Archive for the ‘Gene Therapy Research’ Category

SHARSHERET, Israel--(BUSINESS WIRE)--

Morflora (www.morflora.com), focused on innovative non-transgenic trait delivery technology for plant protection reports today that its TraitUP platform has been successfully used to deliver complex genetic material into seeds, providing protection against diseases and biotic stress for plants grown from treated seeds.

This achievement demonstrates the maturity and power of the TraitUP technology to effectively deliver traits via seed treatment in a fast non-transgenic manner, positioning TraitUP as the technology of choice for companies which engage in functional genomics. Many of the industry players invest substantial resources seeking effective solutions to discover desirable traits in plants and crops, such as protecting crops against diseases and biotic stress, increasing yield and quality, and more. These extensive research operations rely on genetic transformation for the delivery of the desired genes into the target plants, and the testing of their expression and function in the plant of interest.

TraitUP is a key enabling technology for this market, as it can shorten the research process by years, offering a significantly faster alternative to genetic engineering. This is done without changing the plant genome, while expanding the scope of experiments. Utilizing TraitUP increases the immediate availability of seeds of the target crop for experiments in both quantity and variety, providing a proof of concept and allowing researchers to start experimenting on the desired target seed faster than ever.

"We are not transforming plants. We are transforming the industry," said Dotan Peleg, CEO of Morflora. "Our technology follows our vision of increasing and securing the global agricultural production, in a sustainable manner. Morfloras technology will accelerate and broaden the trait research industry as the first step, and upon up-scaling of the seed treatment protocols for commercial use in mass-production of seeds, the next step will be to significantly reduce time and cost to market of numerous genetically optimized crops. The technology has not yet fully matured to meet all the challenges of our vision, yet it is making consistent progress towards fulfilling it. The recent achievement of delivering such a complex genetic construct into seeds without transforming the plants, while enabling them to express disease-tolerance, is a significant milestone."

The research of the delivery of disease control genes using TraitUP seed treatment is held under collaborations with several institutes and researchers, including Prof. Ilan Sela and Prof. Haim Rabinowitch who serve as Professional Board Members on Morflora's advisory board, Prof. Yaacov Katan - an expert in soil borne diseases from the Department of Plant Pathology and Microbiology, The Robert H. Smith Faculty of Agriculture atthe Hebrew University of Jerusalem, and experts from Volcani Center, the Israeli Agriculture Research Organization of the Ministry of Agriculture the Rural Development. These researches indicated that TraitUP treated vegetable seeds express specific antifungal trait, based on the delivery of the PRN genetic operon. Results demonstrate control of Fusaruim, Botrytis and other pathogens.

TraitUP has been recently short-listed in the crop protection focused AGROW awards competition in the 'Best Novel Agricultural Biotechnology' category. The company researchers together with hundreds of industry leaders will attend the award ceremony to be held on 7th November 2012 at London. Earlier this year Morflora was selected as a winner for Red Herring's Top 100 Europe award, a prestigious list honoring the years most promising private technology ventures from the European business region.

About Morflora Morflora develops generic and non transgenic trait delivery solutions into plants, to protect them from a wide variety of diseases, as well as introduce new desired traits for plant enhancement. The company targets the seed and plant treatment markets, offering technology and solutions to increase global crop yield and reduce dependency on chemical treatments and lengthy breeding processes.

Established in 2008, Morfloras mission is to become a leading supplier of plant protection and enhancement solutions for a variety of agricultural markets. For additional information please log on to http://www.morflora.com.

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A Breakthrough In Agricultural Biotechnology –Trait Delivery Innovator Morflora Accelerates Gene Delivery Process in ...

CAMBRIDGE, Mass.--(BUSINESS WIRE)--

FierceBiotech today named Foundation Medicine, Inc. as one of 2012's Fierce 15, designating it as one of the most promising private biotechnology companies in the industry. This is FierceBiotech's tenth annual Fierce 15 selection.

This company is fast. In just two years Foundation Medicine has developed a diagnostic test that helps investigators manage the fast-changing genetic information needed in clinical research and gives physicians a better tool to make some rational decisions on the drugs they choose to treat cancer victims, says FierceBiotech Editor John Carroll. Its drawn the backing of some high-profile tech investors like Google Ventures. And, a lineup of cancer drug developers has signed on to work with the company on key cancer drug programs.

We are honored to be named to the 2012Fierce15and believe this award is a testament to the progressFoundationMedicine continues to make toward our vision of transforming cancer care through the development of our fully informative genomic profile, said Michael J. Pellini, M.D., president and chief executive officer ofFoundationMedicine.

The Fierce 15 celebrates the spirit of being fierce championing innovation and creativity, even in the face of intense competition.

An internationally recognized daily newsletter reaching more than 100,000 biotech and pharma industry professionals, FierceBiotech provides subscribers with an authoritative analysis of the day's top stories. Every year FierceBiotech evaluates hundreds of private companies for its annual Fierce 15 list, which is based on a variety of factors such as the strength of its technology, partnerships, venture backers and a competitive market position.

The 2012 Fierce 15 companies will be recognized today at the BioPharm America conference in Boston. A complete list of "Fierce 15" companies the online newsletter's tenth annual selection is available online at http://www.fiercebiotech.com.

About Foundation Medicine

Foundation Medicine is a molecular information company dedicated to a transformation in cancer care in which treatment is informed by a deep understanding of the genomic changes that contribute to each patients unique cancer. The companys initial clinical product, FoundationOneTM, is a fully informative genomic profile to identify a patients individual molecular alterations and match them with relevant targeted therapies and clinical trials. Foundation Medicines molecular information platform aims to improve day-to-day care for patients by serving the needs of clinicians, academic researchers and drug developers to help advance the science of molecular medicine in cancer. For more information, please visit http://www.foundationmedicine.com.

Foundation Medicine is a registered trademark, and FoundationOneTM is a trademark of Foundation Medicine, Inc.

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FierceBiotech Names Foundation Medicine as One of 2012’s Fierce 15

MENLO PARK, Calif. & GRAMBACH/GRAZ, Austria--(BUSINESS WIRE)--

DNA2.0, the leading bioengineering solutions provider and VTU Technology, the leader in Pichia pastoris protein expression services, today announced a partnership to develop and refine a gene design algorithm to enable maximized protein production in the yeast P. pastoris. The collaboration will combine VTUs deep P. pastoris expertise and AOX1 promoter technology with DNA2.0s gene design technology for robust translation.

