Archive for the ‘Gene Therapy Research’ Category

Doctors at the Royal Brompton Hospital in London will treat 200 patients next month as part of the first ever gene therapy trial for heart failure, which is taking place in 50 centres around the world.

A separate trial, which will test the same therapy in 24 patients who have been fitted with mechanical heart pumps, is expected to begin later this year.

Prof Sian Harding of Imperial College London, who developed the treatment, said: "It's been a painstaking, 20-year process to find the right gene and make a treatment that works, but we're thrilled to be working with cardiologists to set up human trials that could help people living with heart failure."

Prof Peter Weissberg, Medical Director of the British Heart Foundation, which is co-funding the research, said: "While drugs can offer some relief, there is currently no way of restoring function to the heart for those suffering with heart failure. Gene therapy is one of the new frontiers in heart science."

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Gene therapy for heart failure

By Ben Hirschler

LONDON (Reuters) - British scientists are stepping up clinical tests of gene therapy in a bid to help people with advanced heart failure pump blood more efficiently.

Researchers said on Tuesday they planned to enroll patients into two new clinical trials using Mydicar, a gene therapy treatment made by privately held U.S. biotech company Celladon.

After more than 20 years of research, the ground-breaking method for fixing faulty genes is starting to deliver, with European authorities approving the first gene therapy for an rare metabolic disease last November.

In the case of heart failure, the aim is to insert a gene called SERCA2a directly into heart cells using a modified virus, delivered via a catheter infusion. Lack of SERCA2a leads to ever weaker pumping in people with heart failure.

Although drugs offer some relief, there is currently no way of restoring heart function and the prognosis for those with advanced disease is worse than for many cancers.

One of the studies, led by scientists at Imperial College London, is part of a wider mid-stage Phase II project sponsored by Celladon that involves 200 patients worldwide, some of whom have already been treated in the United States and Denmark.

The second trial, which is due to start in the summer, will test the same treatment in 24 British patients already fitted with mechanical heart pumps to see how the approach may help in this particular setting.

It promises to be a long haul, with extensive Phase III studies still needed once results of the current mid-stage tests are received, which Celladon expects in the first half of 2015.

Gene therapy has experienced a series of advances and setbacks over the decades. The most notable blow came in 1999 when an Arizona teenager died in a gene therapy experiment. More recent results, however, have been promising in fields ranging from immune system diseases to blindness.

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New gene therapy trials aim to mend broken hearts

GAITHERSBURG, Md.--(BUSINESS WIRE)--

MaxCyte, Inc., the pioneer in scalable, high performance cell transfection systems, is hosting a series of events at Cambridge Health Institutes PEGS Summit, the premier conference in the protein and antibody biotherapeutic arena, being held April 29 May 3 in Boston, MA. During the conference, MaxCyte will present break-through transient gene expression (TGE) data in a scientific podium presentation and detail unmatched antibody production capabilities in two technical posters. MaxCyte scientists will be available throughout the conference at Booth #216 to provide further technical details about the use of flow electroporation for large scale transient gene expression and rapid stable cell line generation.

Dr. James Brady, Director of Technical Applications at MaxCyte, will present data on flow electroporation in a podium presentation entitled Streamlining Antibody Development Using Large Scale, CHO Transient Gene Expression (TGE) followed by Rapid Production of CHO Stable Clones on Wednesday, May 1, at 3:05 PM within a session dedicated to discussing protein expression in CHO cells, the standard manufacturing cell line for bioproduction.

Dr. Bradys presentation demonstrates the unmatched performance of the MaxCyte Scalable Transfection Systems, says Dr. Karen Donato, Executive Vice President of Global Business Development & Marketing at MaxCyte. No other transient transfection system has the capabilities of MaxCyte electroporation, namely CHO-based expression with antibody titers of over 1 gram/liter, combined with the rapid creation of high yield stable cell lines.

MaxCyte will also present two scientific posters, both available for viewing on Thursday, May 2nd, from 3:10 PM - 4:00 PM and Friday, May 3rd, from 10:05 AM - 10:50 AM. The first poster, entitled CHO Transient Gene Expression (TGE) Optimization for Multi-Gram Level Antibody Production: Effects of Expression Construct, Post Transfection Cell Density and Feed Conditions highlights the transfection and post transfection flexibility of flow electroporation which allows for the full optimization of antibody expression producing antibody titers that can exceed 1 gram/liter within 14 days of transfection. This poster is presented in collaboration with Vivalis, a key client and leading provider of innovative cell-based solutions to the pharmaceutical industry for the manufacture of vaccines and recombinant proteins.

