has announced the addition of John Wiley and Sons Ltd's new book "Applied Statistics for Network Biology. Quantitative and Network Biology (VCH)" to their offering.

This book introduces a number of cutting edge statistical methods which can be used for the analysis of genomic, proteomic and metabolomic data sets. In particular in the field of systems biology, researchers are trying to analyze asmuch data as possible in a given biological system (such as a cell or an organ). The appropriate statistical evaluation of these large scale data is critical for the correct interpretation and different experimental approaches require different approaches for the statistical analysis of these data. This book is written by biostatisticians and mathematicians but aimed at experimental researcher as well as computational biologists who often lack an appropriate background in statistical analysis.

Key Topics Covered:

MODELING, SIMULATION AND MEANING OF GENE NETWORKS.

Network Analysis to Interpret Complex Phenotypes

Stochastic Modelling of Regulatory Networks

Modeling eQTL in Multiple Populations

INFERENCE OF GENE NETWORKS.

Transcriptional Network Inference based on Information Theory

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Research and Markets: Applied Statistics for Network Biology: Quantitative and Network Biology (VCH)

Recommendation and review posted by Bethany Smith

25.09.2012 - (idw) Julius-Maximilians-Universitt Wrzburg

Many genes are suspected of being involved in the development of attention deficit hyperactivity disorder (ADHD). A Franco-German research group has now examined the role of one of these more closely and discovered clear indications of its complicity. Its scientific name is lphn3. In humans, this gene lies on chromosome 4 and codes the protein latrophilin 3, which may play a role as a synaptic protein and receptor in the brain when the typical characteristics of attention deficit hyperactivity disorder emerge: people affected struggle to focus their attention over longer periods, they are easily distracted, they tire quickly, they often react impulsively, and they demonstrate obvious motor restlessness.

Focus on the latrophilin 3 gene

Latrophilin 3 has long been suspected of being partly responsible for the typical characteristics of ADHD. Though, not all that much is known to date about its role within the physiological processes of the nervous system, says Professor Klaus-Peter Lesch.

Lesch is Chairman of the Department of Molecular Psychiatry and Spokesman for the ADHD Clinical Research Group at the University of Wrzburgs Department of Psychiatry, Psychosomatics, and Psychotherapy. He has had his sights on this protein for a few years now. And he is not alone: Researchers from the USA and Spain have recently shown that a particular variant of the latrophilin 3 gene is frequently found in the genetic material of patients who are still suffering from ADHD in adulthood, says Lesch. What is more, the gene has also been identified as one of a total of 86 risk genes that are suspected of triggering drug dependency. The occurrence of drug dependency is above average in ADHD patients.

Experiments on zebrafish larvae

To improve understanding of the role that latrophilin 3 plays in the development of ADHD symptoms, Lesch and scientists from the Institute of Neurobiology in Gif-sur-Yvette, France, conducted experiments with zebrafish larvae. Zebrafish have now become the standard model in science for examining the genetic fundamentals of brain development and behavior, explains Lesch.

In their experiments, the researchers inhibited the lphn3 gene during a particular development phase and then examined the behavior of the fish larvae. They concentrated primarily on the movement activity of the larvae as an easily measurable expression of motor restlessness.

The results

The outcome: We observed a significant increase in swimming distances and average speed in these fish larvae compared to a control group, write the authors. This effect was also evident during the night-time sleep phases in the same way as human ADHD patients can demonstrate hyperactivity symptoms in their sleep.

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ADHD: A gene makes fish larvae hyperactive

Recommendation and review posted by Bethany Smith

LEXINGTON, Mass., Sept. 26, 2012 /PRNewswire/ --Shire plc (LSE: SHP; NASDAQ: SHPG), today announced the appointment of Frederic Chereau as Senior Vice President and Franchise Lead, Angioedema, for its Human Genetic Therapies (HGT) business. In this role, Frederic will oversee the development and execution of the global strategy for the angioedema franchise. He will report to Sylvie Gregoire, President of Shire HGT. Frederic will be based in Shire's office in Lexington, Massachusetts.

"Frederic brings a wealth of experience from top pharmaceutical and biotech companies to Shire HGT, and we know he will be an important asset as we continue to grow and develop our Angioedema Franchise," said Sylvie Gregoire, President, Shire HGT. "With our recent strategic hires, we continue to strengthen our leadership team at HGT, and Frederic will support our goal of helping those with rare diseases lead better lives."

Frederic was previously President and CEO of Pervasis Therapeutics, which was recently acquired by Shire Regenerative Medicine. Prior to Pervasis, he spent nine years with Genzyme Corporation where he held a number of positions of increasing responsibility in Europe and the US, including Vice President and General Manager, leading the company's global cardiovascular business unit. Frederic began his career with Hemotech in France where he held various sales and marketing positions.

Frederic is currently a Member of the Board of Directors of the French American Chamber of Commerce of New England and a Member of Strategic Advisory Board of the La Rochelle Business School. Fluent in both French and English, Frederic holds a Bachelor's Degree in Physics from the University of Paris, a Master's Degree in Business Administration from La Rochelle Business School and an Executive MBA from INSEAD.

Notes to editors

Shire enables people with life-altering conditions to lead better lives.

Through our deep understanding of patients' needs, we develop and provide healthcare in the areas of:

as well as other symptomatic conditions treated by specialist physicians.

We aspire to imagine and lead the future of healthcare, creating value for patients, physicians, policymakers, payors and our shareholders.

"SAFE HARBOR" STATEMENT UNDER THE PRIVATE SECURITIES LITIGATION REFORM ACT OF 1995

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Frederic Chereau Joins Shire Human Genetic Therapies to Lead Angioedema Franchise

Recommendation and review posted by Bethany Smith

SADDLE BROOK, N.J., Sept. 25, 2012 /PRNewswire/ -- In a study published by the journal Nature on Sunday, scientists evaluated breast cancer from a genetic perspective and found distinct genetic differences in patients' tumors. The results of the research point to the fact that analyzing genetics is not only helpful for cancer research, but imperative. Based on the study, scientists conclude that breast cancer can be broken down into four different subtypes. Scientists hope to develop more efficient preventions and treatments for the disease based on the genomes studied.

