Category Archives: Gene Medicine

San Jose, California (PRWEB) January 02, 2014

Follow us on LinkedIn DNA Gene chips or DNA microarrays are small chips that are engrafted with DNA molecules. This advanced approach allows researchers to compare gene expressions in multiple cell types, identify active or switched-off genes, and compare various active genes under different settings. The growing focus on genetic testing and screening against a backdrop of increasing popularity of personalized medicine, is expected to drive demand for DNA gene chips. Growing popularity of preventive healthcare practices is also expected to help expand the use of DNA gene chips in preventative genetic diagnostics.

The trend report titled DNA Gene Chips announced by Global Industry Analysts Inc., is a focused research paper which provides cursory insights into the technology, its evolution, applications, and future prospects, in addition to providing coverage on corporate initiatives of key companies worldwide. The report also provides global market estimates and projections for DNA & Gene Chip (Microarray) in US dollars for years 2012 through 2017. Also covered are companies such as Affymetrix Inc., Agilent Technologies Inc., Illumina Inc., and Sequenom Inc., among others.

For more details about this trend report, please visit http://www.strategyr.com/TrendReport.asp?code=146088.

About Global Industry Analysts, Inc. Global Industry Analysts, Inc., (GIA) is a leading publisher of off-the-shelf market research. Founded in 1987, the company currently employs over 800 people worldwide. Annually, GIA publishes more than 1300 full-scale research reports and analyzes 40,000+ market and technology trends while monitoring more than 126,000 Companies worldwide. Serving over 9500 clients in 27 countries, GIA is recognized today, as one of the world's largest and reputed market research firms.

Global Industry Analysts, Inc. Telephone: 408-528-9966 Fax: 408-528-9977 Email: press(at)StrategyR(dot)com Web Site: http://www.StrategyR.com/

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Increasing Investments in Molecular Biology Research Drives the Market for DNA Gene Chips, According to a New Trend ...

PUBLIC RELEASE DATE:

2-Jan-2014

Contact: Lynn Celmer lcelmer@aasmnet.org 630-737-9700 American Academy of Sleep Medicine

DARIEN, IL A new study conducted across Europe found an extraordinary association between narcolepsy and a specific gene variant related to the immune system.

The modified genome-wide association study involved 1,261 people with narcolepsy, representing nearly 90 percent of European patients suffering from narcolepsy with cataplexy who have complete diagnostic work-up and DNA available. They were matched with 1,422 controls. High-resolution genotyping identified genetic variants including those in the human leukocyte antigen (HLA) system, which contains genes related to immune system function. Analysis was performed by logistic regression.

Results show that participants with the HLA allele DQB1*06:02 were 251 times more likely to have narcolepsy with cataplexy than participants without the gene variant. DQB1*06:02 had a remarkably high negative predictive value of 99.32 percent, which means that nearly 100 percent of narcolepsy with cataplexy patients are DQB1*06:02 positive. Four other DQB1 alleles provided protection against narcolepsy, strongly supporting a causal role for DQB1 in narcolepsy.

"For the first time we have tested the HLA association all over Europe," said principal investigator and lead author Mehdi Tafti, professor in the Center for Integrative Genomics at the University of Lausanne and Lausanne Hospital in Switzerland. "This almost 100 percent association with HLA is somehow unique to narcolepsy and suggests a causal implication."

Recent studies suggest that narcolepsy may be caused by an autoimmune response to an environmental trigger such as an infection. In people who are genetically susceptible to narcolepsy, the immune system may respond to the trigger by mistakenly attacking and destroying brain cells that make hypocretin, a hormone that helps promote alertness.

The authors noted that DQB1*06:02 is a common gene variant that is present in about 20 percent of the general European population. As a result, DQB1*06:02 had a low positive predictive value of only 65.68 percent. However, they suggested that high-resolution genotyping could play a valuable role in diagnosing patients suspected of having narcolepsy and evaluating at-risk populations.

"For clinicians these findings indicate they should reconsider the diagnosis of narcolepsy with cataplexy in HLA DQB1*06:02 negative patients," said American Academy of Sleep Medicine spokesperson Dr. Nathaniel Watson.

