Newswise African-Americans dont get kidney stones as frequently as Caucasians.

Are they protected genetically? If so, identifying the genetic factors that retard kidney stone formation could lead to new ways to treat or even prevent this painful condition, according to Vanderbilt University researcher Todd Edwards, Ph.D.

Kidney stones afflict one of every 11 Americans and cost the country more than $2 billion annually. Avoiding them could really make a difference for a lot of people, and could cut health costs dramatically, he said.

Until recently, teasing out complicated kidney stone genetics would have required years of study, tens of thousands of patients and hundreds of millions of dollars. Now thanks to BioVU, Vanderbilts massive DNA databank, the mother lode is within reach.

This month BioVU logged in its 150,000th unique genetic sample. It is now the worlds largest collection of human DNA linked to searchable, electronic health information, said Dan Roden, M.D., assistant vice chancellor for Personalized Medicine at Vanderbilt and BioVUs principal investigator.

BioVU began collecting DNA in 2007. Discarded blood specimens from Vanderbilt patients are sent to the DNA Resources Core, where the genetic material is extracted and stored. If patients check a box on a consent form, their leftover blood will not be used, but few choose to opt out.

The DNA samples are bar-coded and, along with their matching electronic health records, scrubbed of information that could identify individual patients.

The resulting genetic gold mine enables Vanderbilt researchers to quickly pull and analyze the DNA of hundreds of people with particular health conditions or responses to medication.

Before proceeding, BioVU investigators must be approved by Vanderbilts Institutional Review Board, sign a data use agreement, and determine, with the help of a BioVU project manager, the feasibility of their idea. Their proposals are then considered by separate pre-review and full review committees consisting of Vanderbilt faculty members.

To date, more than 50 BioVU studies have been approved and are under way.

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Vanderbilt's BioVU Databank Now World's Largest Human DNA Repository Linked to Searchable, Electronic Health Information

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SAN DIEGO--(BUSINESS WIRE)--

Illumina, Inc. (ILMN) today announced five initial TruSight content sets for use in next-generation sequencing (NGS) in laboratory settings. Designed by recognized experts at leading institutions, the content sets offer cost-effective, streamlined, targeted sequencing for specific genetic diseases or conditions. Customers can immediately leverage this content to develop their own tests, and in the first half of 2013 will have the additional capability to augment the sets with custom content.

These products, developed in conjunction with leading healthcare experts including Childrens Mercy Center for Pediatric Genomic Medicine, Kennedy Krieger Institute, The Institute of Cancer Research, London, and Partners HealthCare (see additional Illumina-Partners HealthCare news today), are designed to provide comprehensive evaluation of genes associated with the following:

The launch of these new NGS products is an exciting milestone for Illumina, said Jay Flatley, President and Chief Executive Officer for Illumina. We worked closely with the community to develop and introduce these first content sets, to ensure we are meeting the needs of laboratories and to enable results of high quality. Combining this content with already proven Illumina next-generation sequencing technology, via the MiSeq platform, will provide a powerful tool.

TruSight content sets are comprised of oligo probes that target specific genes and regions relevant to specific diseases or conditions. They are designed for use by laboratories in the development of their own unique targeted sequencing tests and will work on Illuminas MiSeq system. Additionally, new Nextera Enrichment kits and MiSeq kits will support lower sample throughput options.

We are very excited about the value of the new content and how accessible it will be to laboratories, said Dr. Stephen Kingsmore, Director, Childrens Mercy Center for Pediatric Genomic Medicine, in Kansas City, Mo. Deploying this expert content on Illuminas proven technology streamlines a labs operational efficiency and speed to results. Ultimately, we hope to improve patient care. Thats the true goal.

Added Matt Posard, Senior Vice President and General Manager of Illuminas Translational and Consumer Genomics business, Today, Illumina also announced a strategic alliance with Partners HealthCare to introduce next-generation sequencing clinical interpretation and reporting tools, via their GeneInsight Suite platform. The combination of TruSight products and these new interpretation and reporting tools is a major step forward in realizing the benefits of next generation sequencing.

TruSight content sets are for research use only and not intended for diagnostic use. The products are now available for order with shipment to begin in Q4 2012. For more information, visit http://www.illumina.com/TruSight.

About Illumina

Illumina (www.illumina.com) is a leading developer, manufacturer, and marketer of life science tools and integrated systems for the analysis of genetic variation and function. We provide innovative sequencing and array-based solutions for genotyping, copy number variation analysis, methylation studies, gene expression profiling, and low-multiplex analysis of DNA, RNA, and protein. We also provide tools and services that are fueling advances in consumer genomics and diagnostics. Our technology and products accelerate genetic analysis research and its application, paving the way for molecular medicine and ultimately transforming healthcare.