Genetic Testing Laboratories Inc. offers a DNA test that highlights possible predispositions to some of the most ubiquitous diseases and conditions -- breast cancer included. The company specializes in DNA tests, covering a multitude of specialty tests including ancestral and paternity testing. As the most recent research shows, breast cancer is identifiable through biological details present. Genetic factors undoubtedly influence the onset of breast cancer as well as the treatments necessary to impede the spread of the disease.

As Breast Cancer Awareness Month approaches, people acknowledge the impact the disease has on many families worldwide. Stefan A. Long, Executive Director of GTL continues to stress the importance of taking preventative action:

"Our Genetic Predisposition Test offers a private, convenient way for people to understand and assess their genome. Our test covers 25 genetic predispositions to diseases that plague millions of Americans every year, and will continue to do so unless we take preventative action."

According to the National Cancer Institute, children with one parent carrying the autosomal dominant genetic predisposition have a 50 percent chance of inheriting a predisposition to breast cancer. Similarly, based on self-reports and independently verified cases, 83 to 97 percent of those diagnosed with breast cancer have a family history of the disease. Because genetics so strongly contribute to the likelihood of a positive breast cancer diagnosis, it is crucial to take action through education and preventative measures.

"The main goal of our DNA Predisposition Test is to help people make informed decisions based on their genetics. While it's impossible to control your genes, it's possible to make changes that keep genetic predispositions at bay," says Long.

To learn more about GTL, visit http://www.gtldna.com.

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Breakthrough Research Emphasizes Importance Of Genetics In Breast Cancer

Recommendation and review posted by Bethany Smith

(SACRAMENTO, Calif.) - Deborah K. Lieu, a stem cell scientist in cardiovascular medicine at UC Davis Health System, has received a $1.3 million research grant from the California Institute for Regenerative Medicine (CIRM) to develop stem cells that could serve as a biological alternative to the electronic pacemakers that people now use to regulate heart rhythm.

According to Lieu, each year 350,000 cardiology patients with abnormal heart rhythms receive electronic pacemakers to maintain a normal heart beat. The devices, while effective, have several disadvantages, including limited battery life and poor response to changing heart rates, such as when a person is exercising. Lieu, who is working with colleague Nipavan Chiamvimonvat, the Roger Tatarian Endowed Professor of Cardiovascular Medicine at UC Davis, plans to examine ways to improve the generation of pacemaking cells using human-induced pluripotent stem cells (hiPSCs), potentially creating what she calls a "biopacemaker."

"There are more than 3 million patients around the country who are dependent on electronic pacemakers," said Lieu. "Each one costs about $58,000 to implant and requires follow-up surgery about every 5 to 10 years to change batteries. Creating a biopacemaker from stem cells would avoid the burden of battery replacement and provide the physiological benefit of enabling a person's heart to naturally adapt to a rising heart rate during activities such as exercise."

Lieu's grant was among more than two dozen projects that received support from state stem cell agency's governing board last week as part of CIRM's Basic Biology awards program. The funding focuses on basic research projects that can provide a better understanding about the fundamental mechanisms of stem cell biology and move researchers closer to knowing how best to use stem cells to help patients.

To create the pacemaking cells, Lieu and her colleagues plan to manipulate an ion channel (the SK channels in cardiac myocytes) to alter the calcium signaling mechanisms during hiPSC differentiation. Stem cell scientists create hiPSCs - typically from an adult cell such as a skin cell - by inducing a "forced" expression of specific genes. Once reprogrammed, the cells take on a variety of capabilities (becoming pluripotent) and offer a range of stem cell treatment possibilities.

Development of a biopacemaker could also benefit the one-in-20,000 infants and premature babies suffering from congenital heart-rhythm dysfunction who currently are not suitable candidates for electronic pacemakers. Infants are physically too small for the device. A biological pacemaker could fit with their small stature and then grow as the infant grows.

Collaborating with Lieu and Chiamvimonvat on the research project will be Jan Nolta, director of the UC Davis Institute for Regenerative Cures; Donald Bers, chair of the UC Davis Department of Pharmacology; and James Chan, assistant professor in the Department of Pathology and affiliated with the NSF Center for Biophotonics Science and Technology at UC Davis.

UC Davis is playing a leading role in regenerative medicine, with nearly 150 scientists working on a variety of stem cell-related research projects at campus locations in both Davis and Sacramento. The UC Davis Institute for Regenerative Cures, a facility supported by the California Institute for Regenerative Medicine (CIRM), opened in 2010 on the Sacramento campus. This $62 million facility is the university's hub for stem cell science. It includes Northern California's largest academic Good Manufacturing Practice laboratory, with state-of-the-art equipment and manufacturing rooms for cellular and gene therapies. UC Davis also has a Translational Human Embryonic Stem Cell Shared Research Facility in Davis and a collaborative partnership with the Institute for Pediatric Regenerative Medicine at Shriners Hospital for Children Northern California. All of the programs and facilities complement the university's Clinical and Translational Science Center, and focus on turning stem cells into cures. For more information, visit http://www.ucdmc.ucdavis.edu/stemcellresearch.

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Pacemaker from Stem Cells Receives Research Funding

Recommendation and review posted by simmons

Public release date: 25-Sep-2012 [ | E-mail | Share ]

Contact: Heather Buschman hbuschman@sanfordburnham.org 858-795-5343 Sanford-Burnham Medical Research Institute

LA JOLLA, Calif., September 25, 2012 The process researchers use to generate induced pluripotent stem cells (iPSCs)a special type of stem cell that can be made in the lab from any type of adult cellis time consuming and inefficient. To speed things up, researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) turned to kinase inhibitors. These chemical compounds block the activity of kinases, enzymes responsible for many aspects of cellular communication, survival, and growth. As they outline in a paper published September 25 in Nature Communications, the team found several kinase inhibitors that, when added to starter cells, help generate many more iPSCs than the standard method. This new capability will likely speed up research in many fields, better enabling scientists around the world to study human disease and develop new treatments.

"Generating iPSCs depends on the regulation of communication networks within cells," explained Tariq Rana, Ph.D., program director in Sanford-Burnham's Sanford Children's Health Research Center and senior author of the study. "So, when you start manipulating which genes are turned on or off in cells to create pluripotent stem cells, you are probably activating a large number of kinases. Since many of these active kinases are likely inhibiting the conversion to iPSCs, it made sense to us that adding inhibitors might lower the barrier."

