Archive for February, 2015

Branch Warren: Blessed Genetics or Hard Work? | Generation Iron
Branch Warren is a fierce competitor with a no nonsense approach to his bodybuilding training. His dedication to his craft has seen him have great success in...

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Mutants Genetics Gladiators Campaas Supra Campos De Sangre
A Mi Parecer La Campaa Mas Facil Espero Que Para Ustedes Tanbien.

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Class 12 -Biology-Genetics-Lec2-Introduction To Mendelian Genetics

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Class 12 -Biology-Genetics-Lec2-Introduction To Mendelian Genetics - Video

Stethoscope - Clinical Genetics| Episode 62)
Stethoscope| Clinical Genetics ( ) Episode 62.

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Stethoscope - Clinical Genetics| Episode 62) - Video

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Cancer Gene Therapy -- 8News Anchor Amy Lacey/VCU Massey Cancer Center
It can be devastating to be diagnosed with cancer, but what if you could take drugs tailored to your DNA, drugs that can buy you precious time? 8News Anchor Amy Lacey has more on the new test...

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Cancer Gene Therapy -- 8News Anchor Amy Lacey/VCU Massey Cancer Center - Video

DALLAS, February 21, 2015 /PRNewswire/ --

RnRMarketResearch.com announces addition of Gene Therapy Hematological Disorders Insight and Gene Therapy Metabolic Disorders Insight: Pipeline Assessment, Market Trend, Technology and Competitive Landscape market research reports to its library.

The "Gene Therapy Hematological Disorders Insight: Pipeline Assessment, Market Trend, Technology and Competitive Landscape" research report provides in depth insights into the Hematological Disorders gene therapy. It has covered 20+ gene therapies covering 20+ Pharmaceutical companies. Studies are performed for approximately 10+ specific indications under Hematological Disorders. The Companies are utilizing 12 different technology platforms which have its own uniqueness and robustness. The Report is also giving insights about the vectors usage in Gene therapy which is approximately 63% for viral vectors, 14% for RNAi therapeutics and 23% for Non-Viral vectors. The Report is also giving early winners of the Hematological Disorders gene therapy market using a proprietary Matrix Model. Complete research is available at http://www.rnrmarketresearch.com/gene-therapy-hematological-disorders-insight-pipeline-assessment-market-trend-technology-and-competitive-landscape-market-report.html

The "Gene Therapy Metabolic Disorders Insight: Pipeline Assessment, Market Trend, Technology and Competitive Landscape" research report provides in depth insights into the Metabolic Disorders gene therapy. It has covered 30+ gene therapies covering 20+ Pharmaceutical companies. Studies are performed for approximately 30+ specific indications under Metabolic Disorders. The Companies are utilizing 16 different technology platforms which have its own uniqueness and robustness. The Report is also giving insights about the vectors usage in Gene therapy which is approximately 66% for viral vectors, 25% for RNAi therapeutics and 9% for Non-Viral vectors. The Report is also giving early winners of the Metabolic Disorders gene therapy market using a proprietary Matrix Model. Complete research is available at http://www.rnrmarketresearch.com/gene-therapy-metabolic-disorders-insight-pipeline-assessment-market-trend-technology-and-competitive-landscape-market-report.html

The Marketed Products Scenario for Gene Therapies section of this report profiles Rexin G, Gendicine and Glybera. Assessment of marketed drugs by therapeutic approach, by route of administration and by delivery system is provided in this research. Pipeline gene therapy products under metabolic disorders, gene therapy products distribution on the basis of delivery system developed and on the basis of genetic material transfer techniques are covered along with gene therapies profiles.

The Gene Therapy Hematological Disorders Report provides the target gene name, localization of gene, molecular function of target with descriptive mechanism of action. Using the propriety DelveInsight Competitive Matrix models, the report also provides the first in class market analytics providing predictive analysis of early market winners of the clinical therapies and pre-clinical therapies in a demographic presentation view. It provides the information across the gene therapy value chain covering gene therapy profiles core insights, pre-clinical data, clinical data, technology details, funding and licensing opportunities.