The rest is here:
Study supports a causal role in narcolepsy for a common genetic variant

Dec. 23, 2013 New findings suggest the oxytocin receptor, a gene known to influence mother-infant bonding and pair bonding in monogamous species, also plays a special role in the ability to remember faces. This research has important implications for disorders in which social information processing is disrupted, including autism spectrum disorder. In addition, the finding may lead to new strategies for improving social cognition in several psychiatric disorders.

A team of researchers from Yerkes National Primate Research Center at Emory University in Atlanta, the University College London in the United Kingdom and University of Tampere in Finland made the discovery, which will be published in an online Early Edition of Proceedings of the National Academy of Sciences.

According to author Larry Young, PhD, of Yerkes, the Department of Psychiatry in Emory's School of Medicine and Emory's Center for Translational Social Neuroscience (CTSN), this is the first study to demonstrate that variation in the oxytocin receptor gene influences face recognition skills. He and co-author David Skuse point out the implication that oxytocin plays an important role in promoting our ability to recognize one another, yet about one-third of the population possesses only the genetic variant that negatively impacts that ability. They say this finding may help explain why a few people remember almost everyone they have met while others have difficulty recognizing members of their own family.

Skuse is with the Institute of Child Health, University College London, and the Great Ormond Street Hospital for Children, NHS Foundation Trust, London.

Young, Skuse and their research team studied 198 families with a single autistic child because these families were known to show a wide range of variability in facial recognition skills; two-thirds of the families were from the United Kingdom, and the remainder from Finland.

The Emory researchers previously found the oxytocin receptor is essential for olfactory-based social recognition in rodents, like mice and voles, and wondered whether the same gene could also be involved in human face recognition. They examined the influence of subtle differences in oxytocin receptor gene structure on face memory competence in the parents, non-autistic siblings and autistic child, and discovered a single change in the DNA of the oxytocin receptor had a big impact on face memory skills in the families. According to Young, this finding implies that oxytocin likely plays an important role more generally in social information processing, which is disrupted in disorders such as autism.

Additionally, this study is remarkable for its evolutionary aspect. Rodents use odors for social recognition while humans use visual facial cues. This suggests an ancient conservation in genetic and neural architectures involved in social information processing that transcends the sensory modalities used from mouse to man.

Skuse credits Young's previous research that found mice with a mutated oxytocin receptor failed to recognize mice they previously encountered. "This led us to pursue more information about facial recognition and the implications for disorders in which social information processing is disrupted." Young adds the team will continue working together to pursue strategies for improving social cognition in psychiatric disorders based on the current findings.

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Gene that influences the ability to remember faces identified

Dec. 26 (UPI) -- Neanderthals may have passed down a gene variant to Latin Americans, putting them at a high risk of developing type-2 diabetes.

The largest genome-wide association study involving more than 8,000 Mexicans and other Latin Americans studied many genes in individuals and tried to find links to certain traits.

The high risk gene called SLC16A11 has been found in around half of those with recent Native American ancestry, including Latin Americans. The variant was also found in 20 percent of East Asians, but was rare in Europe and Africa.

"To date, genetic studies have largely used samples from people of European or Asian ancestry, which makes it possible to miss culprit genes that are altered at different frequencies in other populations," said co-author Jose Florez, associate professor of medicine at Harvard Medical School in Massachusetts.

According to Florez, by expanding the scope of research to look at Latin American samples they have found the strongest genetic risk factor discovered to date, which accounts for 20 percent of that population's increased prevalence of type 2 diabetes.

Earlier research has shown that Neanderthals interbred with modern humans nearly 60,000 to 70,000 years ago, and researchers believe this is how SLC16A11 was introduced.

Altering the levels of SLC16A11 protein can change the amount of a fat that has been involved in the risk of diabetes. The study, published in the journal Nature, suggests that the SLC16A11 could be involved in the transport of an unknown metabolite the affects the fat level in cells.

[BBC] [Nature]

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Latin Americans inherited diabetes gene risk from Neanderthals

December 24, 2013

redOrbit Staff & Wire Reports Your Universe Online

The same gene that influences bonding between mothers and their infant children, as well as the attachment between partners in a monogamous relationship, could also be involved in the ability to remember faces.

