Sep. 30, 2013 Scientists of the International Multiple Sclerosis Genetics Consortium (IMSGC) have identified an additional 48 genetic variants influencing the risk of developing multiple sclerosis. This work nearly doubles the number of known genetic risk factors and thereby provides additional key insights into the biology of this debilitating neurological condition. The genes implicated by the newly identified associations underline the central role played by the immune system in the development of multiple sclerosis and show substantial overlap with genes known to be involved in other autoimmune diseases.

Published online September 29 in the journal Nature Genetics, the study, "Analysis of immune-related loci identifies 48 new susceptibility variants for multiple sclerosis," is the largest investigation of multiple sclerosis genetics to date. Led by the University of Miami Miller School of Medicine, this study relied upon an international team of 193 investigators from 84 research groups in 13 countries and was funded by more than 40 local and national agencies and foundations.

Multiple sclerosis (MS) is a chronic disabling neurological condition that affects over 2.5 million individuals worldwide. The disease results in patchy inflammation and damage to the central nervous system that causes problems with mobility, balance, sensation and cognition depending upon where the damage to the central nervous system occurs. Neurological symptoms are often intermittent in the early stages of the disease but tend to persist and progressively worsen with the passage of time for the majority of patients. The risk of developing multiple sclerosis is increased in those who have a family history of the disease. Research studies in twins and adopted individuals have shown that this increased risk is primarily the result of genetic risk factors.

The findings released in this study nearly double the number of confirmed susceptibility loci, underline the critical role played by the immune system in the development of multiple sclerosis, and highlight the marked similarities between the genetic architecture underlying susceptibility to this and the many other autoimmune diseases.

The present study takes advantage of custom designed technology known as ImmunoChip -- a high-throughput genotyping array specifically designed to interrogate a targeted set of genetic variants linked to one or more autoimmune diseases. IMSGC researchers used the ImmunoChip platform to analyze the DNA from 29,300 individuals with multiple sclerosis and 50,794 unrelated healthy controls, making this the largest genetics study ever performed for multiple sclerosis. In addition to identifying 48 new susceptibility variants, the study also confirmed and further refined a similar number of previously identified genetic associations. With these new findings, there are now 110 genetic variants associated with MS. Although each of these variants individually confers only a very small risk of developing multiple sclerosis, collectively they explain approximately 20 percent of the genetic component of the disease.

Explaining the significance of the work and the nature of the collaboration, the Miller School's Jacob McCauley, Ph.D., who led the study on behalf of the IMSGC, said, "With the release of these new data, our ongoing effort to elucidate the genetic components of this complex disease has taken a major step forward. Describing the genetic underpinnings of any complex disease is a complicated but critical step. By further refining the genetic landscape of multiple sclerosis and identifying novel genetic associations, we are closer to being able to identify the cellular and molecular processes responsible for MS and therefore the specific biological targets for future drug treatment strategies. These results are the culmination of a thoroughly collaborative effort. A study of this size and impact is only possible because of the willingness of so many hard working researchers and thousands of patients to invest their time and energy in a shared goal."

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Forty-eight new genetic variants associated with MS

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Public release date: 29-Sep-2013 [ | E-mail | Share ]

Contact: Lisa Worley lworley2@med.miami.edu 305-458-9654 University of Miami

Scientists of the International Multiple Sclerosis Genetics Consortium (IMSGC) have identified an additional 48 genetic variants influencing the risk of developing multiple sclerosis. This work nearly doubles the number of known genetic risk factors and thereby provides additional key insights into the biology of this debilitating neurological condition. The genes implicated by the newly identified associations underline the central role played by the immune system in the development of multiple sclerosis and show substantial overlap with genes known to be involved in other autoimmune diseases.

Published online September 29 in the journal Nature Genetics, the study, "Analysis of immune-related loci identifies 48 new susceptibility variants for multiple sclerosis," is the largest investigation of multiple sclerosis genetics to date. Led by the University of Miami Miller School of Medicine, this study relied upon an international team of 193 investigators from 84 research groups in 13 countries and was funded by more than 40 local and national agencies and foundations.