Few highlights of these gene therapy market insight reports cover global gene therapy overview & pipeline insights, trends in gene therapy partnering deals, current prominent research areas and key players, companies targeting prominent therapeutic areas, number of gene therapies in clinical trials, number of gene therapies by vectors used, technology and their innovative companies and early market winners for gene therapy.

These research reports on gene therapy market insights offer complete market and pipeline intelligence and complete understanding over therapeutics development for gene therapy. They help devise corrective measures for pipeline projects by understanding therapy area specific gene therapies and in developing strategic initiatives to support your gene therapy development activities. Optimize your portfolio and keep you in touch with the rapidly changing pharmaceutical markets, and make the best decisions for your business. Develop and design in licensing and out licensing strategies by identifying prospective partners with the most attractive projects to enhance and expand business potential and Scope. Evaluate the marketing and pipeline strategy for gene therapies and their Funding availabilities. These reports also help in identifying the upcoming leaders in the gene therapy market in the coming years and getting a first mover advantage by identifying the early market winners for clinical and preclinical gene therapies.

Order a copy of Gene Therapy Hematological Disorders Insight: Pipeline Assessment, Market Trend, Technology and Competitive Landscape report at http://www.rnrmarketresearch.com/contacts/purchase?rname=265852

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Gene Therapy Insights on Hematological and Metabolic Disorders Market in 2015 Research Reports

Experience of Mr. Ashwani Rajput with COD-Medialert
COD-Medi Alert is a unique service that gives the user an opportunity to express their care for their loved ones by reminding them to take medicines on time as prescribed by their doctor. The...

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Companion Diagnostics - Streamlining drug development and advancing personalized medicine
The report, Companion Diagnostics - Streamlining drug development and advancing personalized medicine was written to support both the biopharmaceutical and diagnostic industries better ...

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What is Bone Marrow Aspirate Concentrate (BMAC) in Stem Cell Therapy?
Dr. McKenna explains bone marrow aspirate concentrate (BMAC). BMAC contains stem cells and growth factors that can build blood supply and heal tissue. For more information: http://www.rmiclinic.com...

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Stem Cell Therapy Using Fat Cells - Howard Beach, Ozone Park, Queens NY - Dr. Benjamin Bieber, MD
Regenerative Medicine - Dr. Benjamin Bieber, MD - Howard Beach, Ozone Park, Queens NY http://www.crossbaypmr.com Phone: (718) 835-0100 Stem Cell Therapy Using Fat Cells Dr. Benjamin...

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Ryan Benton Discusses Stem Cell Therapy for Duchenne #39;s Muscular Dystrophy
Ryan Benton is the first patient in the United States to receive human umbilical cord-derived mesenchymal stem cell therapy for Duchenne #39;s muscular dystrophy...

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A research team led by investigators from Mayo Clinic's campus in Jacksonville, Florida, and the University of Oslo, Norway, have identified a molecule that pushes normal pancreatic cells to transform their shape, laying the groundwork for development of pancreatic cancer -- one of the most difficult tumors to treat.

Their findings, reported in Nature Communications, suggest that inhibiting the gene, protein kinase D1 (PKD1), and its protein could halt progression and spread of this form of pancreatic cancer, and possibly even reverse the transformation.

"As soon as pancreatic cancer develops, it begins to spread, and PKD1 is key to both processes. Given this finding, we are busy developing a PKD1 inhibitor that we can test further," says the study's co-lead investigator, Peter Storz, Ph.D., a cancer researcher at Mayo Clinic.

"We need a new strategy to treat, and possibly prevent, pancreatic cancer. While these are early days, understanding one of the key drivers in this aggressive cancer is a major step in the right direction," he says.