The second poster, entitled Bioproduction Using Large Scale Transient Transfection: From >1.2 grams/L Antibody Titers via Transient Gene Expression (TGE) to Rapid, High Yield Stable Cell Line Generation, summarizes data demonstrating the utility of the MaxCyte platform at multiple steps in antibody development including high yield antibody production via transient gene expression and rapid generation of stable cell lines in 6-8 weeks for late stage development and biomanufacturing.

Our clients have already realized the benefits of streamlining progression from early to late stage development by using our one-of-a-kind technology that brings together transient gene expression and rapid stable cell generation, says Douglas Doerfler, President, and CEO of MaxCyte. MaxCyte flow electroporation is a truly enabling technology and we look forward to presenting our latest scientific findings to leaders in the development of biotherapeutics at the PEGS Summit.

About MaxCyte

MaxCyte specializes in cell modification technologies to enable the discovery, development, manufacturing, and delivery of innovative therapeutic products. Drawing on its cell therapy expertise, MaxCyte designed a portfolio of products including the MaxCyte STX Scalable Transfection System and MaxCyte VLX Large Scale Transfection System, ideal tools for use in drug discovery research and screening and protein production environments. These products provide for the rapid development and consistent production of billions of (co)transfected primary cells, stem cells, and cell lines for protein and antibody production and for cell-based assays with comparable results and Seamless Scalability from the bench to HTS and pilot and production scale.

For more information, http://www.maxcyte.com.

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MaxCyte Presents Unprecedented CHO-Based Transient Gene Expression Data for Gram Scale Antibody Production and Rapid ...

THURSDAY, April 25 (HealthDay News) -- Insight into genes that play a key role in disrupting immune system pathways in the brains of people with Alzheimer's disease could offer a potential target for new drugs against the disease, two new studies show.

"Defining the precise steps of the inflammatory response crucial to causing Alzheimer's disease has been elusive. We are pleased to discover these novel insights into that process," Bin Zhang, lead author of one of the studies and an associate professor of genetics and genomic sciences at the Icahn School of Medicine at Mount Sinai in New York City, said in a school news release.

In the study, Zhang's team analyzed brain tissue samples from deceased Alzheimer's patients, as well as healthy people who had died. By measuring the activity level of thousands of genes in these tissue samples, the team identified which gene networks are disrupted in diseased brains.

Specifically, their analysis pinpointed the important role of a gene expressed in immune cells called microglia, which clean up debris and destroy pathogens in the brain.

This gene, called TYROBP, is overactive in the brains of Alzheimer's patients and plays a major role in disrupting the activity of many other genes that control microglia activation, according to the study, which was published April 25 in the journal Cell.

"As a next step, we will evaluate drugs that impact [this] pathway as potential therapies for the disease," Zhang said. "This discovery enables us to design more specific compounds that target these key steps precisely, in contrast to existing anti-inflammatory drugs that may be less ideal for hitting this target."

Another study, published online April 25 in the journal Neuron, may have uncovered another genetic clue to Alzheimer's disease.

Researchers looked at brain samples from deceased Alzheimer's patients and found that higher activity of a gene called CD33 in microglia was linked to higher levels of the beta-amyloid protein plaques that have long been associated with Alzheimer's disease.

In their experiments with mice, switching off CD33 activity seemed to help microglia sweep away the plaques.

"Our findings suggest that pharmaceutical inactivation of CD33 represents a potentially powerful new therapy for the treatment and prevention of Alzheimer's disease, and perhaps other neurodegenerative disorders," senior study author Rudolph Tanzi, of Massachusetts General Hospital and Harvard Medical School in Boston, said in a journal news release.

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Gene Studies Could Point to New Alzheimer's Treatments

IRVINE, Calif., April 25, 2013 (GLOBE NEWSWIRE) -- MRI Interventions, Inc. (MRIC) today announced that its ClearPoint(R) Neuro Intervention System is advancing the minimally-invasive precision delivery of the investigational gene therapy drug Toca 511 into malignant brain tumors. The procedure is being performed under real-time visualization and direct magnetic resonance imaging (MRI) guidance at select clinical trial sites. Highlights of the ClearPoint System's application in the Toca 511 trial include:

Improved flow rates during drug delivery. The recently-introduced SmartFlow(R) large-bore cannula increases the drug delivery rate threefold over documented flow rates of the original SmartFlow cannula. Like the original SmartFlow cannula, the new cannula incorporates a stepped tip design to prevent reflux and leakage of the drug outside of the target area, but the new cannula's large bore allows for a clinically meaningful increased rate of delivery.

Precise delivery of the therapeutic agent into the brain tumor. Direct visualization of the procedure in real-time allows surgeons to monitor and confirm delivery to the tumor of Toca 511 mixed with MRI contrast agent at the time of infusion.