Multiple sclerosis (MS) is a chronic disabling neurological condition that affects over 2.5 million individuals worldwide. The disease results in patchy inflammation and damage to the central nervous system that causes problems with mobility, balance, sensation and cognition depending upon where the damage to the central nervous system occurs. Neurological symptoms are often intermittent in the early stages of the disease but tend to persist and progressively worsen with the passage of time for the majority of patients. The risk of developing multiple sclerosis is increased in those who have a family history of the disease. Research studies in twins and adopted individuals have shown that this increased risk is primarily the result of genetic risk factors.

The findings released in this study nearly double the number of confirmed susceptibility loci, underline the critical role played by the immune system in the development of multiple sclerosis, and highlight the marked similarities between the genetic architecture underlying susceptibility to this and the many other autoimmune diseases.

The present study takes advantage of custom designed technology known as ImmunoChipa high-throughput genotyping array specifically designed to interrogate a targeted set of genetic variants linked to one or more autoimmune diseases. IMSGC researchers used the ImmunoChip platform to analyze the DNA from 29,300 individuals with multiple sclerosis and 50,794 unrelated healthy controls, making this the largest genetics study ever performed for multiple sclerosis. In addition to identifying 48 new susceptibility variants, the study also confirmed and further refined a similar number of previously identified genetic associations. With these new findings, there are now 110 genetic variants associated with MS. Although each of these variants individually confers only a very small risk of developing multiple sclerosis, collectively they explain approximately 20 percent of the genetic component of the disease.

Explaining the significance of the work and the nature of the collaboration, the Miller School's Jacob McCauley, Ph.D., who led the study on behalf of the IMSGC, said, "With the release of these new data, our ongoing effort to elucidate the genetic components of this complex disease has taken a major step forward. Describing the genetic underpinnings of any complex disease is a complicated but critical step. By further refining the genetic landscape of multiple sclerosis and identifying novel genetic associations, we are closer to being able to identify the cellular and molecular processes responsible for MS and therefore the specific biological targets for future drug treatment strategies. These results are the culmination of a thoroughly collaborative effort. A study of this size and impact is only possible because of the willingness of so many hard working researchers and thousands of patients to invest their time and energy in a shared goal."

###

The International Multiple Sclerosis Genetics Consortium was founded in 2003 and today consists of multiple sclerosis and genetics researchers from around the world who coordinate their research activities in the belief that this is the shortest path to understanding the root causes of multiple sclerosis and using that understanding to bring about meaningful improvements for patients and those at risk of this debilitating disease.

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Researchers uncover 48 new genetic variants associated with multiple sclerosis

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Greater than Expected Responses to Salvage Chemotherapy Observed Following Treatment with Algenpantucel-L in Pancreatic Cancer and Tergenpumatucel-L in NSCLC: Data Presented at the 2013 European Cancer Congress

Ames, IA - (Accesswire - September 30, 2013) - NewLink Genetics Corporation (NLNK), an oncology-focused biopharmaceutical company specializing in immunotherapy, today announced the presentation of data on its lead HyperAcute cancer immunotherapy product candidates at the 2013 European Cancer Congress (ESMO) in Amsterdam, The Netherlands. NewLink researchers presented data showing greater than expected responses to salvage chemotherapy following treatment with both algenpantucel-L in patients with pancreatic cancer and tergenpumatucel-L in patients with non-small cell lung cancer (NSCLC). The clinical benefit of chemo-sensitization is being further investigated in a larger number of patients by assessing objective tumor responses to follow-on chemotherapy after HyperAcute immunotherapy in ongoing clinical trials.

"These data indicate that pretreatment with HyperAcute immunotherapy such as algenpantucel-L or tergenpumatucel-L prior to salvage chemotherapy has the potential to increase the sensitivity of cancer cells to chemotherapy that may lead to durable objective and complete responses, commented Nick Vahanian MD, President and Chief Medical Officer of NewLink. In addition, the immunologic responses further support the mechanism for HyperAcute immunotherapy to stimulate the patients immune system to recognize and attack cancer cells."

In a poster presentation entitled "Chemo-sensitization and immunological reactions to hyperacute immunotherapy, a novel approach to cancer treatment," NewLink researchers presented clinical data showing:

Greater than expected responses to follow-on chemotherapy after treatment with algenpantucel-L or tergenpumatucel-L HyperAcute immunotherapy.

- Three pancreatic cancer patients were followed for response to subsequent salvage chemotherapy treatment after progressing on algenpantucel-L therapy. All three patients experienced durable (12-36 months), complete responses.