The gene in question is the oxytocin receptor, a member of the G-protein coupled receptor family which functions receives chemical signals from the hormone and neurotransmitter oxytocin. The receptors modulate a variety of behaviors, including stress, anxiety, bonding, maternal behavior, social memory and recognition.

In a study scheduled to appear in an online Early Edition of Proceedings of the National Academy of Sciences, researchers report that the discovery could help diagnose and treat autism spectrum disorder and other conditions in which a persons ability to process social information is adversely affected.

In addition, the authors report that the findings could also help experts develop new methods of improving social cognition skills in patients suffering from serious psychiatric disorders. Researchers from Emory University, University College London and the University of Tampere in Finland were involved in the research.

According to author Dr. Larry Young of the Emory University School of Medicine and Center for Translational Social Neuroscience (CTSN), this is the first paper to demonstrate that variation in the oxytocin receptor gene has an impact on an individuals facial recognition skill.

He and his colleagues stated that while oxytocin plays an important role in promoting our ability to recognize one another about one-third of the population possesses only the genetic variant that negatively impacts that ability, the university said in a statement. They say this finding may help explain why a few people remember almost everyone they have met while others have difficulty recognizing members of their own family.

Dr. Youngs team analyzed 198 families with one autistic child, as those families had previously been found to demonstrate a wide range of variability when it came to the ability to recognize faces. Approximately 66 percent of the families hailed from the UK, while the rest of them resided in Finland, the university said.

Previously, researchers from Emory University discovered that the oxytocin receptor played a vital role in olfactory-based social recognition in rodents. While attempting to discern whether or not the same gene played a similar role in people, they looked at how subtle differences in the structure of the receptor gene impacted facial memory skills in parents, autistic children and their non-autistic brothers and sisters.

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Gene That Influences Bonding Also Found To Impact Facial Recognition

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Newswise Working in mice, researchers at Washington University School of Medicine in St. Louis report developing a gene delivery method long sought in the field of gene therapy: a deactivated virus carrying a gene of interest that can be injected into the bloodstream and make its way to the right cells.

In this early proof-of-concept study, the scientists have shown that they can target tumor blood vessels in mice without affecting healthy tissues.

Most current gene therapies in humans involve taking cells out of the body, modifying them and putting them back in, said David T. Curiel, MD, PhD, distinguished professor of radiation oncology. This limits gene therapy to conditions affecting tissues like the blood or bone marrow that can be removed, treated and returned to the patient. Today, even after 30 years of research, we cant inject a viral vector to deliver a gene and have it go to the right place.

But now, investigators at Siteman Cancer Center at Barnes-Jewish Hospital and Washington University School of Medicine say they have designed a targetable injectable vector a deactivated virus that homes in on the inner lining of tumor blood vessels and does not get stuck in the liver, a problem that has plagued past attempts.

The findings are reported Dec. 23 in PLOS ONE.

Building on their own previous work and others, the researchers engineered this viral vector to turn on its gene payload only in the abnormal blood vessels that help fuel and nurture tumor growth. But unlike most therapies aimed at tumor vasculature, the goal is not to destroy the cancers blood supply.

We dont want to kill tumor vessels, said senior author Jeffrey M. Arbeit, MD, professor of urologic surgery and of cell biology and physiology. We want to hijack them and turn them into factories for producing molecules that alter the tumor microenvironment so that it no longer nurtures the tumor. This could stop the tumor growth itself or cooperate with standard chemotherapy and radiation to make them more effective. One advantage of this strategy is that it could be applied to nearly all of the most common cancers affecting patients.

In theory, Arbeit pointed out, this approach could be applied to diseases other than cancer in which the blood vessels are abnormal, including conditions like Alzheimers disease, multiple sclerosis or heart failure.

Continue reading here:
Gene Therapy Method Targets Tumor Blood Vessels

PUBLIC RELEASE DATE:

23-Dec-2013

Contact: Lisa Newbern lisa.newbern@emory.edu 404-727-7709 Emory Health Sciences

New findings suggest the oxytocin receptor, a gene known to influence mother-infant bonding and pair bonding in monogamous species, also plays a special role in the ability to remember faces. This research has important implications for disorders in which social information processing is disrupted, including autism spectrum disorder. In addition, the finding may lead to new strategies for improving social cognition in several psychiatric disorders.