Pichia is ideally suited for high-level expression of recombinant proteins for therapeutic and industrial applications, said Dr. Thomas Purkarthofer, Head of Business Development of VTU Technology. We are excited to merge the unparalleled strength of our P. pastoris expression system with DNA2.0s industry-leading gene design and expression optimization technology.

VTUs P. pastoris protein expression platform is based on engineered versions of the AOX1 promoter, one of the strongest eukaryotic promoters known. VTUs approach delivers up to 20 g/L of secreted protein within a few weeks development time, and the company has a proven track record for expressing commercial levels of a wide range of proteins including serum proteins, cytokines, fusion proteins, Fabs, antibody derived fragments, scaffold proteins and enzymes.

The protein target for this collaboration is DNA2.0s IP-free CometGFP, which is part of a novel family of fluorescent and colorimetric proteins developed by DNA2.0. The corresponding IP-free genes are brought to market without expensive, constrained licensing.

We developed our initial Pichia gene design algorithm with the world-leading P. pastoris laboratory of Anton Glieder, and we are thrilled to expand the breadth and scope of our P. pastoris technology for industrial scale applications with the proven commercial leader in the field, VTU Technology, said Jeremy Minshull, Ph.D., cofounder and CEO of DNA2.0. Controllable, consistent and strong protein expression is the goal regardless of the type of research in which you are engaged, and our patented GeneGPS technology has been proven to produce orders of magnitude increases in protein expression.

About VTU Technology:

VTU Technology is a leading provider of comprehensive services based on exclusive and innovative Pichia pastoris protein production technologies. With exclusive know-how and extensive experience, VTUs skilled team delivers fast-track development of high-performance industrial protein production strains enabling high expression yields and economically attractive production processes.

Headquartered in Grambach/Graz, Austria, VTU Technology is a private company and a subsidiary ofVTU Holding, an Austrian enterprise that combines several technology and engineering companies in chemistry, pharma & life science as well as power and fuel industries. For more information, please visit http://www.vtu-technology.com

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DNA2.0 Taps VTU Technology as Research Partner for Industrial Scale Protein Expression

Public release date: 18-Sep-2012 [ | E-mail | Share ]

Contact: Jeremy Moore Jeremy.Moore@aacr.org 215-446-7109 American Association for Cancer Research

PHILADELPHIA Human papillomavirus (HPV) DNA positivity alone, particularly when assessed using polymerase chain reaction methods, is a poor biomarker for HPV-driven head and neck cancers, according to two studies published in Cancer Research, a journal of the American Association for Cancer Research. These studies identified alternative potential markers including viral load, viral gene expression and the evaluation of HPV DNA in combination with certain HPV assays.

Prior research has established that HPV is a cause of some head and neck cancers, including oropharyngeal cancer, and that patients with HPV-associated disease tend to have a better clinical outcome. Consequently, the proper assessment of the clinical status of individual tumors has become a goal of clinicians treating this disease because HPV at the tumor site does not indicate causal involvement in the cancer.

In the first study, Dana Holzinger, Ph.D., of the division of genome modifications and carcinogenesis at the German Cancer Research Center in Heidelberg, Germany, and colleagues analyzed the potential of direct and indirect HPV markers to identify patients with HPV-driven tumors.

They analyzed 199 oropharyngeal squamous cell carcinoma specimens for HPV DNA, viral load, RNA expression patterns seen in cervical carcinomas and the p16 protein, which is associated with tumor suppression.

Results indicated that the cervical cancer RNA expression pattern and viral load were associated with the lowest risk for death from oropharyngeal cancer. In contrast, a weaker association was found for samples that were HPV DNA-positive or that expressed the p16 protein.

"We showed that high viral load and a cancer-specific pattern of viral gene expression are most suited to identify patients with HPV-driven tumors among patients with oropharyngeal cancer," Holzinger said. "Viral expression pattern is a completely new marker in this field and viral load has hardly been analyzed before."

In a second study, researchers evaluated several biomarkers individually and in combination for overall survival among head and neck cancers including polymerase chain reaction-based and serological HPV DNA testing, and p16 immunohistochemistry.

They found that the expression of two oncoproteins, E6 and E7, was associated with improved survival in oropharyngeal disease. In addition, HPV DNA positivity or p16 expression combined with E6 and E7 expression were also associated with enhanced survival. However, neither HPV DNA positivity nor expression of p16 alone yielded a similar result.

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Assessment of HPV DNA alone insufficient to identify HPV-driven head and neck cancers

London, Sep 18:

Scientists have identified a gene, which could be responsible for a womans maternal feelings towards her children.

Researchers at the Rockefeller University in New York found that mice engineered to suppress the gene spent less time licking, nursing and retrieving their pups compared with a control group.

The findings suggest the single gene could be responsible for motivating mothers to protect, feed and raise their young, The Telegraph reported.

Previous studies have found that a brain region called the medial preoptic area controls aggression, sexual receptivity and maternal care in mice.

However, the chemical mechanisms which influence these behaviours have remained largely unclear.

Research has established that nerve cells react to oestrogen, the female sex hormone, and contain high levels of oestrogen receptor alpha, a chemical linked to maternal care and sexual behaviour.

Scientists artificially lowered the levels of the chemical in the medial preoptic area of female mice, to examine how they functioned without it.

They found that the mice spent less time caring for their pups but that their levels of aggression remained unchanged.

The main finding of this paper is manipulation of a specific gene in a specific group of neurons (nerve cells) can drastically alter the expression of a complete, biologically crucial behaviour, said Dr Ana Ribiero, who led the study.

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Gene responsible for ‘maternal feelings’ in women decoded

Public release date: 18-Sep-2012 [ | E-mail | Share ]

Contact: Mattias Lorentzon, University of Gothenburg mattias.lorentzon@medic.gu.se 46-031-342-4929 University of Gothenburg

A big international study has identified a special gene that regulates bone density and bone strength. The gene can be used as a risk marker for fractures and opens up opportunities for preventive medicine against fractures. The study, led by the Sahlgrenska Academy, University of Gothenburg, Sweden, was published in the journal PLoS Genetics.

The international study, which involved more than 50 researchers from Europe, North America and Australia and was led by Associate Professor Mattias Lorentzon and Professor Claes Ohlsson at the Sahlgrenska Academy, University of Gothenburg, is based on extensive genetic analyses of the genetic material of 10,000 patients and experimental studies in mice.