Multiple trajectories in a single case. The ClearPoint System includes a SmartFrame(R) targeting device that works with software to allow convenient repositioning of the cannula for multiple trajectories in a single case, and an adjustable head stabilization device that accommodates a wide range of possible entry points.

Tocagen Inc., the clinical trial sponsor, is developing the investigational drug Toca 511 (vocimagene amiretrorepvec) in combination with Toca FC (an investigational extended-release formulation of 5-FC) for the treatment of recurrent high grade glioma, including glioblastoma multiforme (GBM, Grade IV glioma), the most common and aggressive form of brain cancer. Toca 511 is a retroviral replicating vector (RRV) encoding the genetic instructions for the enzyme cytosine deaminase (CD). Toca 511 is designed to selectively infect dividing cancer cells and spread through the tumor after administration. Each patient then begins a course of Toca FC. Within infected cells the CD enzyme converts 5-FC to the anti-cancer drug 5-FU. By producing 5-FU locally, this technology has the potential to produce much higher concentrations of 5-FU in the tumor than can be safely attained with systemic administration.

"So far we successfully delivered Toca 511 precisely to the brain cancer in three patients, all of whom went home the next day," said Manish Aghi, MD, a neurosurgeon and principal investigator for the Toca 511 trial at University of California, San Francisco. "This new ability to deliver large volumes of Toca 511 rapidly into the tumor at flow rates up to 1.8 ml/h (30 microliters a minute) under real-time visualization represents a major technological advance that will enable the neurosurgeon to accurately deliver large quantities of a therapeutic agent, while providing the patient the benefit and safety of a minimally-invasive procedure."

"Our collaboration with Tocagen underscores the advantages of real-time MRI-guided delivery of therapeutic agents to the brain, and we are pleased to be a key contributor to the rapid progress being achieved," said Kimble Jenkins, CEO of MRI Interventions.

Each year approximately 10,000 new cases of GBM are diagnosed in the US. In a recent population-based study, median survival in all diagnosed patients was 10 months.

Tocagen is presently enrolling patients in its investigational Phase I clinical trials. Currently, University of California, San Francisco, University of California, San Diego, Cleveland Clinic Foundation, and Henry Ford Hospital in Detroit are enrolling patients, and additional sites are in the process of joining this study. For more information about participating in this study, please submit an inquiry form to Tocagen.

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MRI Interventions' ClearPoint(R) System Helps Advance Brain Cancer Clinical Trial of Investigational Gene Therapy Drug ...

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New research published Thursday in the journal Neuron sheds new light on the molecular causes of Alzheimers disease, while also revealing a potential new therapy which could help prevent cognitive decline and brain damage during the early stages of the neurodegenerative disorder.

The study focuses on a variant of a gene known as CD33, which typically contributes to Alzheimers disease by inhibiting the ability of a bodys immune cells to remove toxic molecules from the brain. Those toxins, which are known as beta-amyloid plaques, form between neurons in the brain. Past studies have linked those plaques to neuron death and cognitive deficits such as impaired memory, the researchers explained.

Too much CD33 activity appears to promote late-onset Alzheimers by preventing support cells from clearing out toxic plaques, key risk factors for the disease, explained senior author Dr. Rudolph Tanzi of Massachusetts General Hospital and Harvard University. Future medications that impede CD33 activity in the brain might help prevent or treat the disorder.

Before our study, nothing was known about the function of CD33 in the brain. Moreover, our findings suggest that pharmaceutical inactivation of CD33 represents a potentially powerful new therapy for the treatment and prevention of Alzheimers disease, and perhaps other neurodegenerative disorders, he added. Our findings raise the exciting possibility that the inability of microglia to degrade beta-amyloid in Alzheimers disease could be reversed therapeutically by inhibition of CD33 activity.

Tanzi and his colleagues first became interested in CD33 variations during 2008 research into genes that contribute to late-onset Alzheimers disease. They knew the gene made a protein which regulated the immune system, but its function within the brain was unclear. In order to learn more about how it could contribute to the neurodegenerative condition, they looked at human genetics, biochemistry and human brain tissue, laboratory mice and cell-based experiments, the researchers explained.

They discovered the CD33 gene regulates the clearing of a toxic protein known as amyloid beta (A-beta) in the brains of Alzheimers patients. As part of the Neuron study, Tanzi and his co-authors describe a protective variant of CD33 which promotes clearance of the protein. They also illustrate how reducing the genes expression in immune cells known as microglia boosts their ability to clear-away A-beta, raising the hope the brains immune system could be aided with A-beta removal if CD33 activity is blocked.