- Sixteen NSCLC patients were followed for response to subsequent salvage chemotherapy treatment (list) after progressing on tergenpumatucel-L therapy. Five of the sixteen (31%) achieved partial responses and four of the sixteen (25%) achieved stable disease.

- Immunologic responses, which correlated with improved survival, were observed with both algenpantucel-L and tergenpumatucel-L indicating the ability of HyperAcute immunotherapy to elicit anti-cancer immune responses.

About HyperAcute Immunotherapy

NewLinks HyperAcute immunotherapy platform creates novel biologic products that are designed to stimulate the human immune system to recognize and attack cancer cells. HyperAcute product candidates are composed of human cancer cells that are tumor specific, but not patient specific. These cells have been modified to express alpha-gal, a carbohydrate for which humans have pre-existing immunity. These alpha-gal-modified cells stimulate a rapid and powerful human immune response that trains the bodys natural defenses to seek out and destroy cancer cells. The objective of HyperAcute immunotherapies is to elicit an antitumor response by "educating" the immune system to attack a patients own cancer cells. HyperAcute immunotherapies do not require any tissue from individual patients and use intact whole cells rather than cell fragments or purified proteins. We believe these unique properties of HyperAcute products result in the stimulation of a robust immune response.

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NewLink Genetics Presents Data Demonstrating Potential Chemo-sensitization Activity of its HyperAcute™ Cancer ...

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NASHVILLE, TN--(Marketwired - Sep 30, 2013) - Insight Genetics today announced it has entered into an exclusive, worldwide licensing agreement with St. Jude Children's Research Hospital for a genetic test known as the KIR/KIR-Ligand Assay. The test helps to predict the success of bone marrow transplants by identifying the optimal bone marrow donor subtype. Use of the KIR/KIR-Ligand Assay has been shown to prevent the return of cancer in transplant recipients and reduce risk of death following bone marrow transplantation by about 60 percent. As part of the agreement, Insight Genetics will optimize the KIR/KIR-Ligand Assay for rapid, high-capacity use and make it broadly available to physicians and their patients as well as donor registries.

"When successful, bone marrow transplants can transform patients' lives," said Wing Leung, MD, PhD, Chair of St. Jude's Department of Bone Marrow Transplantation and Cellular Therapy. "This is why it's critical we do everything we can to ensure the best match between donor and recipient. The KIR/KIR-Ligand Assay has great potential in helping to identify the best transplant donors and improve outcomes for patients worldwide."

The U.S. Health Resources and Services Administration estimates that each year more than 18,000 Americans are diagnosed with life-threatening illnesses for which bone marrow transplants are the best treatment option. There are millions of individuals registered as potential bone marrow donors, but effectively matching a patient in need of a transplant with the right donors is a difficult process.

According to the World Health Organization, when donors and recipients are optimally matched, bone marrow transplants can cure more than 90 percent of patients with blood and lymph cancers. The KIR/KIR-Ligand Assay has the potential to make the screening process more efficient and effective, greatly increasing the volume and quality of the donor-patient match. In fact, it is estimated that the test could assist in improving donor matches and increasing life expectancy for as many as 7,500 bone marrow transplant patients in the U.S. annually.

The KIR/KIR-Ligand test was developed by Dr. Leung, Dr. Rafijul Bari and colleagues at St. Jude as part of their research to determine the impact of variations in the KIR2DL1 gene. The group focused on forms of KIR2DL1 carried by natural killer (NK) cells, special immune cells that kill abnormal cells such as cancer cells. Their research found that some forms of KIR2DL1 in NK cells are more active than others, and NK cells carrying the stronger form of KIR2DL1 can destroy cancer cells more effectively than the NK cells with the less active form.

A study conducted by Bari, Leung and colleagues that was featured in the September 16 online version of the Journal of Clinical Oncology (JCO) showed that patients were much more likely to survive a transplant and significantly less likely to experience disease progression when bone marrow transplants came from donors whose NK cells included the stronger form of KIR2DL1.