In the U.S., pancreatic cancer is the fourth most common cause of deaths due to cancer, according to the American Cancer Society. A quarter of patients do not live longer than a year after diagnosis.

Pancreatic cancer can occur when acinar cells -- pancreatic cells that secrete digestive enzymes -- morph into duct-like structures. This usually occurs after injury or inflammation of the pancreas and is a reversible process. However, the presence of oncogenic signaling (Kras mutations, EGF-R) can push these duct cells to develop lesions that are at risk for tumor development.

To test PKD1's effect, the researchers used a 3-D model of pancreatic cells derived from a mouse. They manipulated PKD1 expression by either blocking the gene or inducing its activity. About a week after stimulating PKD1 expression, the researchers could see that acinar cells transformed to duct-like cells. Blocking PKD1 led to decreased formation of duct-like cells and lesions.

"This is a great model for examining what happens in a signaling pathway -- we can see the changes by simply using a microscope. This model tells us that PKD1 is essential for the initial transformation from acinar to duct-like cells, which then can become cancerous," Dr. Storz says. "If we can stop that transformation from happening -- or perhaps reverse the process once it occurs -- we may be able to block or treat cancer development and its spread."

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The above story is based on materials provided by Mayo Clinic. The original article was written by Kevin Punsky. Note: Materials may be edited for content and length.

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Gene that pushes normal pancreas cells to change shape identified

6 hours ago CRISPR systems allow bacteria to adapt to new viral threats. Above, Staphylococcus aureus microbes lacking a CRISPR system are killed off by the bacteria-attacking virus NM4. This plate approximates the concentration of virus particles used in the recent experiments. Credit: Zach Veilleux / The Rockefeller University

Bacteria may not have brains, but they do have memories, at least when it comes to viruses that attack them. Many bacteria have a molecular immune system which allows these microbes to capture and retain pieces of viral DNA that they have encountered in the past, in order to recognize and destroy it when it shows up again.

Research at Rockefeller University described Wednesday (February 18) in Nature offers new insight into the mysterious process by which this system works to encode viral DNA in a microbe's genome for later use as guides for virus-cutting enzymes.

"Microbes, like vertebrates, have immune systems capable of adapting to new threats. Cas9, one enzyme employed by these systems, uses immunological memories to guide cuts to viral genetic code. However, very little is known about how these memories are acquired in the first place," says Assistant Professor Luciano Marraffini, head of the Laboratory of Bacteriology. "Our work shows that Cas9 also directs the formation of these memories among certain bacteria."

These memories are embedded in the bacterial equivalent of an adaptive immune system capable of discerning helpful from harmful viruses called a CRISPR (clustered regularly interspaced short palindromic repeats) system. It works by altering the bacterium's genome, adding short viral sequences called spacers in between the repeating DNA sequences. These spacers form the memories of past invaders. They serve as guides for enzymes encoded by CRISPR-associated genes (Cas), which seek out and destroy those same viruses should they attempt to infect the bacterium again.

Cas9's ability to make precision cuts within a genome - viral or otherwise - has caught the attention of researchers who now use it to alter cells' genetics for experimental or therapeutic purposes. But it is still not well understood just how this CRISPR system works in its native bacteria.

Some evidence suggested that other Cas enzymes managed the memory-making process on their own, without Cas9. But because of the way Cas9 goes about identifying the site at which to make a cut, the researchers, including co-first authors Robert Heler, a graduate student, and Poulami Samai, a postdoc in the lab, suspected a role for Cas9 in memory making.

In addition to matching its CRISPR guide sequence up with the DNA of the virus, Cas9 needs to find a second cue nearby: a PAM (protospacer adjacent motif) sequence in the viral DNA. This is a crucial step, since it is the absence of a PAM sequence that prevents Cas9 from attacking the bacterium's own memory-containing DNA.

"Because Cas9 must recognize a PAM sequence before cutting the viral DNA, it made sense to us that Cas9 would also recognize the PAM sequence when the system is forming a memory of its first encounter with a virus," Heler says. "This is a new and unexpected role for Cas9."