In the current study, the researchers first found that CD33 activity was significantly higher in microglia cells in brain samples from Alzheimers patients than in cells from non-demented controls, Massachusetts General Hospital explained in a statement. Moreover, they showed that the presence of a version of the gene that protected against Alzheimers disease reduced CD33 protein levels in the brain. Importantly, the same protective version of CD33 was found to reduce levels of A-beta 42 the primary constituent of the amyloid plaques that characterize the disease.

Increased numbers of CD33-containing microglia were also linked to higher a-beta levels and total beta-amyloid plaque levels. Their research was conducted using an Alzheimers mouse model, and according to Tanzi, their findings indicate inhibiting CD33 activity in a human patients brain could ultimately become a powerful new approach to treating and possibly preventing Alzheimers disease.

In related research, published online Thursday in the journal Cell, an international team of researchers report they located a network of genes involved in the inflammatory response in the brain which is a critical component in late-onset Alzheimers disease (LOAD).

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Studies Detail Genetic Mechanisms That Could Improve Alzheimer's Treatment

Apr. 25, 2013 An international research consortium led by the Universitat Autnoma de Barcelona (UAB), the CIBERER and the University of Wurzburg (Germany) has discovered a gene that can cause three totally different diseases, depending on how it is altered.

The researchers, using next-generation massive ultrasequencing techniques, have sequenced the over 20,000 genes of a Fanconi anemia patient's genome. By adopting this strategy they have succeeded in identifying pathogenic mutations responsible for this disease in the ERCC4 gene, which had already been linked to two other rare diseases: xeroderma pigmentosum and a type of progeria. The latter are characterised by heightened sensitivity to sunlight, susceptibility to skin cancer and, in the case of progeria, premature aging. Fanconi anemia, on the other hand, is characterised by progressive anemia, congenital malformations and a high risk of developing leukemia and mouth tumours. The ERCC4 gene can therefore be responsible for three different diseases.

The researchers have shown that this gene is involved in two DNA repair mechanisms by which cells maintain the stability of the genome, in such a way that the balance between these two repair systems will determine which of the three diseases the patient will contract. "This is a rather exceptional case, since there are few precedents of a single gene being involved in two independent physiological mechanisms and causing three clinically different diseases," points out UAB professor Dr Jordi Surralls.

These findings, published today in the American Journal of Human Genetics, as well as improving the diagnosis and genetic characterisation of rare diseases, will allow new therapeutic strategies to be applied, like gene therapy or the selection of healthy, compatible embryos to cure siblings through umbilical cord transplants. The findings add to our knowledge of the two DNA repair mechanisms, which are so important for maintaining the stability of our genes and preventing cancer in the general population. In fact, the researchers point to the importance of going on to study this gene's possible role in breast cancer and ovarian cancer.

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Discovery of a gene that controls three different diseases

Apr. 25, 2013 RNA molecules, made from DNA, are best known for their role in protein production. MicroRNAs (miRNAs), however, are short (~22) nucleotide RNA sequences found in plants and animals that do not encode proteins but act in gene regulation and, in the process, impact almost all biological processes -- from development to physiology to stress response.

Present in almost in every cell, microRNAs are known to target tens to hundreds of genes each and to be able to repress, or "silence," their expression. What is less well understood is how exactly miRNAs repress target gene expression.

Now a team of scientists led by geneticists at the University of California, Riverside has conducted a study on plants (Arabidopsis) that shows that the site of action of the repression of target gene expression occurs on the endoplasmic reticulum (ER), a cellular organelle that is an interconnected network of membranes -- essentially, flattened sacs and branching tubules -- that extends like a flat balloon throughout the cytoplasm in plant and animal cells.

"Our study is the first to demonstrate that the ER is where miRNA-mediated translation repression occurs," said lead researcher Xuemei Chen, a professor of plant cell and molecular biology and a Howard Hughes Medical Institute-Gordon and Betty Moore Foundation Investigator. "To understand how microRNAs repress target gene expression, we first need to know where microRNAs act in the cell. Until now no one knew that membranes are essential for microRNA activity. Our work shows that an integral membrane protein, AMP1, is required for the miRNA-mediated target gene repression to be successful. As AMP1 has counterparts in animals, our findings in plants could have broader implications."

Study results appear today in the journal Cell.

Simply put, DNA makes RNA, and then RNA makes proteins. Specifically, RNA encodes genetic information that can be "translated" into the amino acid sequence of proteins. But noncoding RNAs -- RNAs that do not encode proteins -- are increasingly found to act in numerous biological processes. MicroRNAs are a class of noncoding RNAs whose main function is to downregulate gene expression.