According to Tony Hunter, Ph.D., professor in the Molecular and Cell Biology Laboratory at the Salk Institute for Biological Studies and director of the Salk Institute Cancer Center, "The identification of small molecules that improve the efficiency of generating iPSCs is an important step forward in being able to use these cells therapeutically. Tariq Rana's exciting new work has uncovered a class of protein kinase inhibitors that override the normal barriers to efficient iPSC formation, and these inhibitors should prove useful in generating iPSCs from new sources for experimental and ultimately therapeutic purposes." Hunter, a kinase expert, was not involved in this study.

The promise of iPSCs

At the moment, the only treatment option available to many heart failure patients is a heart transplant. Looking for a better alternative, many researchers are coaxing stem cells into new heart muscle. In Alzheimer's disease, researchers are also interested in stem cells, using them to reproduce a person's own malfunctioning brain cells in a dish, where they can be used to test therapeutic drugs. But where do these stem cells come from? Since the advent of iPSC technology, the answer in many cases is the lab. Like their embryonic cousins, iPSCs can be used to generate just about any cell typeheart, brain, or muscle, to name a fewthat can be used to test new therapies or potentially to replace diseased or damaged tissue.

It sounds simple enough: you start with any type of differentiated cell, such as skin cells, add four molecules that reprogram the cells' genomes, and then try to catch those that successfully revert to unspecialized iPSCs. But the process takes a long time and isn't very efficientyou can start with thousands of skin cells and end up with just a few iPSCs.

Inhibiting kinases to make more iPSCs

Zhonghan Li, a graduate student in Rana's laboratory, took on the task of finding kinase inhibitors that might speed up the iPSC-generating process. Scientists in the Conrad Prebys Center for Chemical Genomics, Sanford-Burnham's drug discovery facility, provided Li with a collection of more than 240 chemical compounds that inhibit kinases. Li painstakingly added them one-by-one to his cells and waited to see what happened. Several kinase inhibitors produced many more iPSCs than the untreated cellsin some cases too many iPSCs for the tiny dish housing them. The most potent inhibitors targeted three kinases in particular: AurkA, P38, and IP3K.

Read more from the original source:
Making it easier to make stem cells

Recommendation and review posted by Bethany Smith

ScienceDaily (Sep. 25, 2012) The process researchers use to generate induced pluripotent stem cells (iPSCs) -- a special type of stem cell that can be made in the lab from any type of adult cell -- is time consuming and inefficient. To speed things up, researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) turned to kinase inhibitors. These chemical compounds block the activity of kinases, enzymes responsible for many aspects of cellular communication, survival, and growth.

As they outline in a paper published September 25 in Nature Communications, the team found several kinase inhibitors that, when added to starter cells, help generate many more iPSCs than the standard method. This new capability will likely speed up research in many fields, better enabling scientists around the world to study human disease and develop new treatments.

"Generating iPSCs depends on the regulation of communication networks within cells," explained Tariq Rana, Ph.D., program director in Sanford-Burnham's Sanford Children's Health Research Center and senior author of the study. "So, when you start manipulating which genes are turned on or off in cells to create pluripotent stem cells, you are probably activating a large number of kinases. Since many of these active kinases are likely inhibiting the conversion to iPSCs, it made sense to us that adding inhibitors might lower the barrier."

According to Tony Hunter, Ph.D., professor in the Molecular and Cell Biology Laboratory at the Salk Institute for Biological Studies and director of the Salk Institute Cancer Center, "The identification of small molecules that improve the efficiency of generating iPSCs is an important step forward in being able to use these cells therapeutically. Tariq Rana's exciting new work has uncovered a class of protein kinase inhibitors that override the normal barriers to efficient iPSC formation, and these inhibitors should prove useful in generating iPSCs from new sources for experimental and ultimately therapeutic purposes." Hunter, a kinase expert, was not involved in this study.

The promise of iPSCs

At the moment, the only treatment option available to many heart failure patients is a heart transplant. Looking for a better alternative, many researchers are coaxing stem cells into new heart muscle. In Alzheimer's disease, researchers are also interested in stem cells, using them to reproduce a person's own malfunctioning brain cells in a dish, where they can be used to test therapeutic drugs. But where do these stem cells come from? Since the advent of iPSC technology, the answer in many cases is the lab. Like their embryonic cousins, iPSCs can be used to generate just about any cell type -- heart, brain, or muscle, to name a few -- that can be used to test new therapies or potentially to replace diseased or damaged tissue.

It sounds simple enough: you start with any type of differentiated cell, such as skin cells, add four molecules that reprogram the cells' genomes, and then try to catch those that successfully revert to unspecialized iPSCs. But the process takes a long time and isn't very efficient -- you can start with thousands of skin cells and end up with just a few iPSCs.

Inhibiting kinases to make more iPSCs

Zhonghan Li, a graduate student in Rana's laboratory, took on the task of finding kinase inhibitors that might speed up the iPSC-generating process. Scientists in the Conrad Prebys Center for Chemical Genomics, Sanford-Burnham's drug discovery facility, provided Li with a collection of more than 240 chemical compounds that inhibit kinases. Li painstakingly added them one-by-one to his cells and waited to see what happened. Several kinase inhibitors produced many more iPSCs than the untreated cells -- in some cases too many iPSCs for the tiny dish housing them. The most potent inhibitors targeted three kinases in particular: AurkA, P38, and IP3K.

Working with the staff in Sanford-Burnham's genomics, bioinformatics, animal modeling, and histology core facilities -- valuable resources and expertise available to all Sanford-Burnham scientists and the scientific community at large -- Rana and Li further confirmed the specificity of their findings and even nailed down the mechanism behind one inhibitor's beneficial actions.

More:
Making it easier to make stem cells: Kinase inhibitors lower barrier to producing stem cells in lab

Recommendation and review posted by Bethany Smith

SEATTLE & SAN DIEGO--(BUSINESS WIRE)--

NanoString Technologies, Inc., a privately held provider of life science tools for translational research and developer of molecular diagnostics, today announced the launch of a Single Cell Gene Expression application that provides researchers with a flexible and highly sensitive approach to discovering differences in cell-to-cell gene expression profiles. The new Single Cell Gene Expression application allows a digital measurement of the expression of up to 800 unique transcripts, and offers superior performance to standard single cell microfluidic qPCR protocols. The single tube, highly multiplexed assay eliminates sample splitting and frees researchers from the constraints of fixed-format consumables employed by existing technologies, allowing them to assay genes based on the biology.