To test their hypothesis, Heler swapped the Cas9 enzymes between the immune systems of Streptococcus pyogenes and Streptococcus thermophilus, each of which recognizes a different PAM sequence. As a result, the PAM sequences followed, swapping between the two bugs - evidence that Cas9 is responsible for identifying the PAM during memory formation. In another experiment, he altered the part of Cas9 that binds to the PAM sequence, and found the microbes then began acquiring the target viral sequences randomly, making them unusable.

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Virus-cutting enzyme helps bacteria remember a threat

Precision Medicine: How our Genes Can Help Determine Our Risk and Treatment for Disease
Esteban Burchard, Director, Center for Genes, Environments Health Professor of Bioengineering Therapeutic Sciences Medicine University of California Sa...

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Precision Medicine: How our Genes Can Help Determine Our Risk and Treatment for Disease - Video

Keck Medicine of the University of Southern California (USC) scientists have found a promising new therapeutic target for prostate cancer. The findings offer evidence that a newly discovered member of a family of cell surface proteins called G-protein coupled receptors (GPCRs) promotes prostate cancer cell growth. The protein, GPR158, was found while the researchers were looking for new drug targets for glaucoma.

Prostate cancer is the second most common cancer in American men, after skin cancer, according to the American Cancer Society (ACS). The ACS projects more than 27,000 deaths from prostate cancer in 2015 and is the second leading cause of cancer death in American men, behind lung cancer. One man in seven will be diagnosed with prostate cancer during his lifetime.

"When a prostate cancer tumor is in its early stages, it depends on hormones called androgens to grow," said Nitin Patel, Ph.D., research scientist at the Institute for Genetic Medicine at the Keck School of Medicine of USC, and corresponding author on the research. "Eventually it progresses to a more lethal form, called castration-resistant prostate cancer (CRPC), and is resistant to drugs that block androgen receptors. We found that GPR158, unlike other members of the GPCR family, is stimulated by androgens, which in turn stimulates androgen receptor expression, leading to tumor growth."

The team also discovered that GPR158 is associated with neuroendocrine transdifferentiation (NED) of epithelial prostate tumor cells, which plays a critical role in development of resistance to contemporary androgen receptor-target therapies. The scientists found that prostate cancer patients with elevated GPR158 expression experienced recurrence of prostate cancer. The GPR158 protein is a likely target for new prostate cancer drugs.

The researchers used a conditional Pten knockout mouse model of prostate cancer in collaboration with Keck School of Medicine of USC researchers Mitchell Gross, Chun-Peng Liao and Pradip Roy-Burman.

The team is now exploring the molecular pathways involved in the functional role of GPR158 in NED in the development of CRPC and exploring GPR158-targeted antibody therapeutics.

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New target for prostate cancer treatment discovered

Researchers are beginning to understand how DNA makes some athletes more likely to get hurt.

Injury is a fact of life for most athletes, but some professionalsand some weekend warriors, for that matterjust seem more injury-prone than others. But what is it about their bodies that makes the bones, tendons, and ligaments so much more likely to tear or strainbad luck, or just poor preparation?

A growing body of research suggests another answer: that genetic makeup may play an important role in injury risk.

A review article recently published in the Clinical Journal of Sports Medicine emphasizes that research on the genetics of sports injuries holds great potential for injury prevention for athletes at every level. The authors, from Stanford Universitys department of developmental biology and genetics, believe that genetic testing also gives athletes valuable information that might increase their competitive edge.

Stuart Kim, one of the studys authors and a professor of genetics at Stanford, says his interest in sports injuries began almost by accident. I initially intended to study the genes associated with the large size of NFL lineman, but the athletes werent really interested in finding out the genetic reasons why they were so big, Kim says. But they were extremely interested in figuring out what injuries they were more likely to sustain.