Research on miRNAs has increased tremendously since they were first identified about 20 years ago. In the case of diseases, if some genes are up- or down-regulated, miRNAs can be used to change the expression of these genes to fight the diseases, thus showing therapeutic potential.

MicroRNAs are known to regulate target genes by two major modes of action: they either destabilize the target RNAs, leading to their degradation, or they do not impact the stability of the target RNAs, but simply prevent them from being translated into proteins -- a process known as translation inhibition. The end result of translation inhibition is that the genes do not get expressed. Just how miRNAs cause translational inhibition of their target genes is not well understood.

"We were surprised that the ER is required for the translational inhibition activity of miRNAs," Chen said. "This new knowledge will expedite our understanding of the mechanism of gene silencing. Basically, now we know where to look: the ER. We also suspect it is the rough ER portions that are involved."

Chen explained that the ER has two types: rough and smooth. Rough ER, which synthesizes and packages proteins, looks bumpy; smooth ER, which acts in lipid synthesis and protein secretion, resembles tubes. The ER protein AMP1, she said, is anchored in the rough ER.

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Key cellular organelle involved in gene silencing identified

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Mapping out how an Alzheimers gene works could lead to new treatments.

So far, nearly two dozen genes scattered across four chromosomes have been linked to an increased risk of Alzheimers disease. But identifying such genetic risk factors doesnt mean that researchers fully understand how they contribute to cognitive decline and dementia. And that understanding is often crucial to turning genetic information into effective treatments.

Now a group of scientists report in the journal Neuron that they have pieced together the back story of one gene, known as CD33, that could lead to exciting new ways of removing the amyloid plaques that build up in the brains of Alzheimers patients and cause so many problems with memory and cognitive functions.

(MORE: New Research on Understanding Alzheimers)

Dr. Rudolph Tanzi, director of the genetics and aging research unit at Massachusetts General Hospital and professor of neurology at Harvard Medical School, and his team first identified CD33 in 2008, and at the time, he says, We had no idea what this thing did. And in the [scientific research] literature, little was known about it. So we started from scratch.

Beginning with studies of the where the gene was expressed, he found that a subset of brain cells known as microglia seemed to show high levels of CD33, which makes receptors that pop up on the surface of the cells to bind to neuronal debris, including the residue of inflammatory reactions, and dead and dying nerve cells. CD33 functions as a molecular housekeeper, patrolling the nervous system for any material that doesnt belong and could impair normal brain function. That includes the deposits of amyloid protein that build up in the brains of Alzheimers patients, eventually forming sticky plaques that compromise normal nerve function before destroying them.

(MORE: First Genes Linked to Higher Risk of Alzheimers Disease Among African-Americans)

But when Tanzis team looked at the brains of patients who had died of Alzheimers, they found that CD33 also had a darker side. In patients with a higher burden of amyloid plaques, CD33 also appeared in excess. And so did tons of dead neurons. At some point, as the amyloid is making the cells sick, and forming tangles as lots of neurons are dying, the microglia put on their battle gear and turn radical, killing whatever they think is attacking the brain, says Tanzi. The result is friendly fire, and they start to kill so many neurons that the microglia are now detrimental; they are no longer clearing but theyre rounding up nerve cells and shooting out free radicals and causing a lot of damage.

Instead of engulfing and removing the amyloid, microglia armed with CD33 were targeting healthy nerves instead. To confirm that, Tanzis team conducted a series of tests with cells in culture and in animals, and found that when microglia were stripped of CD33, they went back to performing their housekeeping duties as expected, sniffing out amyloid and pulling the protein out of circulation. Mice genetically engineered to develop Alzheimers plaques but without CD33 showed lower levels of amyloid plaques in their brains than animals with the gene, suggesting that the CD33 was clearing the protein away.

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How an Alzheimer's Gene Could Lead to New Treatments

The Mesothelioma Applied Research Foundation announced today that the educational video covering the BAP1 gene, which is the first gene discovered in mesothelioma, is now available on the organizations website.

Alexandria, VA (PRWEB) April 26, 2013

BAP1 is the first gene discovered in mesothelioma and researchers have just begun embarking on trials to better understand its incidence.

In germ line mutations (inherited mutations), this gene is thought to be extremely rare but has been found to have associations with uveal melanoma (melanoma of the eye), renal cell carcinoma (kidney cancer) and an unpigmented nevi (a skin lesion without color). It is thought that approximately 25% of mesothelioma patients will have somatic mutations (those that occur spontaneously) of this gene.

According to the executive director of the Mesothelioma Applied Research Foundation, Mary Hesdorffer, Nurse Practitioner, this gene has much potential for mesothelioma patients.