Through the combined studies, researchers have succeeded in identifying a special gene, Wnt16, with a strong link to bone density and so-called cortical bone thickness, which is decisive to bone strength.

The genetic variation studied by the international research network could predict, for example, the risk of a forearm fracture in a large patient group of older women.

"In the experimental study, we could then establish that the gene had a crucial effect on the thickness and density of the femur. In mice without the Wnt16 gene, the strength of the femur was up to 61 per cent lower," according to Mattias Lorentzon at the Institute of Medicine, the Sahlgrenska Academy, University of Gothenburg.

The discovery opens up opportunities to develop new medicines to prevent the most common fractures.

"Low cortical bone mass is a decisive factor in, for example, hip and forearm fractures. Unfortunately, the treatments currently used for brittleness of the bones have very little effect on the cortical bone mass," says Mattias Lorentzon.

"If we can learn to stimulate the signaling routes of the Wnt16 gene, we could strengthen the skeleton in these parts too, thereby preventing the most common and serious fractures. The discovery of Wnt16 and its regulation of cortical bone mass is therefore very important," according to Mattias Lorentzon.

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New gene offers hope for preventive medicine against fractures

ScienceDaily (Sep. 17, 2012) The discovery of a new gene could lead to better bug-resistant plants.

Research led by Michigan State University and appearing on the cover of this week's Proceedings of the National Academy of Sciences, demonstrates that domestic tomatoes could re-learn a thing or two from their wild cousins.

Long-term cultivation has led to tomato crops losing beneficial traits common to wild tomatoes. Anthony Schilmiller, MSU research assistant professor of biochemistry and molecular biology, was able to identify a gene that is involved in one of these beneficial traits.

Many tomato secrets are found in its hair. Trichomes, or hair-like protrusions, produce a mixture of specialized chemicals that shape the interactions between the plant and its environment. The location of the chemicals allows some of them to act as the first line of defense against pests.

One class of compounds, acyl sugars, is a frontline defender. Trichomes secrete acyl sugars to fend off pests. Schilmiller teamed with Robert Last, MSU professor of biochemistry and molecular biology, and Amanda Charbonneau, MSU doctoral researcher, to try to understand how these chemicals are made. Little was known about how acyl sugars were produced until now, and this research identifies and describes the first gene that participates in the production of the protective sugars in cultivated tomatoes, Schilmiller said.

"Acyl sugars play a critical role in allowing wild tomatoes to fend off bugs," he said. "Because cultivated tomatoes were not bred for their acyl sugar amounts and quality, they have reduced levels compared to wild ones we do not eat. Understanding how they are made is the first step toward breeding cultivated tomatoes, and other plants in this family, to make them more resistant to herbivores."

Other Solanaceous crops that could benefit from this research include potatoes, peppers, eggplants and petunias.

In addition, this work shows that the newly discovered gene is active only in one specific cell of one trichome type.

"Not only will we be able to potentially engineer heartier tomatoes, but understanding how to specifically target trichome gene expression without affecting the fruit, we'll also be able to add other important chemicals for insect resistance and possibly other beneficial traits to the surface of the plants," Schilmiller said.

The research was funded by the National Science Foundation.

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New gene could lead to better bug-resistant plants

Public release date: 18-Sep-2012 [ | E-mail | Share ]

Contact: Kathryn Ruehle kruehle@liebertpub.com Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, September 18, 2012A child who suffers a moderate or severe traumatic brain injury (TBI) may still have substantial functional disabilities and reduced quality of life 2 years after the injury. After those first 2 years, further improvement may be minimal. Better interventions are needed to prevent long-lasting consequences of TBI in children conclude the authors of a study published in Journal of Neurotrauma, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available free on the Journal of Neurotrauma website at http://www.liebertpub.com/neu.

Frederick Rivara and colleagues from University of Washington, Seattle, and Mary Bridge Children's Hospital, Tacoma, WA, and Children's Hospital of Philadelphia and the University of Pennsylvania, Philadelphia, PA, describe the functional and quality of life outcomes of children who experienced a moderate or severe TBI when they were 0-17 years of age. In the article "Persistence of Disability 24 to 36 Months after Pediatric Traumatic Brain Injury: A Cohort Study" they follow up on a previous report that found improvement in some areas of functioning for up to 24 months. In this expanded study, the authors showed no significant improvement in the children's ability to function, participate in activities, or in their quality of life between 24 and 36 months post-injury, and they suggest that a plateau is reached in the recovery.

"This important communication by Rivara and colleagues reinforces the concept that pediatric traumatic brain injury is associated with significant enduring morbidity, with recovery plateauing over time," says John T. Povlishock, PhD, Editor-in-Chief of Journal of Neurotrauma and Professor, VCU Neuroscience Center, Medical College of Virginia, Richmond. "This finding also reinforces emerging thought that pediatric traumatic brain injury must be viewed in another context, rather than the current perception that the course of such injury parallels that found in the adult population."

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About the Journal Journal of Neurotrauma is an authoritative peer-reviewed journal published in print and online that focuses on the latest advances in the clinical and laboratory investigation of traumatic brain and spinal cord injury. Emphasis is on the basic pathobiology of injury to the nervous system, and the papers and reviews evaluate preclinical and clinical trials targeted at improving the early management and long-term care and recovery of patients with traumatic brain injury. Journal of Neurotrauma is the Official Journal of the National Neurotrauma Society and the International Neurotrauma Society. Complete tables of content and a sample issue may be viewed on the Journal of Neurotrauma website at http://www.liebertpub.com/neu.

About the Publisher Mary Ann Liebert, Inc., publishers is a privately held, fully integrated media company known for establishing authoritative peer-reviewed journals in many promising areas of science and biomedical research, including Therapeutic Hypothermia and Temperature Management, Tissue Engineering, and Brain Connectivity. Its biotechnology trade magazine, Genetic Engineering & Biotechnology News (GEN), was the first in its field and is today the industry's most widely read publication worldwide. A complete list of the firm's 70 journals, books, and newsmagazines is available on the Mary Ann Liebert, Inc., publishers website at http://www.liebertpub.com.

Mary Ann Liebert, Inc. 140 Huguenot St., New Rochelle, NY 10801-5215 Phone: (914) 740-2100 (800) M-LIEBERT Fax: (914) 740-2101 http://www.liebertpub.com

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Disability caused by traumatic brain injury in children may persist and stop improving after 2 years

ScienceDaily (Sep. 17, 2012) Cleveland Clinic researchers have discovered that vitamin E may prevent cancer in patients with an under-recognized genetic disorder.