"The KIR/KIR-Ligand technology developed at St. Jude offers enormous potential to improve the lives of patients who receive bone marrow transplants, and we're looking forward to putting our assay development expertise to work to make it available for widespread clinical use around the world," said David Hout, PhD, Vice President of Research and Development at Insight Genetics. "With this assay, we have the ability to type multiple donor samples simultaneously and generate results rapidly, all at a reduced cost compared to existing screening methods. This test will not only increase the efficiency with which transplants are performed but it also promises to help dramatically improve cure rates by optimally matching each donor and recipient."

Under the terms of the agreement with St. Jude, Insight Genetics obtained the licensing rights to KIR2DL1 coding (cDNA) sequences and the KIR/KIR-Ligand Assay. Using its expertise in assay development, Insight Genetics initially will focus on refining the assay for clinical use, with plans to make it available to clinicians and researchers as a lab-developed test in early 2014. The company will be working to deepen relationships with bone marrow donor registry programs and transplant centers to enhance typing and donor matching for each procedure.

Insight Genetics' work on the KIR/KIR-Ligand Assay aligns with the company's expanding portfolio of advanced diagnostic tools to improve the lives of cancer patients. St. Jude previously licensed to Insight Genetics two other biomarkers, anaplastic lymphoma kinase (ALK) and a series of mutations within the ALK gene that confer resistance to ALK inhibitor therapy. The company is researching and developing additional tests to help physicians diagnose and monitor cancer patients and select the most effective treatments.

More information about St. Jude's work on the KIR/KIR-Ligand Assay can be seen here and here.

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Insight Genetics Inks Deal With St. Jude Children's Research Hospital to Improve Donor Matching in Bone Marrow ...

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NEET BIO - Gene Therapy
This video describes about gene therapy. Gene therapy is a collection of methods that allows correction of a gene defect that has been diagnosed in a child/e...

By: XLClasses

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NEET BIO - Gene Therapy - Video

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Susan Young for MIT Technology Review 2013-09-30 14:11:37 UTC

Though many gene therapies have been tested in patients around the world in hopes of curing hereditary diseases, few governments have approved their sale, and none has been approved in the United States. That could change in coming years as several therapies enter advanced trials.

A big step forward already came in November 2012, when the European Medicines Agency gave the Dutch biotech startup UniQure permission to sell its treatment. That approval came as a relief to many in the field, who had been waiting for a break in the clouds hanging over the technology since failed and fatal trials in the 1990s. You see a resurgence in terms of investors, and in truth, a number of problems have been solved, says Katherine High, a medical researcher at Childrens Hospital of Philadelphia, who is overseeing a late-stage clinical trial for a different gene therapy.

Still, experts say it is likely to be a few years before a treatment is approved in the U.S. With its European approval in hand, UniQure may have a good chance of also getting the first U.S. approval, but the company says it has not yet submitted an application to the FDA.

Like most gene therapies, UniQures treatment uses a modified virus to deliver a working copy of a gene to patients who lack a healthy version. In this case, the gene is needed for the body to break down fats; without it, patients can develop painful and even fatal inflammation of the pancreas. UniQure uses a modified version of a virus that most of us already carry. The choice of virus used to deliver a gene therapy depends in part on where the treatment needs to go in the body and whether the viruses are intended to replicate themselves. Some viruses, for instance, are designed to spread throughout the body to kill cancer cells.

There are several groups that could be the first to develop a U.S.-approved gene therapy (see table). Highs team is one; they are enrolling patients in a late-stage trial of a treatment for a disorder that causes blindness at an early age. The patients in this trial have previously been given the gene therapy in one eye, and now the other will be tested.

In the experimental treatment, doctors inject a virus-based particle just behind a patients retina. The treatment improved some patients vision to the point that they were no longer legally blind. Some patients have been stable for nearly six years. The trial is scheduled to end in April 2015.

Another possibility comes from Massachusetts-based Bluebird Bio, which has published results from patients who have seemingly been cured of a genetic blood disease. The company is about to start testing its approach in a hereditary neurological disorder that is often fatal in young boys.

SEE ALSO: Gene Therapy Combats Hereditary Blood Disease

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When Will Gene Therapy Come to the United States?

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Walking with Spinal Cord Injury

By: CECEKC1

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Walking with Spinal Cord Injury - Video

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Aubrey de Grey - Google vs Death: an Anti Aging Initiative - Progress in Regenerative Medicine
Aubrey de Grey of SENS Foundation on #39;Calico #39;, Google #39;s anti-aging initiative. http://sens.org/outreach/outreach-blog/time-feature-cso-aubrey-de-grey-googles...