Currently, the research goal of the BAP1 gene is for prevention and early detection of mesothelioma, says Ms. Hesdorffer.

According to her, this means that, for example, asbestos exposed individuals who carry the gene can be studied to determine if a cancer signal can be picked up before the development of mesothelioma.

The idea is that down the line, if you have a germ line mutation, you and your immediate family will be screened for cancers associated with this gene in the hope of picking up an early malignancy. If the gene is found to be defective, researchers will be looking for ways to turn it off and avoid the malignancy entirely," added Ms. Hesdorffer.

The Mesothelioma Applied Research Foundation had an entire session devoted to the BAP1 gene at the 2013 Symposium.

Mesothelioma is a malignant tumor of the lining of the lung, abdomen, or heart known to be caused by exposure to asbestos. Medical experts consider it one of the most aggressive and deadly of all cancers. Approximately 3,000 Americans are diagnosed with mesothelioma every year and an estimated one-third were exposed while serving in the Navy or working in Navy shipyards.

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New Mesothelioma Gene Discovered: Educational Video Available

DUBLIN--(BUSINESS WIRE)--

Research and Markets has announced the addition of the "MediPoint: Predictive Breast Cancer Gene Testing - Current and Future Players" report to their offering.

This report focuses on the predictive breast cancer gene testing markets in the US and Europe, and future markets in China, India and Brazil, identifying and competitively assessing current marketed and pipeline products and emerging technologies.

This report identifies the unmet needs in the market, provides an understanding of physician perception of predictive breast cancer gene testing, and future trends. To successfully market new gene tests, companies need to offer gene tests that address the current unmet needs of current predictive breast cancer gene tests and show better efficacy and cost effectiveness to the gene tests currently in the market. This report will identify the opportunities for this technology.

Scope

- Investigation of current and future market competition for predictive breast cancer gene testing.

- Competitor assessment.

- Coverage of key market players and company profiles including business description, financial overview and SWOT analysis.

- Strategic assessment of the device sector through market impact analysis, future market scenario and company analysis.

- Direct quotes from Key Opinion Leaders (KOL) as well as oncologists, geneticists and genetic counselors already using these gene tests.

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Research and Markets: MediPoint: Predictive Breast Cancer Gene Testing - Current and Future Players

The Stream - The baby blueprint
Follow The Stream on Al Jazeera: http://stream.aljazeera.com/story/201304192241-0022689 YOUTUBE: http://www.youtube.com/show/thestream TWITTER: https://twitt...

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The Stream - The baby blueprint - Video

A Beginners Guide to Genetic Engineering
Science Talent Search 2013.

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A Beginners Guide to Genetic Engineering - Video

ALM207 Genetic engineering lecture two
This is a video on the topic Genetic engineering lecture Two. This is part of the topic of technology in Plant and Animal breeding, which is offered in the Agricultural Degree at NMIT. For...

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ALM207 Genetic engineering lecture two - Video

Dr Rasheed Genetic Engineering 23-4

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New Gift - Supriyo Sen - GE FOCUS FOWARD
Subscribe to the GE Channel: http://full.sc/12xcByI In today #39;s context of biological and ecological destruction caused by chemical farming, industrial agricu...

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Genetic Engineering: Somewhat Defined
These are my comrades explaining their own impromptu definition of genetic engineering.

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Genetic Engineering on Genetically Modified Food
"A multimedia project for the 2013 Student Bio Expo by Abbey Landicho and Lucy Lu." This audio slideshow is about the topic Genetic Engineering about Genetic...

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Genetic Engineering on Genetically Modified Food - Video

Genetic engineering The world_s greatest scam_ 1)

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Genetic engineering The world_s greatest scam_ 1) - Video

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Contact: Kathryn Ruehle kruehle@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, April 25, 2013Delving into controversial and unsettling subjects such as the gender basis of violence, the new refereed journal Violence and Gender, launching in fall 2013, will explore the difficult issues that are vital to threat assessment and prevention of the epidemic of violence. Edited by Mary Ellen O'Toole, PhD, Violence and Gender is the first and only peer-reviewed journal focusing on the understanding, prediction, and prevention of acts of violence, and will be published online with Open Access options and in print by Mary Ann Liebert, Inc., publishers.

"We have an urgent imperative," says Mary Ann Liebert, President and CEO of the company that bears her name. "There are differences in the way men and women exhibit violent behavior, and they need to be better understood and addressed to prevent tragic acts of murder and massive, often irreversible, injury. It is a serious public health issue."