Several genetic mutations are known to be present in Cowden Syndrome (CS) -- a disease that predisposes individuals to several types of cancers, including breast and thyroid cancers. One type of mutation in the succinate dehydrogenase (SDH) genes may be responsible for cancer development, according to research by Charis Eng, M.D., Ph.D., Hardis Chair and Director of the Genomic Medicine Institute and Director of its Center for Personalized Genetic Healthcare at Lerner Research Institute, published September 17 in Clinical Cancer Research.

Dr. Eng discovered that mutations in SDH genes, responsible for energy production, result in an accumulation of reactive oxygen species (ROS). These changes damage the cells and make them resistant to apoptosis -- our bodies' natural method of weeding out cancerous cells.

However, when vitamin E was applied to the mutant cells, ROS accumulation decreased, as well as the accompanying cellular damage.

"These findings support the notion that vitamin E may be useful as an anti-cancer therapeutic adjunct or preventive agent, especially for CS patients harboring SDH mutations, and its protective properties should be further explored," said Dr. Eng.

CS predisposes individuals to several types of cancers -- an 85 percent lifetime risk of breast cancer, a 35 percent risk for epithelial thyroid cancer, and increased risk of other cancers as well. Approximately one in 200,000 people are affected by CS.

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The above story is reprinted from materials provided by Cleveland Clinic, via EurekAlert!, a service of AAAS.

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Vitamin E may decrease cancer risk in Cowden syndrome patients

Featured Article Academic Journal Main Category: Smoking / Quit Smoking Also Included In: Lung Cancer;Genetics Article Date: 17 Sep 2012 - 12:00 PDT

Current ratings for: Smokers With Lung Cancer Have Tenfold Genetic Damage

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Senior author Richard K. Wilson is director of The Genome Institute at Washington University School of Medicine in St. Louis in the US. He says in a media statement that none of his team was surprised that the genomes of smokers with lung cancer had more mutations than the genomes of never-smokers with the disease:

"But it was surprising to see 10-fold more mutations. It does reinforce the old message - don't smoke," he adds.

Within non-small cell there are also three further classifications: adenocarcinomas (usually found in an outer area of the lung); squamous cell carcinomas (usually found in the center of the lung next to a bronchus or air tube); and large cell carcinomas (these can occur in any part of the lung and tend to grow and spread faster than the other two classes).

In their paper, the researchers describe how they carried out "whole-genome and transcriptome sequencing of tumor and adjacent normal tissue samples" from all 17 patients.

Across all 17 patients they identified just over 3,700 mutations, with an average mutation frequency more than 10-fold higher in the smokers compared to the never-smokers.

However, the researchers can't say whether these will work on these mutations in lung cancer patients, as first author Ramaswamy Govindan, an oncologist who treats patients at Siteman Cancer Center at Barnes-Jewish Hospital and Washington University, explains:

"Whether these drugs will actually work in patients with these DNA alterations still needs to be studied."

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Smokers With Lung Cancer Have Tenfold Genetic Damage

Enlarge David Paul Morris/Bloomberg via Getty Images

Slides containing DNA sit in a bay waiting to be analyzed by a genome sequencing machine.

Slides containing DNA sit in a bay waiting to be analyzed by a genome sequencing machine.

Ever since James Watson and Francis Crick cracked the genetic code, scientists have been fascinated by the possibilities of what we might learn from reading our genes.

But the power of DNA has also long raised fears such as those dramatized in the 1997 sci-fi film Gattaca, which depicted a world where "a minute drop of blood determines where you can work, who you should marry, what you're capable of achieving."

That was science fiction. Just three years later, President Bill Clinton announced that the once-futuristic dream of reading someone's entire genetic code their genome had become a reality. It took hundreds of scientists nearly a decade to painstakingly piece together the first real look at the entire human genetic blueprint. It cost $3 billion just to make that rough draft.

Twelve years later, the cost of deciphering a person's genetic instructions has dropped faster than the price of flat-screen TVs. And the sequencing can be done much quicker.

Over the past decade, the cost of sequencing a human-sized genome has dropped dramatically. Since 2008, those cost reductions have outpaced Moore's Law, a famous forecast predicting the doubling of computing power every two years. Technology that keeps pace with Moore's Law is thought to be in good shape.

Instead of years, it can take just weeks. Instead of an army of scientists, all it takes is a new high-speed sequencing machine and a few lab techs. Instead of billions, it can cost as little as $4,000. And many are predicting the $1,000 genome is coming soon.

"It's incredible to me today to see how far we've advanced," said Robert Blakesley, who directs the National Institutes of Health's Intramural Sequencing Center.

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As Genetic Sequencing Spreads, Excitement, Worries Grow

Alan McStravick for redOrbit.com Your Universe Online

A recent study, conducted by researchers at the Washington University School of Medicine in St. Louis and their partners at the Joslin Diabetes Center in Boston and the Novartis Institutes for Bio Medical Research, has managed to identify a specific genetic mechanism connected to mutations in the WFS1 gene that affects insulin-secreting beta cells.

It is believed that this discovery will be paramount in increasing the understanding of the rare genetic disorder Wolfram Syndrome (WS) and may also be an important development in the treatment of milder forms of diabetes and related disorders. The full study has been published online in the journal Nature Cell Biology.

Wolfram Syndrome is a rare genetic condition that is caused by mutations in a single gene. This minute mutation, however, has far reaching effects on the body leading to conditions such as diabetes, hearing and vision loss and nerve cell damage that can cause motor difficulties and, ultimately, early death.

WS was first observed in 1938 as a combination of familial juvenile-onset diabetes and optic atrophy. It was understood even then that for most of the patients with this progressive disorder, premature death and widespread atrophic changes throughout the brain were the most probable outcomes. This insulin-requiring type of diabetes typically develops at around age 6.

Examination showed that pancreatic islets were atrophic and the insulin-producing beta cells were selectively absent. WS is believed to account for 1 out of every 150 patients suffering from juvenile or adolescent onset insulin-requiring diabetes mellitus.

The mechanism by which WS works is still unknown, although in 1994 researchers discovered a link between the WFS1 gene and genetic markers on the 4p chromosome.

The reported frequency of those who carry the recessive genetic trait in the U.S. population is approximately 1%. While those that carry the recessive trait do not necessarily show the full range of WS symptoms, they are at a higher risk of developing various forms of mental illness.