By: Adam Ford

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Aubrey de Grey - Google vs Death: an Anti Aging Initiative - Progress in Regenerative Medicine - Video

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Professor Arnold Caplan discusses mesenchymal stem cell therapy for multiple sclerosis
Professor Caplan is "The father of the mesenchymal stem cell (MSC)". In this clip, he describes a mouse experiment using human MSCs in a mouse model of MS. T...

By: http://www.cellmedicine.com

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Professor Arnold Caplan discusses mesenchymal stem cell therapy for multiple sclerosis - Video

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Insurance Covered Stem Cell Therapy in California at TeleHealth (888) 828-4575
http://stemcelltherapyincalifornia.com Stem Cell Therapy procedures at TeleHealth are offered for a number of conditions and often covered by insurance. Thes...

By: USPainNetwork

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MANILA, PhilippinesStem cell therapy should only apply to skin grafting for burn patients and not for anti-aging purposes, according to the Food and Drug Administration (FDA).

Up to now, there is no evidence that stem cell therapy has anti-aging effects, said FDA acting Director General Kenneth Hartigan-Go.

The FDA recognizes only hematopoietic (pertaining to the formation and development of blood cells) stem cell transplantation, corneal resurfacing with limbal stem cells and skin regeneration with epidermal stem cells as generally accepted standards of health care.

Asked if this meant anti-aging stem cell therapies would not be allowed in the Philippines, Go said: It means that if the health claim is for burn patients, requirements that need to be submittedlike clinical trial reportsare expected to be complete, whereas if the claim is for anti-aging, then the requirements may be more extensive and intensive considering that products for anti-aging claims are still controversial.

Facility accreditation

The FDA said it had been continuously collaborating with the Department of Healths Bureau of Health Facilities and Services (BHFS) in accrediting facilities that deal with human cells, tissues, and cellular and tissue-based products (HCT/Ps), laboratory and therapeutic activities or services.

As of Sept. 24, 51 facilities have applied for accreditation, and 11 of these have been inspected by the BHFS, the FDA said.

No automatic approval

Submission of an application, however, does not necessarily result in automatic approval.

The FDA guidelines require that all stem cell and cellular-based treatments offered in the country should first pass the agencys standards for safety, efficacy and quality.

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Stem cell therapy for burns, not aging, says FDA

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Healing With Stem Cell Therapy
http://www.ihealthtube.com http://www.facebook.com/ihealthtube Stem cell treatments have long been controversial, mostly because they started with the use of...

By: iHealthTube.com

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Healing With Stem Cell Therapy - Video

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A research team at the Massachusetts General Hospital have discovered two gene mutations that could cause late onset Alzheimers disease in humans. The good news, according to the researchers, this can help in the prevention and treatment of the disease.

A gene, called ADAM10, is where the new mutations were found. The mutations are similar to the same mutations found in Alzheimers, which is usually founded in people over the age of 60. This is the second gene confirmed to cause late onset Alzheimers as well as the fifth to be linked overall to the disease according to the Massachusetts General Hospital researchers.

The two mutations the researchers found in the ADAM10 gene, showed an increase in producing the beta-amyloid protein. The beta-amyloid protein is founded in people who suffer from Alzheimers. The mutations also stop the creation of new nerve related cells in the hippocampus. The hippocampus is critical as it main purpose is to help with the brains function to learn and retain memory.

This is the first report to document, in animal models, new [disease-causing] gene mutations for Alzheimers since the reports of the original four genes in the 1990s. , study senior author Rudolph Tanzi, director of the genetics and aging unit the Mass General Institute for Neurodegenerative Disease, said at the hospital news release.

What we found regarding the many effects of these two rare mutations in ADAM10 strongly suggests that diminished activity of this enzyme can cause [Alzheimer's disease], and these findings support ADAM10 as a promising therapeutic target for both treatment and prevention. he said.

Similar findings from animal models does not mean it will be founded in humans, but it is a potential help in the fight against Alzheimers. Video via NDN

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Alzheimer’s: A Discovery of Two New Gene Mutations

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Public release date: 29-Sep-2013 [ | E-mail | Share ]

Contact: Glenna Picton picton@bcm.edu 713-798-7973 Baylor College of Medicine

HOUSTON -- (Sep. 29, 2013) As so many genome studies do, this study published online in the journal Nature Genetics began with a single patient and his parents who were in search of a diagnosis.