A team of researchers from Yerkes National Primate Research Center at Emory University in Atlanta, the University College London in the United Kingdom and University of Tampere in Finland made the discovery, which will be published in an online Early Edition of Proceedings of the National Academy of Sciences.

According to author Larry Young, PhD, of Yerkes, the Department of Psychiatry in Emory's School of Medicine and Emory's Center for Translational Social Neuroscience (CTSN), this is the first study to demonstrate that variation in the oxytocin receptor gene influences face recognition skills. He and co-author David Skuse point out the implication that oxytocin plays an important role in promoting our ability to recognize one another, yet about one-third of the population possesses only the genetic variant that negatively impacts that ability. They say this finding may help explain why a few people remember almost everyone they have met while others have difficulty recognizing members of their own family.

Skuse is with the Institute of Child Health, University College London, and the Great Ormond Street Hospital for Children, NHS Foundation Trust, London.

Young, Skuse and their research team studied 198 families with a single autistic child because these families were known to show a wide range of variability in facial recognition skills; two-thirds of the families were from the United Kingdom, and the remainder from Finland.

The Emory researchers previously found the oxytocin receptor is essential for olfactory-based social recognition in rodents, like mice and voles, and wondered whether the same gene could also be involved in human face recognition. They examined the influence of subtle differences in oxytocin receptor gene structure on face memory competence in the parents, non-autistic siblings and autistic child, and discovered a single change in the DNA of the oxytocin receptor had a big impact on face memory skills in the families. According to Young, this finding implies that oxytocin likely plays an important role more generally in social information processing, which is disrupted in disorders such as autism.

Additionally, this study is remarkable for its evolutionary aspect. Rodents use odors for social recognition while humans use visual facial cues. This suggests an ancient conservation in genetic and neural architectures involved in social information processing that transcends the sensory modalities used from mouse to man.

See original here:
Researchers identify gene that influences the ability to remember faces

Gene therapy is a novel approach to treat, cure, or ultimately prevent disease by changing the expression of a persons genes. Gene therapy is in its infancy, and current therapies are primarily experimental, with most human clinical trials still in the research stages.

How does gene therapy work? Genes are composed of DNA that carries information needed to make proteins the building blocks of our bodies. Variations in the DNA sequence or code of a gene are called mutations, which often are harmless but sometimes can lead to serious disease. Gene therapy treats disease by repairing dysfunctional genes or by providing copies of missing genes.

To reverse disease caused by genetic damage, researchers isolate normal DNA and package it into a vehicle known as a vector, which acts as a molecular delivery truck. Vectors composed of viral DNA sequences have been used successfully in human gene therapy trials. Doctors infect a target cell usually from a tissue affected by the illness, such as liver or lung cellswith the vector. The vector unloads its DNA cargo, which then begins producing the proper proteins and restores the cell to normal. Problems can arise if the DNA is inserted into the wrong place in the genome. For example, in rare instances the DNA may be inserted into a regulatory gene, improperly turning it on or off, leading to cancer.

Researchers continue to optimize viral vectors as well as develop non-viral vectors that may have fewer unexpected side effects. Nonviral gene delivery involves complexing DNA with an agent that allows it to enter a cell nonspecifically. DNA delivered in this manner is usually expressed for only a limited time because it rarely integrates into the host cell genome.

Initial efforts in gene therapy focused on delivering a normal copy of a missing or defective gene, but current programs are applying gene delivery technology across a broader spectrum of conditions. Researchers are now utilizing gene therapy to :

What diseases could be treated with gene therapy? About 4,000 diseases have been traced to gene disorders. Current and possible candidates for gene therapy include cancer, AIDS, cystic fibrosis, Parkinsons and Alzheimers diseases, amyotrophic lateral sclerosis (Lou Gehrig's disease), cardiovascular disease and arthritis.

In cases such as cystic fibrosis or hemophilia, disease results from a mutation in a single gene. In other scenarios like hypertension or high cholesterol, certain genetic variations may interact with environmental stimuli to cause disease.

Has gene therapy been successfully used in humans? Gene therapy is likely to be most successful with diseases caused by single gene defects. The first successful gene therapy on humans was performed in 1990 by researchers at the National Institutes of Health. The therapy treated a four-year-old child for adenosine deaminase (ADA) deficiency, a rare genetic disease in which children are born with severe immunodeficiency and are prone to repeated serious infections.