Genetic information can be valuable for amateur athletes, tooregardless of skill level, someone about to join a recreational basketball league or a tennis club would be well-served to know if theyre at risk of blowing out an ACL or tearing an Achilles. Each year, around 2 million adults go to the emergency room for sports-related injuries, many of them acquired during pickup games or matches in recreational leagues.

Within the field of sports-injury genetics, some studies have focused on variations in the genes that control the production of collagen, the main component of tendons and ligaments. Collagen proteins also form the backbone of tissues and bones, but in some people, structural differences in these proteins may leave the bodys structures weaker or unable to repair themselves properly after injury. In a study published in the British Journal of Sports Medicine in 2009, South African researchers found that specific variations of a collagen gene named COL1A1 were under-represented in a group of recreational athletes who had suffered traumatic ACL injuries. Those who had torn their ACL were four times as likely as the uninjured study subjects to have a blood relative who had suffered the same injury, suggesting that genetics are at least partially responsible for the strength of the ligament.

The same COL1A1 gene has also been linked to other soft-tissue injuries, like Achilles-tendon ruptures and shoulder dislocations. In a review article that combined the results of multiple studies on the COL1A1 gene, published in the British Journal of Sports Medicine in 2010, researchers concluded that those with the TT genotypeone of three potential variants of the gene, found only in 5 percent of the populationare extremely unlikely to suffer a traumatic ligament or tendon injury.

However, because of the vast complexity of the human genome, its highly improbable that a single variant within a gene can determine a persons genetic risk for a given soft-tissue injury. Researchers agree its much more likely that these injuries, like complex conditions such as obesity or type 2 diabetes, are influenced by multiple genes.

The COL5A1 gene, another one associated with collagen production, has been linked to a higher risk of injury of the ACL and Achilles tendon, as well as greater susceptibility to exercise-induced muscle cramping. A 2013 study in the Clinical Journal of Sports Medicine found that specific variants of COL5A1 were strongly correlated with muscle cramping among runners in the Two Oceans Marathon in South Africa.

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The Genetics of Being Injury-Prone

Gene therapy leads to promising avenue for HIV vaccine
Gene therapy leads to promising avenue for HIV vaccine.

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Gene therapy leads to promising avenue for HIV vaccine - Video

Stamford, CT (PRWEB) February 20, 2015

World-renowned scientist and University of Pittsburgh School of Medicine genetics and biochemistry professor Joseph Glorioso III, PhD has been named Chairman of the Scientific Advisory Council at Alliance for Cancer Gene Therapy.

Glorioso, known for his work on the molecular and genetic aspects of the herpes simplex virus and how to better engineer this organism as a vector for transporting therapeutic genes, will take the helm from Dr. Savio L.C. Woo, the founding Chairman of ACGTs Scientific Advisory Council; Dr. Woo has also been named Chairman Emeritus of the Council.

Savio has been a remarkable and dynamic leader who has steered the Council from the beginning to focus on young investigators and groundbreaking clinical translation, Glorioso said. This work has resulted in ACGT pioneering breakthroughs in gene and cell therapy treatments for cancer. We now look forward, to expanding our vision to include later-stage research, which will be very exciting.

Glorioso received his bachelors degree and doctorate from Louisiana State University before joining the University of Michigan Medical School in the late 1970s. He attained the rank of professor and assistant dean for research and graduate studies there, and then joined the University of Pittsburgh School of Medicine in 1989. At Pittsburgh, Glorioso served as Professor and Chair of the Department of Molecular Genetics and Biochemistry, as well as the McEllroy Professorship in Biochemistry until 2009. He continues his groundbreaking work in the development of herpes viral vectors for the treatment of cancer, chronic pain and diseases of the central nervous system. Glorioso has served on ACGTs Scientific Advisory Council since 2005.

Joe has been a valuable member of our Scientific Advisory Council and has made tremendous strides in his own work to improve the quality of life for patients fighting cancer and other diseases; that same vision will advance ACGTs own pursuit of effective cell and gene therapy treatments, said Barbara Netter, President and Co-founder of ACGT.