The parents of this first patient sought genetic testing for Prader-Willi syndrome when he was only a year old, but the test, which was still in its infancy, came back negative. For the next 12 years, his parents were left in limbo. He had many features of the disease including lack of muscle tone, feeding difficulties and failure to thrive early on. Autism spectrum disorder and mild intellectual disability became evident as he grew older.

Dr. C. Thomas Caskey, then with UTHealth and now with Baylor College of Medicine, referred the patient to Dr. Christian Schaaf, an assistant professor of molecular and human genetics at Baylor College of Medicine and a faculty member at the Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital, for an evaluation. Schaaf agreed that the boy had many of the outward signs consistent with Prader-Willi, but others were lacking, such as the morbid obesity, which is typically caused by a very aggressive appetite.

Dr. Manuel L. Gonzalez-Garay (co-first and co-corresponding author), assistant professor and bioinformatics expert at the University of Texas Health Science Center at Houston's Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, identified a single change (called a point mutation) in the gene MAGEL2 using highly accurate whole genome sequencing information from Complete Genomics, Inc., of Mountain View California. This gene is located in the area of chromosome 15, which researchers knew was involved in Prader-Willi syndrome. The single base deletion found in this GC-rich and difficult to sequence gene is a frame-shift mutation that disrupts activity of the protein product of MAGEL2.

Prader-Willi syndrome is an imprinted disease, which means only one of the two copies of the gene inherited from your parents is working. The other is "silenced," usually during the formation of eggs or sperm. In this case, neither parent had a mutation, meaning that the mutation occurred first in this child. However, it still mattered whether the mutation came from the mother or the father.

The team from UTHealth and Complete Genomics then performed an involved analysis that determined that the mutated gene was on the paternal chromosome 15.

"Because the mom's copy of the gene is silenced and the dad's copy is deficient, there is no functional copy of the gene in his body," said Schaaf. "It was a nice collaboration among Baylor, UTHealth and Complete Genomics. But it was only one patient. When you identify a new gene and want to prove that it is the real cause of disease, you really need to identify several patients with mutations in the same gene, and show that they also have similar clinical manifestations. You also ought to consider the severity of the mutation and how rare the mutation is."

To start, they began to look for other patients. They asked the Baylor Whole Genome Sequencing Laboratory to find out if there had been similar mutations found in patients who had their exomes or protein-coding portions of the genome sequenced. They searched through the records of 1,200 and found three more patients with mutations in the same gene. One of the three had classic Prader-Willi syndrome, the other two were classified as Prader-Willi like. All three children had the standard molecular testing for Prader-Willi when they were infants, with negative results.

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Sequencing studies help pinpoint gene in Prader-Willi syndrome

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Gene is only second linked to late-onset Alzheimer's, fifth overall linked to the disease.

Published: Sept. 28, 2013 at 8:20 PM

Researchers at Massachusetts General Hospital identified two gene mutations that can increase a person's chance of developing late-onset Alzheimer's disease.

The research, published in the October issue of Neuron magazine, found that the two rare mutations are found in the ADAM10 gene, the second gene found to play a role in Alzheimer's developed after the age of 60. It's the fifth gene overall linked to the disease.

"This is the first report to document, in animal models, new [disease-causing] gene mutations for Alzheimer's since the reports of the original four genes in the 1990s," study senior author Rudolph Tanzi, director of the genetics and aging unit at the MassGeneral Institute for Neurodegenerative Disease, said in a hospital news release.

"What we found regarding the many effects of these two rare mutations in ADAM10 strongly suggests that diminished activity of this enzyme can cause [Alzheimer's disease], and these findings support ADAM10 as a promising therapeutic target for both treatment and prevention," Tanzi said.

More here:
Alzheimer's: Two additional gene mutations linked to disease

Recommendation and review posted by Bethany Smith

Gene is only second linked to late-onset Alzheimer's, fifth overall linked to the disease.

Published: Sept. 28, 2013 at 8:20 PM

Researchers at Massachusetts General Hospital identified two gene mutations that can increase a person's chance of developing late-onset Alzheimer's disease.