In side-by-side gene expression experiments using identical total RNA samples, reflecting RNA yields from 1 to 100 cells, the nCounter protocol demonstrated superior sensitivity compared to microfluidic qPCR. Specifically, the nCounter Single Cell Assay was able to quantify the expression of 70 percent more transcripts than the Fluidigm BioMark HD System run by a commercial service provider using an optimized single cell protocol (Citri et. al. , Nature Protocols (2012) Vol. 7(1):118-127). Results of this study will be presented today at the 2012 Select Sciences Single Cell Analysis Summit in San Diego.

Our Single Cell Assay allows cancer, stem cell and immunology researchers to profile gene expression with unmatched sensitivity and flexibility, said Barney Saunders, Ph.D., Senior Vice President and General Manager, Life Sciences at NanoString Technologies. Researchers who currently enjoy the digital precision, ease-of-use and ability to run challenging sample types such as FFPE tissue, can now utilize the nCounter system for more experiments using as little as 10pg of total RNA or even single cells.

Brad Gray, President and CEO of NanoString commented: Single cell gene expression is an area of rapidly growing interest from researchers who are already using nCounter technology as well as those who are getting to know our technology for the first time, said Brad Gray, President & CEO of NanoString Technologies. We are committed to constantly expanding the nCounter Analysis System application suite, and this new offering is just one of many new capabilities being developed by our R&D team.

The nCounter Analysis System is a fully automated, multi-application digital detection and counting system with a very simple workflow. The nCounter system has been employed in basic and translational research since it was first introduced in 2008. NanoString provides assays for gene expression, miRNA analysis and copy number variation.

Researchers attending the Single Cell Analysis Summit in San Diego can learn more about the new Single Cell Gene Expression application by attending NanoStrings workshop on Tuesday, September 25, 2012 from 12:45 1:30pm Pacific Standard Time or by visiting the NanoString booth. More information is available at http://www.NanoString.com.

About NanoString Technologies, Inc.

NanoString Technologies is a privately held provider of life science tools for translational research and developer of molecular diagnostics. The companys nCounter Analysis System is the first and only technology platform to deliver highly multiplexed, direct profiling of individual molecules in a single reaction without amplification. The nCounter Analysis System offers a cost-effective way to easily profile hundreds of gene transcripts, copy number variations, or miRNAs simultaneously with high sensitivity and precision. The companys technology enables a wide variety of basic research and translational medicine applications, including biomarker discovery and validation. NanoString is also developing the technology for use in molecular diagnostics.

The nCounter platform is for Research Use Only. Not for use in diagnostic procedures.

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NanoString Launches Single Cell Gene Expression Solution for its nCounter® Analysis System

Recommendation and review posted by Bethany Smith

By Peggy McCarthy, Conn. Health I-Team Writer

A recent study that discovered a genetic link to Post Traumatic Stress Disorder (PTSD) could ultimately lead to breakthroughs in treatment or prevention, but advances are at least a decade away because additional research is needed, according to the studys lead researcher.

Ultimately, there could be significant implications for the military where PTSD prevalence is estimated to be at least twice that of the general population because of severe trauma associated with combat duty.

Were onto something important, said Mark W. Miller, Ph.D, the researcher. Miller is a clinical research psychologist in Boston for the VAs National PTSD Center, and is an associate professor of psychiatry at Boston University School of Medicine. But he said studies with more participants that replicate his findings are needed before talking about policy implications or screening or anything like that.

Dr. Joel Gelernter, a Yale psychiatrist and chief of the VAs Molecular Genetics lab in West Haven, was not involved in this study, but does research on the genetics of PTSD. He said if the Boston study results are replicated in future research, it opens the possibility for much-needed, new drug development for treatment of PTSD.

Drug development is a very promising avenue for research if this line of evidence pans out, Gelernter said, adding that now, there is nothing really fantastic available to treat PTSD.

According to Miller, the study, which began in 2006, is the first of its kind for PTSD because it was genome-wide, which means it analyzed the entire genetic makeup of participants, giving researchers 1.5 million pieces of genetic data per person.

It was conducted by the Department of Veterans Affairs National Center for PTSD and the BU School of Medicine. Researchers interviewed and took DNA samples from about 500 participants comprised of veterans and their spouses or partners. All participants have experienced trauma, and about half have PTSD.

Participants with PTSD were found to share a variant of a gene known in scientific shorthand as RORA. The same variant had previously been linked to a range of other psychiatric conditions, including bipolar disorder, autism, depression and attention deficit hyperactivity disorder.

Patrick Bellon, executive director of the advocacy group, Veterans For Common Sense, said the study is significant for veterans. We are glad to see research that furthers our understanding and possible treatment options for PTSD, he said. This research is more important than ever with approximately 1 million new veterans returning to civilian life in the next five years. A complete understanding of this invisible wound of war, which afflicts at least 20 percent of veterans will be crucial to a successful transition for our service members.

More:
PTSD: Genetic link could lead to vet drug treatment

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A sequencing study of breast-cancer-tumor genomes suggests that cancers should be categorized by their genetic heritage, rather than where they reside in the body

Visuals Unlimited, Inc./Anne Weston/Cancer Research UK / Getty Images

In recent years, scientists have come to appreciate that breast cancer is a complex disease, triggered by myriad genetic and lifestyle factors. But the latest study of the genetics behind the disease, published in the journal Nature, shows that it may actually be slightly simpler than researchers had thought.

As part of the Cancer Genome Atlas (TCGA), a government project that is aiming to sequence tumor genomes from dozens of different cancers to help scientists better understand tumor development and treatment, scientists sequenced 510 tumors from 507 patients with breast cancer. All told, they found 30,626 mutations in these cancer cells, but those aberrations fell into four main groups.

In one subtype, basal-like tumors that account for 10% of all breast cancers, the researchers found that the mutations resembled those found in ovarian cancers, thus explaining the link between the two diseases: women at higher risk of developing breast cancer are also more vulnerable to getting ovarian cancer.

(MORE: Cracking Cancers Code)

In two related subtypes, luminal A and luminal B, which include breast cancers that contain receptors for estrogen and progesterone, the scientists found that while the mutation rate in these cancers was lower, genetic aberrations occurred in a larger number of genes, suggesting that a more complex interaction of abnormal genes contribute to these types of breast cancer.