ACGTs Scientific Advisory Council, composed of preeminent physicians and researchers in cell and gene therapy, serves without remuneration and establishes the scientific criteria for the review of all grants. Council members are also tasked with developing strict accountability guidelines requiring periodic progress reports. At present, the Council is composed of 15 members, including Glorioso.

Based in Stamford, Connecticut, ACGT funds top physicians and researchers at medical institutions in the U.S. and Canada. The Foundation supports a number of gene and cell therapy treatments, including immunotherapy, which activates patients own immune systems to battle cancerous cells. In 2014, the FDA granted fast-track status to 2 immunotherapy treatments for leukemia, for which ACGT provided critical early funding.

About Alliance for Cancer Gene Therapy (ACGT): Established in 2001, ACGT (http://www.acgtfoundation.org) is the nations only not-for-profit dedicated exclusively to cell and gene therapy treatments for all types of cancer. One-hundred percent of contributions go directly to research. ACGT has funded 46 grants in the U.S. and Canada since its founding in 2001 by Barbara Netter, President, and her late husband, Edward, to conduct and accelerate critically needed innovative research. Since its inception, ACGT has awarded 31 grants to Young Investigators and 15 grants to Clinical Investigators, totaling more than $25 million in funding. ACGT is located at 96 Cummings Point Road, Stamford, CT 06902.

ACGT on Facebook: http://www.facebook.com/ACGTfoundation ACGT on Twitter: http://www.twitter.com/ACGTfoundation ACGT on YouTube: http://www.youtube.com/user/ACGTfoundation

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Alliance for Cancer Gene Therapy (ACGT) Thanks Dr. Savio L.C. Woo For His Service; Names Dr. Joseph Glorioso ...

Denny Ross - 16 January 2015 - 2
Denny is a charismatic and resilient individual who loves to challenge himself with the latest and fastest adventures in life. His most recent adventure has ...

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Wheelchair Van Transfer Video: Jennifer Hastings | MedBridge
Watch a demonstration of a wheelchair van transfer. Read FREE related article: https://www.medbridgeeducation.com/h/october-newsletter-independent-transfers-exercise-filters-back-pain-stroke-rehab ...

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Wheelchair Van Transfer Video: Jennifer Hastings | MedBridge - Video

Non-Surgical Regenerative Medicine For Joint Pain- Flexogenix
For millions of patients experiencing joint pain, facing the prospect of joint replacement surgery along with all of the associated risks and potential unwan...

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Genetically modified crops have long drawn fire from opponents worried about potential contamination of conventional crops and other plants. Now a plant gene discovered by University of Guelph scientists might help farmers reduce the risk of GM contamination and quell arguments against the use of transgenic food crops, says Sherif Sherif, lead author of a new research paper describing the findings.

This is believed to be the first-ever study to identify a gene involved in altering fruit trees that normally cross-pollinate -- needing one plant to fertilize another -- into self-pollinators, said Sherif.

The paper was published recently in the journal BMC Biology.

Sherif said researchers might one day insert this gene into GM crops to prevent their pollen from reaching other plants.

Plant agriculture professor Jay Subramanian, Sherif's PhD supervisor and a co-author on the paper, said: "There are a lot of transgenic crops worldwide. There is concern about pollen from them being able to fertilize something in the wild population, thus creating 'super weeds.'"

The researchers found a gene making a protein that naturally allows a small handful of plants to self-pollinate and make fruit before the flower opens. Peaches, for example, have closed flowers, unlike their showy-flowered plum and cherry cousins that need pollen from another tree to fertilize and set fruit.

Subramanian studies tree fruits at the Vineland Research and Innovation Centre in Vineland, Ont. Sherif worked with him on studies of plant responses to stresses such as drought or disease.