Violence and Gender will be the international forum for the critical examination of biological, genetic, behavioral, psychological, racial, ethnic, and cultural factors as they relate to the gender of perpetrators of violence. Papers in the Journal will cover topics such as gender biology; genetics; psychopathy; mental health; planned predatory behavior; testosterone, hormones, and neurochemicals; nature vs. nurture; films, television, and video games; and pyromania.

The Editor-in-Chief of Violence and Gender, Mary Ellen O'Toole, PhD, is recognized as the FBI's leading expert in psychopathy. Her expertise is in criminal investigative analysis, offender behavior, targeted school violence, workplace violence, and threat assessment. How gender impacts these subjects must be better understood to prevent the growing number and nature of violent episodes.

"We are becoming immune to tragic events such as Columbine," Dr. O'Toole says. "The mandate for this journal to help us better understand and hopefully prevent these tragedies is absolute."

Dr. O'Toole has helped develop a better understanding of infamous offenders, including Green River Killer Gary Ridgway and Unabomber Ted Kaczynski, and high-profile crimes, such as the Columbine shootings, Zodiac serial murder case, and 2002 Salt Lake City Olympics bombing.

"I spent my career studying the criminal violent mind," says Dr. O'Toole, "and now gratuitous violence is at an all-time high. This violence is well-planned, lethal, and extremely callous. The offenders are nearly always male. Does gender really make a difference in the commission of violent crime? It's time for a journal to take on this question."

Violence and Gender will be a primary resource for psychologists and mental health providers; sociologists; criminologists; educators; cultural anthropologists; probation, parole, and corrections officers; and law enforcement professionals at federal, state, local, and international agencies that assess threats and deal with violent behaviors.

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Violence and Gender Journal launching fall 2013

Even as the final report of the Supreme Court-appointed Technical Expert Committee (TEC) on open field trials of genetically modified crops is awaited, 51 independent international scientists with expertise in genetic engineering and biosafety protocols have approved the panels Interim Report. The report has called for a 10-year moratorium on open field trials of Bt food crops until adequate regulatory mechanisms and safety standards are put in place.

With Bt brinjal being the first-ever food crop sought to be introduced in India, its dossier went through international appraisal and evoked much interest throughout the world.

The TEC report attracted attention because of intense polarisation over the use of GM agri-biotechnologies in food and the environment and the large number of public and private researchers, investors and companies engaged in developing GM crops and associated Intellectual Property Rights claims, the renowned GM scientists said in a statement.

Since the Interim Report was made public, the Union Agriculture Ministry filed an affidavit in the Supreme Court in favour of GM technology. After hearing the Ministry, the court appointed a sixth member on the panel.

This was opposed by Aruna Rodrigues, lead PIL petitioner, through her lawyer Prashant Bhushan, who said that in the matter of regulation of GM crops, the Ministry of Environment and Forests stood over the Agriculture Ministry.

Underscoring the need for science to operate free of commercial and political goals, the scientists said the review of previous approvals in India for Bt crops left the TEC in no doubt that India was not ready to make reliable safety judgments because of failures in procedure, inadequate attention to development of competent and independent regulatory bodies and lack of appropriate management of conflict of interest among scientific consultants.

The TEC provided competence and independence to achieve credibility. The science used by the TEC is sound and its recommendations are reasonable. It has not imposed any new rules or suggested a moratorium on research. It has simply called for adequate standards to be established, said the 51 signatories, including fellows of Royal Societies or National Academies of Science, scientists representing a range of research disciplines including plant genetic engineering and the creation of first GM food crop, tomato, in the U.S., which was later withdrawn for health concerns.

The TEC made 11 specific recommendations for properly regulating the development and commercialisation of genetically modified crops in India.

It recommended that product testing outside of the laboratory [field trials] be stopped until a comprehensive and effective process for such testing could be implemented. Except for a ban on testing GM crops for which India is a centre of biodiversity or origin, all testing can restart as soon as the government provides a robust and proper procedure, the statement said.

Taking note of the concerns expressed by the scientists, three eminent citizens the former Supreme Court judge, V.R. Krishna Iyer; the former Election Commissioner, J.M. Lyngdoh; and the former Chief Justice of the Delhi High Court, A.P. Shah endorsed and forwarded their statement to Prime Minister Manmohan Singh and UPA chairperson Sonia Gandhi.

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Global scientists back 10-year moratorium on field trials of Bt food crops

How TPP will hurt America
On Wednesday, the Senate Finance Committee met to discuss the opportunities and challenges the Trans-Pacific Partnership could pose on the United States. The...

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FORT MYERS NeoGenomics is winning market share.

That was one of the major takeaways from an earnings call it held for investors Thursday.