Teasing apart such connections will be critical for improving treatment for women with these mutations: those with luminal-A cancers generally have good outcomes, while those with luminal-B tumors have more mixed results. Isolating which mutations distinguish the two subtypes may help doctors treat women with luminal-B cancers in order to make them progress more like luminal-A cases, for example.

(MORE: Why Having a Large Baby May Raise Your Risk of Breast Cancer)

In the final subtype, which are those that contain the HER2 receptors, the scientists found two smaller subgroups of HER2 cancers, which could explain why some women respond better to HER2-specific therapies like Herceptin than others. The good responders may have tumors with mutations that make the HER2 receptors more active and therefore enriched, making those cells better targets for the drug than those without the mutations.

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Genetic Study Identifies Four Main Types of Breast Cancer

Recommendation and review posted by Bethany Smith

One of the most agonizing questions that parents of children with autism ask iswhy? Now, a growing number of genetic tests are providing some answers.

Scientists say that roughly 20 percent of autism cases can be linked to known genetic abnormalities, and many more may be discovered.

Pinpointing a genetic explanation can help predict whether siblings are likely to have the disorderand even point to new, targeted treatments. Last week, for example, researchers reported that an experimental drug, arbaclofen, reduced social withdrawal and challenging behaviors in children and adults with Fragile X syndrome, the single most common genetic cause of autism.

Related: Experimental drug to treat Fragile X syndrome shows promise

No single blood test or brain scan can diagnose autism spectrum disordersin part because environmental factors also play a major role. But once a child is diagnosed, on the basis of symptoms and behavioral tests, researchers can work backward looking for genetic causes.

Both the American Academy of Pediatrics and the American College of Medical Genetics recommend that all children diagnosed with ASD be tested for Fragile X Syndrome and other chromosome abnormalities. The newest tests, called chromosomal microanalysis, can identify submicroscopic deletions or duplications in DNA sequences known to be associated with autism. Together, these tests find genetic explanations for more than 10 percent of autism cases.

Experts estimate that 400 to 1,000 individual genes may play a role in the complex neurological issues involved in autism. Tests are proliferating that look for mutations in some of those genes, thanks to new technologies that let scientists sequence many genes at once.

Mount Sinai School of Medicine in New York City, for example, is offering a new blood test that examines 30 different genes for mutations known to be associated with autism or other developmental delays.

Some autism-related genetic disorders also carry a high risk of cancer, seizures, heart disease or other health problems, so knowing about them allows families and physicians to be vigilant for such issues.

Identifying genetic causes can also help families find support groups, research programs and potential treatments tailored to their child's specific needs. For example, one of the abnormalities Mount Sinai tests for is the SHANK3 mutation on chromosome 22. It causes an autism-spectrum disorder and Phelan-McDermid Syndrome, in which communication between nerve cells is disrupted, impairing learning and memory. Researchers at Mount Sinai found that an insulin-like growth factor could reverse that disruption in mice and are now testing it in children aged 5 to 17 with SHANK3 mutations.

Read more:
New tests indicate progress in identifying the genetic roots of autism

Recommendation and review posted by Bethany Smith

SAN FRANCISCOGenetic mapping of hundreds of breast cancer tumours confirmed there are four main subtypes and discovered that one closely resembles ovarian cancer, suggesting the two may be attacked with similar therapies.

The study, in which the genomes of 825 breast tumours were sequenced, was the most comprehensive of its type involving the disease. It is part of a U.S. research project into the genetics of 20 types of cancers. Earlier this month, the group, called the Cancer Genome Atlas project, released a similar report on new DNA mutations affecting a type of lung malignancy.

The breast cancer findings, published Sunday in the journal Nature, support the expanding medical view that cancers should be categorized by their genetic origins, rather than where theyre found on the body. The link found between breast and ovarian cancer gives scientists added leverage to compare treatments and outcomes across both tumours.

There are certain mutations you can find across cancers in different organs, said Eric Topol, a professor at the Scripps Research Institute in La Jolla, Calif., who was not involved in the research. This is a real transition point, and we have to move toward more sequencing to give patients the best shot toward curing their cancer.

The personalized medicine approach has fuelled a move among drugmakers to identify treatments targeting genetic mutations, such as Roche Holdings Zelboraf and Pfizers Xalkori.

For years, doctors have classified breast cancers according to measures such as how they invade other tissues, their cellular variability, and their appearance when stained with certain chemicals, said Paul Billings, a geneticist who is medical director Life Technologies Corp., a maker of DNA sequencers in Carlsbad, Calif.

Thats the old world, Billings said. The new world is a diagnostic system that will be based on targetable DNA mutations present in breast cancer.

In the breast cancer study, a computer analysis suggests the form known as basal-like, named for its resemblance to basal skin cells, may be treatable with drugs that either cut off the tumours blood supply or prevent blood vessel growth, or chemotherapy, according to a statement from the National Cancer Institute.

The new research backed up earlier work segmenting breast cancer into four groups according to genetic markers: HER2-enriched, Luminal A, Luminal B and basal-like.

More than 72 gene-based therapies are available already, five times as many as in 2006, according to the Personalized Medicine Coalition, an industry advocacy group based in Washington.

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Genetic study points to new breast cancer treatments

Recommendation and review posted by Bethany Smith

FOSTER CITY, Calif.--(BUSINESS WIRE)--

VitaPath Genetics, Inc., a privately held company leading the exploration of the Vitanome, the subset of information that lies within our genomes that plays a critical role in how we metabolize vitamins, today announced healthcare industry veteran Catherine Burzik has been appointed Chair of its Board of Directors.

Ms. Burzik is a seasoned senior executive in the healthcare industry who has led major medical device, diagnostic, diagnostic imaging and life sciences businesses. Most recently, she served as President, Chief Executive Officer and Director of Kinetic Concepts, Inc., a leading medical device company specializing in the fields of wound care and regenerative medicine. Previously, she was President of Applied Biosystems and held senior executive positions at Eastman Kodak and Johnson & Johnson. Ms. Burzik is currently Chair of the San Antonio Branch of the Dallas Federal Reserve Board; Chair of the Canisius College Board of Trustees; and member of the Board of Directors of InHealth and the Board of Trustees of Keck Graduate School of Applied Life Sciences. She founded and chairs the Catherine M. and Francis N. Burzik Foundation, a philanthropic organization focused on bolstering science, technology, engineering and mathematics programs in higher education.