Other co-authors on the paper are Guelph professors Jaideep Mathur, Department of Molecular and Cellular Biology and Gopi Paliyath, Department of Plant Agiruclture, along with Islam El-Sharkawy, a former research associate with Subramanian; and colleagues at the National University of Singapore.

Besides aiding crop farmers and food producers, their discovery might be a boon to perfume-makers, said Subramanian.

Used in fragrant perennials such as jasmine, the gene might keep flowers closed and allow growers to collect more of the aromatic compounds prized by perfume-makers. "That's when volatile compounds are peaking," said Subramanian. "When the flower opens, you lose almost 80 per cent of those volatiles."

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Gene may help reduce GM contamination

Single-letter genetic variations within parts of the genome once dismissed as 'junk DNA' can increase cancer risk through wormhole-like effects on far-off genes, new research shows.

Researchers found that DNA sequences within 'gene deserts' -- so called because they are completely devoid of genes -- can regulate gene activity elsewhere by forming DNA loops across relatively large distances.

The study, led by scientists at The Institute of Cancer Research, London, helps solve a mystery about how genetic variations in parts of the genome that don't appear to be doing very much can increase cancer risk.

Researchers developed a new technique to study the looping interactions and discovered that single-letter DNA variations linked to the development of bowel cancer were found in regions of the genome involved in DNA looping.

Their study, published today in Nature Communications, is the first to look comprehensively at these DNA interactions specifically in bowel cancer cells, and has implications for the study of other complex genetic diseases.

It was funded by the EU, Cancer Research UK, Leukaemia & Lymphoma Research, and The Institute of Cancer Research (ICR).

The researchers developed a technique called Capture Hi-C to investigate long-range physical interactions between stretches of DNA -- allowing them to look at how specific areas of chromosomes interact physically in more detail than ever before. Previous techniques used to investigate long-range DNA interactions were not sensitive enough to produce definitive results.

The researchers assessed 14 regions of DNA that contain single-letter variations previously linked to bowel cancer risk. They detected significant long-range interactions for all 14 regions, confirming their role in gene regulation.

These interactions are important because they can control how genes behave, and alterations in gene behaviour can lead to cancer -- in fact most genetic variations that have been linked to cancer risk are not in genes themselves, but in the areas of the genome that regulate them.

Study leader Professor Richard Houlston, Professor of Molecular and Population Genetics at The Institute of Cancer Research, London, said: "Our new technique shows that genetic variations are able to increase cancer risk through long-range looping interactions with cancer-causing genes elsewhere in the genome. It is sometimes described as analogous to a wormhole, where distortions in space and time could in theory bring together distant parts of the universe.

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Cancer risk linked to DNA 'wormholes'

Using advanced DNA sequencing methods, researchers have identified a new gene that is associated with sporadic amyotrophic lateral sclerosis (ALS), or Lou Gehrig's disease. ALS is a devastating neurodegenerative disorder that results in the loss of all voluntary movement and is fatal in the majority of cases. The next-generation genetic sequencing of the exomes (protein-coding portions) of 2,874 ALS patients and 6,405 controls represents the largest number of ALS patients to have been sequenced in a single study to date.

Though much is known about the genetic underpinnings of familial ALS, only a handful of genes have been definitively linked to sporadic ALS, which accounts for about 90 percent of all ALS cases. The newly associated gene, called TBK1, plays a key role at the intersection of two essential cellular pathways: inflammation (a reaction to injury or infection) and autophagy (a cellular process involved in the removal of damaged cellular components). The study, conducted by an international ALS consortium that includes scientists and clinicians from Columbia University Medical Center (CUMC), Biogen Idec, and HudsonAlpha Institute for Biotechnology, was published today in the online edition of Science.