Since 1990, gene therapy had been tested in human clinical trials for treating such diseases as severe combined immunodeficiency disease (SCID), cystic fibrosis, Canavan's disease, and Gaucher's disease. In 2003, more than 600 gene therapy clinical trials were under way in the United States but only a handful of these are in advanced stages. SCID, in which children lack natural defenses against infection and can only survive in isolated environments, remains the only disease cured by gene therapy.

Are genetic alterations from gene therapy passed on to children? Gene therapy can be targeted to somatic (body) or germ (egg and sperm) cells. In somatic gene therapy, the patients genome is changed, but the change is not passed along to the next generation. In germline gene therapy, the patients egg or sperm cells are changed with the goal of passing on changes to their offspring. Existing gene therapy treatments and experiments are all somatic.

Continue reading here:
Gene Therapy - American Medical Association

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Gene Therapies

Takara Bio advances clinical development of the following gene therapies:

Takara Bio acquired the HF10 business from M's Science Corporation in November 2010 and is currently conducting a Phase I clinical trial in the United States for the treatment of head and neck cancer and other solid tumors, which is sched-uled for completion in fiscal 2014. HF10 is a spontaneously occurring attenuated mutant of Herpes Simplex virus Type 1 that displays strong antitumor activity (oncolytic activity) when locally injected into tumors. Moreover, preclinical data suggests that HF10 also contributed to the acquisition of immunity against the tumors.

In Japan, three clinical studies were conducted in patients with breast cancer, head and neck cancer, and pancreatic cancer at Nagoya University School of Medicine. The results of these studies showed oncolytic activity and tolerability of HF10.

In December 2011, Mie University Hospital began a clinical study on solid tumors. Further, in April 2013, Nagoya University School of Medicine commenced a clinical study with patients suffering from non-resectable pancreatic cancer for the treatment in combination of HF10 with existing anticancer drugs.

MolMed S.p.A, of Italy, which has in-licensed the RetroNectin method from Takara Bio, is now conducting a Phase III clinical trial of HSV-TK gene therapy for high-risk, acute hematological malignancies in Europe. Takara Bio has exclusive rights to this treatment technology in most Asian countries.

In 2008, Takara Bio began conducting a Phase I clinical trial of HSV-TK gene therapy (project code: TBI-0301) at the National Cancer Center Hospital for treatment of patients with relapsed leukemia after hematopoietic stem cell transplantation. However, the number of existing patients with this condition remained low. In order to accelerate this gene therapy project, the TBI-0301 trial was discontinued and a new joint clinical trial in Japan and South Korea (phase I / II clinical trial, project code: TBI-1101) is in preparation to commence in fiscal 2016. The new trial will focus on patients with hematological malignancy after having undergone HLA mismatched hematopoietic stem cell transplantation.

Takara Bio, in a joint effort with both the University of Pennsylvania and Drexel University, commenced an endoribonuclease MazF based gene therapy Phase I clinical trial in the United States for patients that have been infected the human immunodeficiency virus (HIV, otherwise known as the AIDS virus). This clinical trial is scheduled for completion in fiscal 2016.

In the mechanism of AIDS, replication of the virus in infected HIV immune cells causes However, the MazF-modified T-cells (a type of immune cells) are expected to remain functional even if infected by HIV, by preventing replication of the virus. MazF genes are transduced into patient-derived T-cells ex vivo using retroviral vectors that express MazF conditionally upon HIV infection. The MazF-modified T-cells that are infused back into the patients will cleave the RNA strand of HIV and thereby block the replication of the virus when it infects the transduced T-cells. As a result, this method has the potential to become a gene therapy treatment for HIV infections.

Takara Bio, in collaboration with Mie University Hospital, is preparing a Phase I clinical trial in fiscal 2014 on MAGE-A4 antigen-specific T-cell receptor (TCR) gene therapy utilizing next-generation retroviral vectors developed by the Company. The main mechanism of TCR gene therapy is that the gene-transduced lymphocytes, which acquire the capability to specifically recognize cancer cells, attack and eliminate the cancer. TCR genes that are capable of recognizing cancer antigens are tranceduced into the patient's own lymphocytes, which are then re-infused into the patient.

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