Full-fledged WS only occurs in the offspring of two parents who both carry the recessive form of the gene WFS1, and multiple incidences within a genetically predisposed family are not uncommon. There doesnt appear to be any increase or decrease in frequency based on the sex of the offspring.

As we currently understand WS, it is the result of either nuclear or mitochondrial genetic dysfunction. In addition to diabetes mellitus, other typical symptoms include diabetes insipidus, impaired vision and hearing loss. Additional WS complications can include urinary tract and seizure disorders.

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Researchers Link Genetic Mutation To Rare Form Of Diabetes

GlaxoSmithKline (GSK) recently announced it has hiked its stake in Response Genetics Inc. (RGDX), a company focused on the development and sale of molecular diagnostic testing services for cancer, to 15.2%. Glaxo made an investment of $5.5 million and purchased 5 million newly issued shares of Response Genetics at $1.10 per share.

Response Genetics and Glaxo have a long standing relationship focused on Glaxos immunotherapy and oncology candidates, wherein Response Genetics conducts companion diagnostic tests and other related activities for Glaxos candidates.

We currently have an Underperform recommendation on Glaxo. The stock carries a Zacks #3 Rank (Hold rating) in the short run.

Several products in Glaxos portfolio including Valtrex, Arixtra, Evoclin, Lamictal, Imitrex, Requip, Combivir and Epivir are facing declining sales due to intense generic competition. We expect the company's top line and gross margins to remain under pressure in the coming quarters. The EU pricing pressure will continue to affect sales.

Glaxos second quarter 2012 earnings of 79 cents per American Depository Share (ADS) was well below the Zacks Consensus Estimate of 84 cents. Earnings fell 2.5% year over year. Revenues also decreased 7.3% year over year to $10.2 billion and came in below the Zacks Consensus Estimate of $10.4 billion. The company lowered its revenue guidance and expects revenues to remain flat year over year (at CER). We note that earlier Glaxo was expecting revenues to grow from 2011 levels.

Glaxo is looking towards deals and acquisitions to drive growth. The company is focusing on increasing the rights on its partnered products and promising pipeline candidates, so that it stands to benefit more from their success.

Glaxos acquisition of Cellzome and Human Genome Sciences and increasing investment in Theravance Inc. (THRX) and Amicus Therapeutics (FOLD) indicate its efforts to expand the pipeline.

Apart from this, Glaxo continues to make progress with its cost-cutting initiative, which should help reduce the impact of increasing generic competition over the next few years and help earnings grow.

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Glaxo Increases Stake in RGDX

ScienceDaily (Sep. 16, 2012) The rare disorder Wolfram syndrome is caused by mutations in a single gene, but its effects on the body are far reaching. The disease leads to diabetes, hearing and vision loss, nerve cell damage that causes motor difficulties, and early death.

Now, researchers at Washington University School of Medicine in St. Louis, the Joslin Diabetes Center in Boston and the Novartis Institutes for BioMedical Research report that they have identified a mechanism related to mutations in the WFS1 gene that affects insulin-secreting beta cells. The finding will aid in the understanding of Wolfram syndrome and also may be important in the treatment of milder forms of diabetes and other disorders.

The study is published online in the journal Nature Cell Biology.

Insulin-secreting beta cells in the pancreas (above) cannot make enough cyclic AMP in patients with Wolfram syndrome. As a result, the pancreas produces and secretes less insulin, and the cells eventually die.

"We found something we didn't expect," says researcher Fumihiko Urano, MD, PhD, associate professor of medicine in Washington University's Division of Endocrinology, Metabolism and Lipid Research. "The study showed that the WFS1 gene is crucial to producing a key molecule involved in controlling the metabolic activities of individual cells." That molecule is called cyclic AMP (cyclic adenosine monophosphate).

In insulin-secreting beta cells in the pancreas, for example, cyclic AMP rises in response to high blood sugar, causing those cells to produce and secrete insulin.

"I would compare cyclic AMP to money," Urano says. "You can't just take something you make to the store and use it to buy food. First, you have to convert it into money. Then, you use the money to buy food. In the body, external signals stimulate a cell to make cyclic AMP, and then the cyclic AMP, like money, can 'buy' insulin or whatever else may be needed."

The reason patients with Wolfram syndrome experience so many problems, he says, is because mutations in the WFS1 gene interfere with cyclic AMP production in beta cells in the pancreas.

"In patients with Wolfram syndrome, there is no available WFS1 protein, and that protein is key in cyclic AMP production," he explains. "Then, because levels of cyclic AMP are low in insulin-secreting beta cells, those cells produce and secrete less insulin. And in nerve cells, less cyclic AMP can lead to nerve cell dysfunction and death."

By finding that cyclic AMP production is affected by mutations in the WFS1 gene, researchers now have a potential target for understanding and treating Wolfram syndrome.

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Mechanism that leads to diabetes, blindness, identified

The findings, published in the Proceedings of the National Academy of Sciences, suggest the single gene could be responsible for motivating mothers to protect, feed and raise their young, the scientists said.

Earlier research has established that nerve cells react to oestrogen, the female sex hormone, and contain high levels of oestrogen receptor alpha, a chemical linked to maternal care and sexual behaviour.

In the new study, scientists artificially lowered the levels of the chemical in the medial preoptic area of female mice, to examine how they functioned without it.

They found that the mice spent less time caring for their pups but that their levels of aggression remained unchanged.

Dr Ana Ribiero, who led the study, said: "The main finding of this paper is manipulation of a specific gene in a specific group of neurons (nerve cells) can drastically alter the expression of a complete, biologically crucial behaviour."

The effects were "remarkably specific" to maternal care because even related behaviours, such as aggression, remained unchanged, she added.

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'Maternal gene' identified in mice

Germline therapy - the alteration of genes in eggs or sperm - could be made legal by Parliament next year Critics say it's wrong to tamper with the sanctity of life and consequences for future generations are uncertain

By Fiona Macrae

PUBLISHED: 18:17 EST, 16 September 2012 | UPDATED: 01:46 EST, 17 September 2012

The creation of genetically-modified babies could win Parliaments backing next year.

A law change would allow for children to be designed to be free of horrific diseases that can kill within hours of birth.

The children would effectively have two mothers and one father.

Green light ahead: A change in the law could soon permit the creation of genetically modified babies free from congenital diseases. (File picture)

Supporters say the genetic engineering of eggs and embryos will help couples who have suffered the trauma of multiple miscarriages and the deaths of their newborns because of genetic diseases.