I am honored to be named Chair of the VitaPath Board of Directors, said Ms. Burzik. One of the many great outcomes from the Human Genome Project has been the increased understanding of the complexity of individual genetic variation. VitaPaths goal is to identify how genetic variations in vitamin-responsive genes can lead to specific diseases and, importantly, how the effect of these variations can be mitigated through vitamin therapy. I look forward to working with the company to realize its full potential.

Dennis Gilbert, Ph.D., President, Chief Executive Officer and Founder of VitaPath commented: For 60 years, the recommended daily allowance of vitamins has remained essentially unchanged and homogenous across the population. Our research has shown that individual genetic differences can play a large and medically important role in many common conditions. The VitaPath approach has broad applicability across several hundred genes involved in vitamin metabolism that have been implicated in dozens of diseases. These conditions may be remediated with vitamin therapy, provided that the at-risk individuals can be identified through simple genetic tests.

Cathys deep experience and strategic vision will be a tremendous asset to us as we seek to develop our platform that can suggest vitamin-based therapeutic interventions based on an individuals genetic profile, added Dr. Gilbert.

The first test developed on VitaPaths platform identifies women at highest risk of having children with spina bifida which may be prevented by using prescription-dose folic acid before pregnancy. The test is expected to be offered in doctors offices in 2013.

For more information about VitaPath Genetics, please visit http://www.vpgenetics.com.

About VitaPath Genetics

VitaPath Genetics, Inc. has developed a platform for genomic-based tests that determine an individuals need for vitamin therapy in medically actionable conditions. Using its platform, VitaPath develops specific assays that test for the risk of vitamin-remediable diseases and that can help manage the use of $30 billion of supplements purchased in the U.S. each year. The first test developed by VitaPath measures genetic risk factors associated with spina bifida to identify women who would benefit from prescription-strength folic acid supplementation. VitaPath is privately held and has received investment from Mohr Davidow Ventures, X/Seed Capital Management and Alere Inc. The company is based in Foster City, California.

The rest is here:
Catherine Burzik Appointed Chair of VitaPath Genetics Board of Directors

Recommendation and review posted by Bethany Smith

CAMBRIDGE, Mass. & BOTHELL, Wash.--(BUSINESS WIRE)--

Seattle Genetics, Inc. (SGEN) and Millennium: The Takeda Oncology Company, a wholly owned subsidiary of Takeda Pharmaceutical Company Limited (TSE:4502), today announced the completion of patient enrollment in a phase III clinical trial of ADCETRIS (brentuximab vedotin) for post-transplant Hodgkin lymphoma (HL) patients. The phase III trial, also known as the AETHERA trial, is evaluating ADCETRIS versus placebo for the treatment of patients at high risk of residual Hodgkin lymphoma following autologous stem cell transplant (ASCT). ADCETRIS is an antibody-drug conjugate (ADC) directed to CD30, a defining marker of classical HL.

We are pleased to complete the enrollment of this important phase III trial, evaluating the use of ADCETRIS for Hodgkin lymphoma patients who are at high risk of residual disease following an ASCT, said Thomas C. Reynolds, M.D., Ph.D., Chief Medical Officer of Seattle Genetics. The AETHERA trial is designed to provide the medical community with valuable insight into the potential for ADCETRIS to consolidate responses in Hodgkin lymphoma patients following a transplant, and will be the first data on the use of ADCETRIS in a maintenance-type setting. We anticipate data from this trial will be available in late 2013 or early 2014.

Completing enrollment of the AETHERA trial in the post-transplant Hodgkin lymphoma patient population at high risk for residual disease is a significant milestone for our ADCETRIS clinical development program, said Karen Ferrante, M.D., Chief Medical Officer, Millennium. We look forward to continuing to work with our partner Seattle Genetics to determine the potential benefit of this targeted treatment in other CD30-expressing tumors.

The AETHERA trial is a randomized, double-blind, placebo-controlled phase III study, comparing progression-free survival in 329 post-ASCT patients receiving ADCETRIS to those receiving placebo. Patients must be at high risk for residual HL, defined as those with a history of refractory HL, those who relapse or progress within one year from receiving front-line chemotherapy and/or those who have disease outside of the lymph nodes at the time of pre-ASCT relapse. Secondary endpoints of the trial include overall survival, safety and tolerability. Patients receive ADCETRIS every three weeks for up to approximately one year. This international multi-center trial is being conducted in the United States, Europe and Russia.

About ADCETRIS

ADCETRIS (brentuximab vedotin) is an ADC comprising an anti-CD30 monoclonal antibody attached by a protease-cleavable linker to a microtubule disrupting agent, monomethyl auristatin E (MMAE), utilizing Seattle Genetics proprietary technology. The ADC employs a linker system that is designed to be stable in the bloodstream but to release MMAE upon internalization into CD30-expressing tumor cells.

ADCETRIS received accelerated approval from the U.S. Food and Drug Administration (FDA) for two indications: (1) the treatment of patients with Hodgkin lymphoma after failure of autologous stem cell transplant (ASCT) or after failure of at least two prior multi-agent chemotherapy regimens in patients who are not ASCT candidates, and (2) the treatment of patients with systemic anaplastic large cell lymphoma (sALCL) after failure of at least one prior multi-agent chemotherapy regimen. The indications for ADCETRIS are based on response rate. There are no data available demonstrating improvement in patient-reported outcomes or survival with ADCETRIS.

ADCETRIS is not approved for use outside the United States. The marketing authorization application for ADCETRIS in relapsed or refractory Hodgkin lymphoma and sALCL, filed by Takeda Global Research & Development Centre (Europe), was accepted for review by the European Medicines Agency (EMA) in June 2011. In July 2012, the Committee for Medicinal Products for Human Use (CHMP) of the EMA issued a positive opinion for the conditional approval of ADCETRIS, supporting an approval decision in the European Union.

Seattle Genetics and Millennium are jointly developing ADCETRIS. Under the terms of the collaboration agreement, Seattle Genetics has U.S. and Canadian commercialization rights and the Takeda Group has rights to commercialize ADCETRIS in the rest of the world. Seattle Genetics and the Takeda Group are funding joint development costs for ADCETRIS on a 50:50 basis, except in Japan where the Takeda Group will be solely responsible for development costs.