The Fort Myers-based company, focused on genetic testing for cancer, saw its test volume grow by 19 percent in the first quarter. Along with that growth came record quarterly revenue of $15.7 million, up 3 percent from a year ago.

Another takeaway? The company continues to aggressively develop new tests, adding to its already extensive menu of choices.

Innovation is very important to what we do. We are in an era of personalized medicine and we are introducing a lot of new molecular tests that are not only helping the company to grow, but also helping physicians diagnose and treat cancer better, said Douglas VanOort, the companys chairman and CEO, in a phone interview after the call.

NeoGenomics handles testing for pathologists, clinicians, oncologists and hospitals throughout the country.

The company reported profits of $300,000 for the first quarter, down from $603,000 a year ago.

During the conference call, VanOort highlighted the companys efforts to become more efficient and to regain profitability in the aftermath of a big regulatory change. The change, related to its Medicare billing practices, has cost the company about $1.3 million quarterly since it took effect last year. The company expects to overcome that hurdle later this year.

In the first quarter, the average revenue per test decreased by 13 percent from a year ago, primarily because of the regulatory change. But through newfound efficiencies, the company cut its cost per test by 5 percent from the fourth quarter, and its down 12 percent from a year ago.

We are not cutting costs, VanOort said in the phone interview. We are just finding more efficient ways to do what we do.

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Fort Myers-based genetic testing company sees record quarterly revenue

Newswise New Brunswick, NJ Your genetic makeup can help determine how well your body will respond to weight loss efforts aimed at controlling high blood pressure, a new study confirms.

The multi-institutional study, led by researchers at The Cardiovascular Institute, part of the University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, may help clarify how hypertension develops and progresses in certain individuals and also identify people for whom weight loss programs are most likely to help reduce blood pressure. Results were published in the current issue of Hypertension 2013;61:857-863.

The Trial of Nonpharmacologic Interventions in the Elderly (TONE) looked at 21 polymorphisms that have been identified as relating to hypertension, obesity, and diabetes mellitus to see what impact weight loss and sodium-reduction programs would have on blood pressure. Polymorphisms are the elements of a persons DNA that make it different from anothers and allow for diversity in such varied areas as eye color, hair texture, and even blood type. The TONE study identified several polymorphisms that relate to weight sensitivity with regard to hypertension, according to principal investigator John B. Kostis, MD, John G. Detwiler professor of cardiology, professor of medicine and pharmacology, associate dean for cardiovascular research, and director of The Cardiovascular Institute of Robert Wood Johnson Medical School.

The study sheds some light on an issue that has received little attention in the past, the researchers said.

There are more than a thousand papers discussing the question of what the impact is on blood pressure of decreasing the amount of salt you consume in your dietwhat is called salt sensitivity. But, there is nobody talking about weight sensitivity, and weight loss is equally or more important in controlling blood pressure, Dr. Kostis said.

Our work describes the variability of blood pressure drop in response to weight loss, according to a number of genetic polymorphisms, added William J. Kostis, PhD, MD, clinical and research fellow in medicine, Massachusetts General Hospital, Cardiology Division, alumnus of Robert Wood Johnson Medical School, and member of The Cardiovascular Institute, who was the first author of the study.

Participants in the TONE studyindividuals age 60 to 80 who were already taking one or two anti-hypertensive medicationswere randomly assigned to one of four interventions: Intensive dietary intervention focused on sodium reduction Weight loss program Combination of weight loss and sodium-reduction programs Attention control, in which individuals attended meetings that discussed dentistry, podiatry, or other topics unrelated to hypertension, weight loss, or sodium reduction

Regardless of the intervention, participants levels of anti-hypertensive medication remained the same throughout, to remove medication changes as a variable.

The study showed that both weight loss, if individuals are overweight, and decreased sodium intake may each lead to lower blood pressure, and the combination of weight loss and sodium restriction is more effective than either strategy alone, noted Dr. William Kostis.

Physicians can put these findings to use today through a blood test or even saliva test that measures genotype, Dr. John Kostis said. They can compare the patients genetic background with the polymorphisms that have been identified in the study and counsel patients accordingly, offering advice as to which type of intervention may be more successful in lowering that patients blood pressure, he said.

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New Study Confirms Link between Weight Loss and Blood Pressure for Individuals with Specific Genetic Polymorphisms

Undoing aging: Aubrey de Grey at TEDxDanubia 2013
Aubrey de Grey is a biomedical gerontologist and the Chief Science Officer of SENS Foundation, a charity dedicated to combating the aging process. He is also...

By: TEDxTalks

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Undoing aging: Aubrey de Grey at TEDxDanubia 2013 - Video