But critics say it is wrong to tamper with the sanctity of life, especially when the consequences for future generations are uncertain.

Germline therapy, or the alteration of genes in eggs or sperm, is banned in most countries.

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Dawn of the GM baby: Technique that gives children three parents may only be a year away

Public release date: 16-Sep-2012 [ | E-mail | Share ]

Contact: Hilary Graham hngraham@mdanderson.org 713-794-4383 University of Texas M. D. Anderson Cancer Center

HOUSTON A new study published online in Nature Medicine, led by scientists at The University of Texas MD Anderson Cancer Center, describes the discovery of a novel drug combination aimed at a subset of melanoma patients who currently have no effective therapeutic options.

Melanoma patients have different responses to therapy, depending on what genes are mutated in their tumors. About half of melanomas have a mutation in the BRAF gene; while a quarter have a mutation in the NRAS gene.

New BRAF inhibitor drugs are effective against BRAF-mutant melanoma, but no comparable therapies are currently available against NRAS-mutant melanoma. For the first time, this study provides new hope for patients with NRAS-mutant melanoma that an effective targeted treatment might be developed in the coming years.

By analyzing a sophisticated, genetically engineered mouse model of NRAS-mutant melanoma with a novel systems biology approach, scientists discovered that combining two different classes of drugs shrinks these tumors.

The researchers, led by Lynda Chin, M.D., chair of the Department of Genomic Medicine and scientific director of the Institute for Applied Cancer Science, at MD Anderson together with colleagues from the Dana-Farber Cancer Institute at Harvard Medical School and from Boston University discovered that the two drugs, which inhibit proteins Mek and Cdk4, complement one another by targeting unique cancer features.

"The lack of a drug like the BRAF inhibitor that works against NRAS means that there is still no effective treatment option for NRAS-mutant patients to fall back on," said Chin. "Developing an effective combination using existing drugs or drugs already in clinical development is a path to address this unmet need for this population of melanoma patients."

A roadmap for effective drug combinations

Researchers must first know what an effective treatment actually looks like before they can identify and develop effective drug combinations. To accomplish this, Chin and her colleagues generated an inducible NRAS (iNRAS) mouse model. In the model, activating mutant NRAS caused melanomas to form, while turning it off caused the melanomas to shrink exactly what an effective drug therapy should do.

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Drug combination against NRAS-mutant melanoma discovered

Public release date: 17-Sep-2012 [ | E-mail | Share ]

Contact: Stephanie Jansky janskys@ccf.org 216-636-5869 Cleveland Clinic

Saturday, September 15, 2012, Cleveland: Cleveland Clinic researchers have discovered that vitamin E may prevent cancer in patients with an under-recognized genetic disorder.

Several genetic mutations are known to be present in Cowden Syndrome (CS) a disease that predisposes individuals to several types of cancers, including breast and thyroid cancers. One type of mutation in the succinate dehydrogenase (SDH) genes may be responsible for cancer development, according to research by Charis Eng, M.D., Ph.D., Hardis Chair and Director of the Genomic Medicine Institute and Director of its Center for Personalized Genetic Healthcare at Lerner Research Institute, published today in Clinical Cancer Research.

Dr. Eng discovered that mutations in SDH genes, responsible for energy production, result in an accumulation of reactive oxygen species (ROS). These changes damage the cells and make them resistant to apoptosis our bodies' natural method of weeding out cancerous cells.

However, when vitamin E was applied to the mutant cells, ROS accumulation decreased, as well as the accompanying cellular damage.

"These findings support the notion that vitamin E may be useful as an anti-cancer therapeutic adjunct or preventive agent, especially for CS patients harboring SDH mutations, and its protective properties should be further explored," said Dr. Eng.

CS predisposes individuals to several types of cancers an 85 percent lifetime risk of breast cancer, a 35 percent risk for epithelial thyroid cancer, and increased risk of other cancers as well. Approximately one in 200,000 people are affected by CS.

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Dr. Eng's research was supported by the Breast Cancer Research Foundation and National Institutes of Health National Cancer Institute (NIH/NCI) grant P01CA124570-04S1.

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Cleveland Clinic study shows vitamin E may decrease cancer risk in Cowden syndrome patients

By Jacqueline Savard. First published in The Conversation.

17 September 2012

Jacqueline Savard explores the growing prevalence of genetic testing and what impact they have on over-diagnosis.

Genetic testing and screening is increasingly becoming a presence in our lives. Daily news reports discuss new associations between genes and common conditions. And these associations are used to calculate risks for individuals who have the genes for the conditions, but don't display any symptoms.

In essence, these people become the "worried well", a group of people not yet ill, but at risk of developing diseases.

Genetic tests and over-diagnosis

Once restricted to the domain of the clinic, genetic testing is now available to most people, either through their doctor or via the internet. There are a variety of tests in the market, some of which can provide risk estimates associated with complex common diseases such as diabetes, obesity, Alzheimer's disease and cancer.

A major concern with such tests is that they're the beginning of a path toward over-diagnosis, where the potential to develop a disease or being at risk for the disease is strong enough to constitute a label of sickness.

Over-diagnosing includes, but is not limited to, widening disease definitions, early detections of abnormalities that may or may not cause symptoms or death and the use of increasingly sensitive technologies that detect "abnormalities," the causes and consequences of which are unknown at this time.

Genetic testing and screening could be seen as the ultimate test (the most fundamental part of one's body and life is used to classify a person as ill or potentially ill), so what are the implications of using this technology to assist in diagnosing and classifying people?

Originally posted here:
How genetic testing is swelling the ranks of the 'worried well'

SAN DIEGO--(BUSINESS WIRE)--

Pathway Genomics Corporation, a San Diego-based clinical laboratory that offers its genetic tests internationally, has partnered with innovative La Jolla-based medical practiceMD Revolution. Founded byDr. Samir DamaniandDr. Sunil Bhoyrul, MD Revolution is the first clinical practice to systematically incorporate genomic and mobile health technologies into chronic disease management and prevention. Dr. Damani,a board-certified cardiologistwho currently serves as the practices primary physician, has fully integrated Pathway Genomics premier nutrigenetic test,Pathway Fit, into his practice, and has experienced exceptionally positive results in patient outcomes.

We have enrolled over 50 patients into one of our programs. Among patients that have completed the program, we found dramatic clinical and statistically significant improvements in at least one of four key health parameters including weight loss, visceral fat reduction, increases in metabolism and allowable daily caloric intake, said Dr. Damani. Other parameters have included improved blood pressure control and marked improvements in cardiorespiratory fitness as measured by sub-maximal VO2 (oxygen consumption) testing.