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Seattle Genetics and Millennium Complete Enrollment in Phase III AETHERA Trial of ADCETRIS® for Post-Transplant ...

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(SACRAMENTO, Calif.) - Deborah K. Lieu, a stem cell scientist in cardiovascular medicine at UC Davis Health System, has received a $1.3 million research grant from the California Institute for Regenerative Medicine (CIRM) to develop stem cells that could serve as a biological alternative to the electronic pacemakers that people now use to regulate heart rhythm.

According to Lieu, each year 350,000 cardiology patients with abnormal heart rhythms receive electronic pacemakers to maintain a normal heart beat. The devices, while effective, have several disadvantages, including limited battery life and poor response to changing heart rates, such as when a person is exercising. Lieu, who is working with colleague Nipavan Chiamvimonvat, the Roger Tatarian Endowed Professor of Cardiovascular Medicine at UC Davis, plans to examine ways to improve the generation of pacemaking cells using human-induced pluripotent stem cells (hiPSCs), potentially creating what she calls a "biopacemaker."

"There are more than 3 million patients around the country who are dependent on electronic pacemakers," said Lieu. "Each one costs about $58,000 to implant and requires follow-up surgery about every 5 to 10 years to change batteries. Creating a biopacemaker from stem cells would avoid the burden of battery replacement and provide the physiological benefit of enabling a person's heart to naturally adapt to a rising heart rate during activities such as exercise."

Lieu's grant was among more than two dozen projects that received support from state stem cell agency's governing board last week as part of CIRM's Basic Biology awards program. The funding focuses on basic research projects that can provide a better understanding about the fundamental mechanisms of stem cell biology and move researchers closer to knowing how best to use stem cells to help patients.

To create the pacemaking cells, Lieu and her colleagues plan to manipulate an ion channel (the SK channels in cardiac myocytes) to alter the calcium signaling mechanisms during hiPSC differentiation. Stem cell scientists create hiPSCs - typically from an adult cell such as a skin cell - by inducing a "forced" expression of specific genes. Once reprogrammed, the cells take on a variety of capabilities (becoming pluripotent) and offer a range of stem cell treatment possibilities.

Development of a biopacemaker could also benefit the one-in-20,000 infants and premature babies suffering from congenital heart-rhythm dysfunction who currently are not suitable candidates for electronic pacemakers. Infants are physically too small for the device. A biological pacemaker could fit with their small stature and then grow as the infant grows.

Collaborating with Lieu and Chiamvimonvat on the research project will be Jan Nolta, director of the UC Davis Institute for Regenerative Cures; Donald Bers, chair of the UC Davis Department of Pharmacology; and James Chan, assistant professor in the Department of Pathology and affiliated with the NSF Center for Biophotonics Science and Technology at UC Davis.

UC Davis is playing a leading role in regenerative medicine, with nearly 150 scientists working on a variety of stem cell-related research projects at campus locations in both Davis and Sacramento. The UC Davis Institute for Regenerative Cures, a facility supported by the California Institute for Regenerative Medicine (CIRM), opened in 2010 on the Sacramento campus. This $62 million facility is the university's hub for stem cell science. It includes Northern California's largest academic Good Manufacturing Practice laboratory, with state-of-the-art equipment and manufacturing rooms for cellular and gene therapies. UC Davis also has a Translational Human Embryonic Stem Cell Shared Research Facility in Davis and a collaborative partnership with the Institute for Pediatric Regenerative Medicine at Shriners Hospital for Children Northern California. All of the programs and facilities complement the university's Clinical and Translational Science Center, and focus on turning stem cells into cures. For more information, visit http://www.ucdmc.ucdavis.edu/stemcellresearch.

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Pacemaker from Stem Cells Receives Research Funding

Recommendation and review posted by sam

NEWTON, MA--(Marketwire - Sep 24, 2012) - Recombinant, a provider of data warehousing and clinical intelligence solutions for healthcare performance management, personalized medicine and translational research, will deliver two presentations with client executives from the Northern New England Accountable Care Collaborative (NNEACC) and UCLA Health System at the 20th Annual College of Healthcare Information Management Executives (CHIME) Fall CIO Forum, October 16 - 19 in Indian Wells, CA. Sessions include managing information within an Accountable Care Organization (ACO) model and capitalizing on big data assets. The presentations are part of the Organizational Performance and Emerging Issues in Healthcare and Health Information Technology tracks, respectively. Recombinant is a CHIME Foundation member.

Healthcare Data-as-a-Service for Big Data Challenges

Virginia McFerran, CIO, UCLA Health System, and Jason Oliveira, Managing Director, Health System Consulting, Recombinant, will present "Healthcare Data-as-a-Service for our Big Data Challenges" on Wednesday, October 17 from 11:15 a.m. - 12 p.m. The session will recount the journey of UCLA Health System and its academic partners in strategizing, designing and establishing its xDR data-as-a-service architecture, including best practices and lessons learned.

"Emerging data sources such as EHRs, HIEs, patient portals, and the increasing availability of genomics and proteomics information are pushing health systems into the reality of having to manage massive amounts of data. As more health systems pursue secondary uses of data many quickly realize that they lack an enterprise data management strategy to efficiently exploit their big data assets," said Oliveira. "Virginia and I will help attendees gain a deeper understanding of what managing 'big data' means in terms of new information technology requirements, and what emerging approaches are being taken by the industry by focusing on the experience of our client, UCLA Health System."

Defining and Meeting the Core Data Requirements of ACOs

David Wennberg MD, MPH, Chief Executive Officer, NNEACC, and Mark Golberg, Managing Director, Healthcare Provider ACO, Recombinant will present "Defining and Meeting the Core Data Requirements of ACOs" on Thursday, October 18 from 11:15 a.m. - 12 p.m.

"ACOs cannot deliver on the promise of improving healthcare delivery and patient outcomes and reducing cost without the ability to identify, prioritize, access, and integrate data from internal and external clinical, claims, financial and other critical systems," said Golberg. "The scope, reliability and timeliness of data, in turn, impact downstream applications including knowledge management, decision support, business intelligence, and advanced analytics systems. Dr. Wennberg and I will discuss key issues of ACO data and information management and practical trade-offs often required in ACO network development based on our experience with NNEACC."