The research, published in the October issue of Neuron magazine, found that the two rare mutations are found in the ADAM10 gene, the second gene found to play a role in Alzheimer's developed after the age of 60. It's the fifth gene overall linked to the disease.

"This is the first report to document, in animal models, new [disease-causing] gene mutations for Alzheimer's since the reports of the original four genes in the 1990s," study senior author Rudolph Tanzi, director of the genetics and aging unit at the MassGeneral Institute for Neurodegenerative Disease, said in a hospital news release.

"What we found regarding the many effects of these two rare mutations in ADAM10 strongly suggests that diminished activity of this enzyme can cause [Alzheimer's disease], and these findings support ADAM10 as a promising therapeutic target for both treatment and prevention," Tanzi said.

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Alzheimer's: Two new gene mutations linked to disease

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September 2013 Breaking News Genetic engineering
September 2013 Breaking News Genetic engineering.

By: utoob bornagain

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September 2013 Breaking News Genetic engineering - Video

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Asa Mathat | All Things D

Last week more than a dozen companies had IPOs and among them was an interesting bio-tech company called Foundation Medicine.

Foundation offers to the public the kind of in-detailed genetic cancer testing made famous by Steve Jobs. Jobs was the first well-known person to try this sort of thing.

For about $6,000, this test uncovers all the genetic mutations that lead to a persons tumor. It's helping to usher in a new era of "personalized medicine" where doctors choose cancer treatments based on genetic knowledge.

Jobs spent some $100,000 to have this kind of test done, according to Walter Isaacsons biography, and in the end, it obviously didn't save him.

But he believed deeply in the value of the attempt, saying Im either going to be one of the first to be able to outrun a cancer like this, or Im going to be one of the last to die from it, reports Antonio Regalado, MIT Technology Review.

After Jobs died, the doctors who reportedly worked on the test at the Broad Institute of MIT and Harvard, left Broad to start Foundation, Regalado reports. Bill Gates and Larry Page both visited Jobs shortly before his death, according toIsaacson, and while they could do nothing to help him, they did help fund Foundation.

Bill Gates was part of the company's initial $13.5 million round and still owns 4%, according to documents filed with the SEC.

Google Ventures, the venture capital arm of Google, was part of a long list of VCs that later kicked in cash, and still owns 9%. In fact, foundation raised a whopping $251 million from investors in two years.

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Steve Jobs' Final Vision Is Coming True Thanks (In Part) To Bill Gates And Google

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FD Genetics
Why I think psychology is the excuse for genetics.

By: Francis Diet TALKS

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FD Genetics - Video

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AMERICAN GENETICS
http://www.cacciaedintorni.it.

By: Caccia e Dintorni

Link:
AMERICAN GENETICS - Video

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Genetics - Don #39;t Give Up @ Teatro Coliseo, Bs As, 21/09/13.
Genetics - Don #39;t Give Up (Peter Gabriel single, 1986). Teatro Coliseo, Bs As, Argentina. Sábado 21 de Septiembre de 2013. HD Stereo.

By: Gino Zolezzi

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Genetics - Don't Give Up @ Teatro Coliseo, Bs As, 21/09/13. - Video

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Gene therapy relieving chronic pain in pets
9/26 10 pm -- A revolutionary gene therapy developed in Colorado could relieve people #39;s chronic pain, such as arthritis or fibro but first, it is being teste...

By: 7NEWS and TheDenverChannel.com

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Gene therapy relieving chronic pain in pets - Video

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Gene therapy part 2 : ex vivo gene therapy
For more information, log on to- http://shomusbiology.weebly.com/ Download the study materials here- http://shomusbiology.weebly.com/bio-materials.html Gene ...

By: Suman Bhattacharjee

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Gene therapy part 2 : ex vivo gene therapy - Video

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Gene therapy part 1 : basics of gene therapy
For more information, log on to- http://shomusbiology.weebly.com/ Download the study materials here- http://shomusbiology.weebly.com/bio-materials.html Gene ...

By: Suman Bhattacharjee

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Gene therapy part 1 : basics of gene therapy - Video

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Gene therapy part 3 in vitro gene therapy
For more information, log on to- http://shomusbiology.weebly.com/ Download the study materials here- http://shomusbiology.weebly.com/bio-materials.html Gene ...

By: Suman Bhattacharjee

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Gene therapy part 3 in vitro gene therapy - Video

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