Through its patent pending processes, MD Revolution is defining how genomic and mobile health technologies can be leveraged for superior clinical outcomes for adults of any age who have a range of health goals, from simply optimizing their health to treating chronic conditions such as diabetes.

One of Dr. Damanis patients, Mitch Thrower, can attest to the benefits of Pathway Fit and the positive impact that MD Revolutions program had on his life. As a seasoned triathlete and former owner and chairman ofTriathletemagazine, Thrower realizes the importance of understanding how ones body responds to food and exercise.

Going through the MD Revolution process, we tested for basic metabolic rate and we tracked my diet everything I ate for a couple of weeks. I was going to bed at least 1,500 calories deficient every night and was eating the wrong foods, said Thrower. Thats where Pathway Fit was helpful, in terms of determining what kinds of foods are best over what timeframe. After he started MD Revolutions program, Thrower was able to successfullymanage his weight, and he improved his overall health and wellness. Ive never felt healthier, he explained.

While Throwers background is somewhat unique, the successful outcome he experienced is one that is very familiar to Dr. Damani. Nutrigenomics provides valuable insight into how we process nutrients, respond to exercise, maladaptive eating behaviors, and our propensity for vitamin deficiencies. It enables a more tailored approach to diet and exercise, said Dr. Damani. Patients no longer have to be pushed from one fad diet to another. While the field of genomics and its implications on disease and health is evolving, we cannot ignore the tools available today that enable better prevention and treatment of chronic disease.

About Pathway Genomics

Pathway Genomics owns and operates an on-sitegenetic testinglaboratory that is accredited by the College of American Pathologists (CAP), accredited in accordance with the U.S. Health and Human Services Clinical Laboratory Improvement Amendments (CLIA) of 1988, and licensed by the state of California. Using only a saliva sample, the company incorporates customized and scientifically validated technologies to generate personalized reports, which address a variety of medical issues, including an individuals carrier status for recessive genetic conditions, food metabolism and exercise response, prescription drug response, and propensity to develop certain diseases such as heart disease, type 2 diabetes and cancer. For more information about Pathway Genomics, visitwww.pathway.com.

About MD Revolution

Originally posted here:
Genetic Testing and Mobile Health Technology Combine to Provide Significant Improvements in Patient Results

Published on 24 August 2012 Hits: 682 Written by AFP

PARIS: Scientists on Wednesday said that they had developed a strain of rice that grows well in soils lacking the nutrient phosphorus, a feat that could boost crop yields for some farmers by as much as a fifth.

The announcement ends a quest to pinpoint a mystery gene that helps the roots of baby rice plants tease phosphorus from the soil, enabling them to notch up strong, early growth.

The gene has now been transferred to modern varieties of rice using classic methods of cross-breeding, not genetic engineering, said Sigrid Heuer at the International Rice Research Institute (IRRI) in Los Baos town, Laguna province.

Next week, national rice breeders from Bangladesh, India, and Thailand will be briefed on the exciting find, which should benefit small farmers most of all, Heuer said in a phone interview from Manila.

I would expect to see [an improvement in yield of about] 20 percent, but it depends so much on the type of the soil and how severe the stress is, Heuer said.

But realistically, we are talking conservatively of an average of 10 to 20 percent, and locally a little more if the [phosphorus] stress is severe, she added.

The breakthrough seeks to address one of the biggest problems facing rice growers from the southeastern United States to South America, Southeast Asia and China.

Many soil types bond tightly to phosphorus, surrendering only a tiny amount of the precious mineral to plant roots.

To get around this, farmers look to phosphorus fertilizers, which are spread on the field.

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Gene breakthrough could boost rice yields

Love it or hate it, the one thing you can say for sure about California's ballot initiative process is that it's the absolute worst way to craft policy dealing with complex scientific issues.

That doesn't stop advocates on one side or another from constantly trying, with the result that the public's understanding of the underlying facts plummets faster than you can say, well, "Proposition 37."

Proposition 37 is on November's ballot. The measure would require some, but not all, food sold in California and produced via genetic engineering to be labeled as such. (There are exemptions for milk, restaurant food and other products.)

Genetic engineering, or genetic modification, which involves manipulating DNA or transferring it from one species to another, is increasingly common in agriculture and food processing, and wouldn't be banned or even regulated by the measure. Genetic engineering has pluses and minuses. It can increase crop yields and pest resistance. But it can also affect the environment in negative ways pollen or seeds from genetically engineered crops can be spread by wind, birds or insects to territory where they're unwanted, for example.

Once you've said that, you've said pretty much everything that's known to be relevant to Proposition 37. The rest is baloney, of the non-genetically engineered variety.

So what does this mean for you? It means that between now and election day your airwaves are likely to be filled with steaming piles of fatuous nonsense about genetically engineered foods (which will be depicted as horrifically perilous or absolutely safe), about trial lawyers, about struggling mom-and-pop grocery stores, about the evils of multinational agribusinesses and federal regulators. You'll be presented with learned scientific and economic studies on both sides, and they'll almost certainly be misleading, incomplete or irrelevant, though they'll sound pretty danged convincing.

This will all come to you courtesy of war chests that are already in the neighborhood of $30 million, total.

Great initiative system we have here in the Golden State. As a procedure for producing rational law, it could only be designed by a mad scientist working with rogue DNA.

Let's start with the Yes on 37 campaign. It describes its bottom line as your right to know what's in your food; so what's wrong with mandating explicit labeling? That's fair as far as it goes, but it doesn't go very far. The danger in enacting rules like this is that while they sound perfectly reasonable, they distract from the need for thoughtful and effective regulation and for action at the Legislature, not the ballot box.

"All consumers should have a right to know how their food is produced," observes Gregory Jaffe, head of the biotechnology project at the Center for Science in the Public Interest, which is no crony of the food industry. "But that includes not merely genetic engineering, but irradiated foods and those produced from cloning."

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Prop. 37: Another example of the perils of the initiative process

A mutated gene that increases the chances of obesity could also lower the risk of diabetes, despite the proven link between the two conditions, a study has shown.

Researchers at the Oxford BioBank in the UK measured insulin resistance, which is associated with obesity. They found that the subjects who had a mutation in the phosphate and tensin homologue (PTEN) gene had a low level of insulin resistance but were more likely to be obese.