"The identification of TBK1 is exciting for understanding ALS pathogenesis, especially since the inflammatory and autophagy pathways have been previously implicated in the disease," said Lucie Bruijn, PhD, Chief Scientist for The ALS Association. "The fact that TBK1 accounts for one percent of ALS adds significantly to our growing understanding of the genetic underpinnings of the disease. This study, which combines the efforts of over two dozen laboratories in six countries, also highlights the global and collaborative nature of ALS research today.

"This study shows us that large-scale genetic studies not only can work very well in ALS, but that they can help pinpoint key biological pathways relevant to ALS that then become the focus of targeted drug development efforts," said study co-leader David B. Goldstein, PhD, professor of genetics and development and director of the new Institute for Genomic Medicine at CUMC. "ALS is an incredibly diverse disease, caused by dozens of different genetic mutations, which we're only beginning to discover. The more of these mutations we identify, the better we can decipher--and influence--the pathways that lead to disease." The other co-leaders of the study are Richard M. Myers, PhD, president and scientific director of HudsonAlpha, and Tim Harris, PhD, DSc, Senior Vice President, Technology and Translational Sciences, Biogen Idec.

"These findings demonstrate the power of exome sequencing in the search for rare variants that predispose individuals to disease and in identifying potential points of intervention. We are following up by looking at the function of this pathway so that one day this research may benefit the patients living with ALS," said Dr. Harris. "The speed with which we were able to identify this pathway and begin our next phase of research shows the potential of novel, focused collaborations with the best academic scientists to advance our understanding of the molecular pathology of disease. This synergy is vital for both industry and the academic community, especially in the context of precision medicine and whole-genome sequencing."

"Industry and academia often do things together, but this is a perfect example of a large, complex project that required many parts, with equal contributions from Biogen Idec. Dr. Tim Harris, our collaborator there, and his team, as well as David Goldstein and his team, now at Columbia University, as well as our teams here at HudsonAlpha, said Dr. Myers. "I love this research model because it doesn't happen very frequently, and it really shows how industry, nonprofits, and academic laboratories can all work together for the betterment of humankind. The combination of those groups with a large number of the clinical collaborators who have been seeing patients with this disease for many years and providing clinical information, recruiting patients, as well as collecting DNA samples for us to do this study, were all critical to get this done."

Searching through the enormous database generated in the ALS study, Dr. Goldstein and his colleagues found several genes that appear to contribute to ALS, most notably TBK1 (TANK-Binding Kinase 1), which had not been detected in previous, smaller-scale studies. TBK1 mutations appeared in about 1 percent of the ALS patients--a large proportion in the context of a complex disease with multiple genetic components, according to Dr. Goldstein. The study also found that a gene called OPTN, previously thought to play a minor role in ALS, may actually be a major player in the disease.

"Remarkably, the TBK1 protein and optineurin, which is encoded by the OPTN gene, interact physically and functionally. Both proteins are required for the normal function of inflammatory and autophagy pathways, and now we have shown that mutations in either gene are associated with ALS," said Dr. Goldstein. "Thus there seems to be no question that aberrations in the pathways that require TBK1 and OPTN are important in some ALS patients."

The researchers are currently using patient-derived induced pluripotent embryonic stem cells (iPS cells) and mouse models with mutations in TBK1 or OPTN to study ALS disease mechanisms and to screen for drug candidates. Several compounds that affect TBK1 signaling have already been developed for use in cancer, where the gene is thought to play a role in tumor-cell survival.

"This is a great example of the potential of precision medicine," said Tom Maniatis, PhD, the Isidore S. Edelman Professor, chair of biochemistry and molecular biophysics, and coauthor on the paper. Dr. Maniatis is also a member of the Zuckerman Mind Brain Behavior Institute and director of Columbia's university-wide precision medicine initiative. "It now seems clear that future ALS treatments will not be equally effective for all patients because of the disease's genetic diversity. Ultimately, as candidate therapies become available, we hope to be able to use the genetic data from each ALS patient to direct that person to the most appropriate clinical trials and, ultimately, use the data to prescribe treatment."

Link:
New ALS gene, signaling pathways identified