"The CHIME Fall CIO Forums combine the best speakers and healthcare IT educators in the nation with unparalleled opportunities for CIOs and healthcare IT executives to network with their peers and collectively share solutions, solve problems and address challenges," said Peter Emerson, Chief Executive Officer, Recombinant. "We are pleased to join with our clients the Northern New England Accountable Care Collaborative and UCLA Health System to share our pragmatic experience and expertise at the 20th CIO Fall Forum."

About Recombinant

Recombinant provides leading-edge data warehousing and clinical intelligence solutions to healthcare providers, academic medical centers and life science researchers to deliver higher quality outcomes, accelerate personalized medicine, and lower costs. Our team of industry veterans is focused on improving the flow of reliable data to power clinical and research applications in a secure, compliant environment. For more information about Recombinant's products and services, visit http://www.recomdata.com.

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Recombinant to Address ACO Data Management and Big Data Opportunities in Healthcare at CHIME12 Fall CIO Forum

Recommendation and review posted by sam

NEW YORK, Sept. 24, 2012 /PRNewswire/ --Reportlinker.com announces that a new market research report is available in its catalogue:

Competitive Handbook towards Personalized Medicine in Prostate Cancer

http://www.reportlinker.com/p0980851/Competitive-Handbook-towards-Personalized-Medicine-in-Prostate-Cancer.html#utm_source=prnewswire&utm_medium=pr&utm_campaign=Drug_and_Medication

Personalized medicine is very much about fitting target profiles of drugs towards disease mechanism(s). This report is a new and unique way of stratifying and analyzing the global prostate cancer pipeline towards personalized medicine and presents actionable analysis which allows you to discover:

* Where the competition is; Which targets, compound types and companies are setting the path?

* How much R&D effort has gone towards different targets and what is known about the target?

* Which pathways are targeted, by what and how?

* What is truly new and unique in the prostate cancer pipeline?

* How new and unique your target strategy really is

* What overlapping competition you have from other companies and compound types towards your therapeutic targets

Follow this link:
Competitive Handbook towards Personalized Medicine in Prostate Cancer

Recommendation and review posted by sam

VEGA -- On Fri., Sept. 28, during the halftime show of the Vega High School football game vs. Sunray High School, Gridiron Heroes Spinal Cord Injury Foundation will present a wheelchair-accessible van to Luis Morales.

Morales, played for the Vega High School football team and is currently a student, suffered a spinal cord injury during a game in September 2011.

Friday's game starts at 7:30 p.m. at Vega High Schools Longhorn Field.

This will be the first wheelchair-accessible vehicle the Morales family has used since his injury. The handicapped-accessible van is the eighth that Gridiron Heroes has donated in nine years to high school football players who have sustained a spinal cord injury during a game. The van will be driven out on the field during the halftime show, followed by a special presentation to the Morales family.

Gridiron Heroes is a non-profit organization that supports individuals who have sustained catastrophic spinal cord injuries on the football field. The organization also works to educate about the importance of player safety. For more information about Gridiron Heroes and all of its heroes on and off the field, visit http://www.gridironheroes.org.

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Readers Feel...

Recommendation and review posted by sam

SUNDAY, Sept. 23 (HealthDay News) -- A comprehensive look at the genetic blueprint of breast cancer has revealed new insights into the disease -- including the discovery that certain breast and ovarian tumors may be closely related.

Basal-like breast tumors -- one of the most deadly subtypes of breast cancer -- are genetically more similar to ovarian cancer than to other breast cancers, the new research found.

In this study, the scientists used six different technologies to analyze 348 tumors from women with breast cancer. They looked for defects in DNA, RNA and proteins in the tumors.

They confirmed the existence of four main subtypes of breast cancer -- luminol A, luminal B, HER2 and basal-like -- and found unique genetic and molecular signatures within each of the subtypes.

The findings add to growing evidence suggesting that tumors should be catalogued and treated based on the genes that are disrupted rather than their location in the body, the researchers said.

"With this study, we're one giant step closer to understanding the genetic origins of the four major subtypes of breast cancer," study co-leader Dr. Matthew Ellis, chair of medical oncology at Washington University School of Medicine in St. Louis, said in a university news release.

One oncologist said the findings on breast cancer's diversity echo her own experience in treating patients.

"The diversity of breast cancer is instinctual to a practicing breast surgeon who has seen women with breast cancer, presumably the same stage, have differing outcomes with respect to recurrence and survival," said Dr. Donna-Marie Manasseh, director of breast surgery at the Maimonides Breast Cancer Center in New York City. "This research validates what we have suspected."

According to Ellis, the new study suggests that most basal-like breast tumors and ovarian tumors have similar genetic origins and potentially could be treated with the same drugs.

Basal-like tumors account for about 10 percent of all breast cancers and disproportionately affect younger and black women in the United States. Basal-like tumors include most triple-negative breast tumors, which are often aggressive and do not respond to therapies that target hormone receptors or to standard chemotherapies.

Read more here:
Gene study yields new clues to breast cancer

Recommendation and review posted by Bethany Smith

September 24, 2012

Lee Rannals for redOrbit.com Your Universe Online

A new study has confirmed a link between sugary sodas, and genetic susceptibility to high body mass index (BMI) and increased risk of obesity.

The team wrote in the New England Journal of Medicine that their findings reinforce the view that environmental and genetic factors shape obesity risk.

Our study for the first time provides reproducible evidence from three prospective cohorts to show genetic and dietary factorssugar-sweetened beveragesmay mutually influence their effects on body weight and obesity risk, Lu Qi, assistant professor in the Department of Nutrition at Harvard School of Public Health (HSPH) and senior author of the study, said in a press release.

Consuming sugary drinks in the past three decades has increased worldwide, and there has been little research on whether environmental factors like drinking these drinks can influence genetic predisposition.

For the study, the team used data from 121,700 women in the Nurses Health Study (NHS), 51,529 men in the Health Professionals Follow-up Study (HPFS), and 25,000 in the Womens Genome Health Study (WGHS).

All of the participants in the research had completed food-frequency questionnaires detailing their food and drink consumption.

The team analyzed data from 6,934 women from NHS, 4,423 men from HPFS, and 21,740 women from WGHS who were of European ancestry.

Participants were divided into four groups depending on how many sugar drinks they consumed. The groups were broken up into those who consumed less than one serving of a sugar beverage a month, between one to four servings per month, between 2 to six servings per week, and one or more servings per day.

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Sugary Sodas Lead To An Increased Risk Of Obesity

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