A high level of insulin resistance is associated with pre-diabetes, which almost inevitably leads to diabetes.

The link between diabetes and obesity has long been accepted, and this is the first study to show that there isnt a connection in all cases. In an article accompanying the studys publication in the New England Journal of Medicine, Ulf Smith, MD, of the University of Gothenburg in Sweden, said the research had both expected and unexpected results.

The findings may have implications for treatment of type 2 diabetes, since physicians may be unaware that trying to reduce the action of the PTEN gene could make the illness worse.

Free Diabetic Recipe Book Get your free meal guide and recipe booklet today, packed with more than 60 recipes to help you or your loved ones better manage diabetes symptoms. Click here to get yours!

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An "Obesity Gene" May Decrease Diabetes Risk

WASHINGTON, Sept. 13, 2012 (GLOBE NEWSWIRE) -- Genomind, LLC, a neuropsychiatric personalized medicine company, recently announced the addition of a new member to its leading Scientific Advisory Board.

Rudolph E. Tanzi, Ph.D., is the director of the Genetics and Aging Research Unit at the MassGeneral Institute for Neurodegenerative Disease in Boston. He is also a professor of neurology and holder of the Joseph P. and Rose F. Kennedy Endowed Chair in Neurology and Mental Retardation at Harvard University.

Dr. Tanzi is an internationally respected researcher focusing on the molecular and genetic factors of neurological diseases, with significant interest in Alzheimer's disease. For the last 30 years, he has been dedicated to gene research on neurodegenerative disease and co-discovered the three genes that cause early-onset familial Alzheimer's.

Dr. Tanzi is also responsible for co-discovering genes that trigger Huntington's disease, Wilson's disease, Autism, and other neurological disorders. He is the head of the Alzheimer's Genome Project, a research project of the Cure Alzheimer's Fund, which identified four new related genes - a finding that was named one of the Top Ten Medical Breakthroughs of 2008 by Time magazine. He is the co-author of the book Decoding Darkness: The Search for the Genetic Causes of Alzheimer's Disease, and has co-authored more than 340 articles, making him one of the top ten most cited researchers on Alzheimer's. Dr. Tanzi has been honored with a significant number of awards for his work, which include the Metropolitan Life Foundation Award and The Potamkin Prize.

Dr. Tanzi received his BS from the University of Rochester with a double major in microbiology and history and his Ph.D. in neurobiology from Harvard University.

"It is an honor to welcome Dr. Tanzi to our Scientific Advisory Board," said Genomind Co-founder and Chief Scientific Officer Dr. Jay Lombard. "He is recognized by his peers as the preeminent expert internationally on the genetic basis of Alzheimer's disease pathogenesis. He has dedicated his career to investigating the molecular and genetic causes of Alzheimer's disease, and his discovery of all three genes causing early-onset familial AD is groundbreaking for patients. His discoveries give us hope that there will be more sophisticated ways to develop preventive strategies when diagnosing and treating Alzheimer's disease."

"I am looking forward to working with the Genomind Scientific Advisory Board and the impressive team already in place," said Dr. Tanzi. "Genomind's philosophy of improving patient lives through neurological research aligns perfectly with my research and beliefs, and I hope my past and future findings will help them bring the findings of recent scientific research into real-world use."

Dr. Tanzi joins a distinguished group of thought leaders on the Scientific Advisory Board, all known for their work at the forefront of psychiatric and neurologic research. Board members include Scott T. Aaronson, MD; P. Murali Doraiswamy, MD; Maurizio Fava, MD; Allan I. Levey, MD, PhD; Anil Malhotra, MD; Roy H. Perlis, MD, MSc; and Stephen M. Stahl, MD, PhD.

About Genomind

Genomind is a personalized medicine company comprised of innovative researchers and expert leaders in psychiatry and neurology. Genomind is committed to discovery of the underlying causes of neuropsychiatric disorders and supports the development of personalized medicine that improves patients' lives. Genomind was founded by Ronald I. Dozoretz, MD, a psychiatrist who has devoted his career to improving mental health. Jay Lombard, DO, a neurologist and co-founder of Genomind, is a critically acclaimed author and nationally recognized thought leader in neuropsychiatry practice and research. Learn more at http://www.genomind.com.

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Rudolph E. Tanzi, Ph.D. Joins Genomind's Scientific Advisory Board

The war on cancer is poised to enter a new phase that promises more precise treatments, fewer side effects and, most of all, more survivors.

And none too soon. Although death rates from many cancers have slowly but steadily declined over the decades, experts agree that current treatments are mostly too blunt, too scattershot and too dangerous for the patients they are intended to save.

Today, treating cancer often means an all-out chemical assault on tumors. Doctors bombard patients' bodies with drugs that aim to destroy cancer cells. But like shelling an entire city to wipe out a few rebels, the strategy leaves civilian casualties in its wake: Standard cancer treatments destroy healthy cells alongside diseased ones, taking a toll on a patient's body and strength.

Now, however, the battle tactics are shifting. Researchers have learned how to gather intelligence on a cancer's traits, turn off the tumor's defenses and precisely target only the cells that are causing disease.

"We have the confluence of all these advances coming together at once," says Dr. Ronald DePinho, president of the University of Texas MD Anderson Cancer Center in Houston. "I'm not saying we can cure cancer within 10 years. But we've been handed a complete toolbox. Within this decade, there's no question that we're going to accelerate the decline in mortality due to cancer."

DePinho says the recent revolution in genetics has reignited the world of cancer research. Scientists can sequence all the genes in a cancer cell faster than ever before, compare the cancer genes with those in the rest of the body and even turn genes on and off.

Using these technologies, researchers have discovered that similar-looking cancers can have very different genetic makeups. Understanding the world of mutations can help doctors predict how quickly cancer will grow and which drugs will kill it.

"Oncology as a discipline has always divided itself around body sites," says geneticist Elaine Mardis of Washington University School of Medicine in St. Louis. "There are people who focus on lung cancer and people who focus on breast cancer and people who focus on pancreatic cancer." But the field has realized that cancers are defined as much by their genetic mutations as by location, she says.

When new cancer drugs are in clinical trials, it's already standard practice to see whether the patients who respond have any telltale genetic markers. And in some, cases, such genetic signatures have been found.

Last year, the Food and Drug Administration approved vemurafenib, a melanoma drug that works only in patients with a particular mutation in a gene called BRAF. The drug has no effect in patients without the mutation, so a genetic test is required before a doctor can prescribe it.

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Genetics to determine cancer treatments