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Illumina Launches TruSightTM Targeted Sequencing Content Sets

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Being told you have a genetic predisposition to alcoholism could make you feel you have less control over your drinking, a new study suggests.

The unique study adds to growing concern about the potential perils of direct-to-consumer genetic tests.

Psychologist Ilan Dar-Nimrod from the University of Sydney and colleagues report their findings in the journal Genetics in Medicine.

He says the latest findings show how genetic information has the power to change a person's emotional state, behaviour and attitudes.

"We have about 1,600 genetic tests available now," Dar-Nimrod tells the Australian Broadcasting Corporation. "We should have better knowledge about how to communicate these results in a manner that doesn't create harm."

He says for a few genetic-related diseases, having a particular gene means you will definitely get the disease, unless you die of other causes first.

But in 98 per cent of cases the gene only increases your risk of a condition and that risk may be very small or very uncertain.

Despite the lack of certainty around the impact of many disease-related genes, Dar-Nimrod says there is some evidence that people who test positive for them can become fatalistic and believe they will definitely develop the condition in question.

He says such "genetic determinism" is encouraged by media reports that imply a greater risk from such genes than there actually is.

Dar-Nimrod and colleagues set up the first randomized experiment to investigate the psychological and behavioural impact of receiving personalized genetic information of this kind.

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Home genetic testing for alcoholism carries perils

Recommendation and review posted by Bethany Smith

Public release date: 11-Sep-2012 [ | E-mail | Share ]

Contact: Anita Kar anita.kar@mcgill.ca 514-398-3376 McGill University

This press release is available in French.

Have you ever wondered why some people find it so much easier to stop smoking than others? New research shows that vulnerability to smoking addiction is shaped by our genes. A study from the Montreal Neurological Institute and Hospital - The Neuro, McGill University shows that people with genetically fast nicotine metabolism have a significantly greater brain response to smoking cues than those with slow nicotine metabolism. Previous research shows that greater reactivity to smoking cues predicts decreased success at smoking cessation and that environmental cues promote increased nicotine intake in animals and humans. This new finding that nicotine metabolism rates affect the brain's response to smoking may lead the way for tailoring smoking cessation programs based on individual genetics.

Smoking cues, such as the sight of cigarettes or smokers, affect smoking behavior and are linked to relapse and cigarette use. Nicotine metabolism, by a liver enzyme, also influences smoking behavior. Variations in the gene that codes for this enzyme determine slow or fast rates of metabolism and therefore, the level of nicotine in the blood that reaches the brain. In the study smokers were screened for their nicotine metabolism rates and their enzyme genotype. Participants were aged 18 35 and smoked 5-25 cigarettes daily for a minimum of 2 years. People with the slowest and fastest metabolism had their brain response to visual smoking cues measured using functional MRI. Fast metabolizers had significantly greater response to visual cigarette cues than slow metabolizers in brain areas linked to memory, motivation and reward, namely the amygdala, hippocampus, striatum, insula, and cingulate cortex.

"The finding that nicotine metabolism rate has an impact on the brain's response to smoking cues supports our hypothesis that individuals with fast nicotine metabolism rates would have a greater brain response to smoking cues because of close coupling in everyday life between exposure to cigarettes and surges in blood nicotine concentration. In other words they learn to associate cigarette smoking with the nicotine surge," says clinician-scientist Dr. Alain Dagher, lead investigator at The Neuro. "In contrast, individuals with slow metabolism rates, who have relatively constant nicotine blood levels throughout the day, are less likely to develop conditioned responses to cues. For them, smoking is not associated with brief nicotine surges, so they are smoking for other reasons. Possibilities include maintenance of constant brain nicotine levels for cognitive enhancement (ie, improved attention, memory), or relief of stress or anxiety. "

Future research could focus on improving smoking cessation methods by tailoring treatments for different types of smokers. One possibility is to measure the rate of nicotine metabolism as part of the therapeutic decision-making process. For example, targeting cue-induced relapse risk may not help those with slow nicotine metabolism, who are more likely to benefit from long-acting cholinergic drugs such as the nicotine patch, consistent with previous clinical trials. Conversely the use of non-nicotine based therapies aimed at reducing craving may help fast metabolizers, as demonstrated for buproprion, an anti-depressant that has been used for smoking cessation.

###

This research was supported by the Canadian Tobacco Control Research Initiative (AD), Fonds de Recherche en Sant du Qubec (AD), and the Canadian Institutes of Health Research.

About The Neuro

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How genetics shape our addictions

Recommendation and review posted by Bethany Smith

DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/zzkm43/plunketts_biotech) has announced the addition of Plunkett Research Ltd's new book "Plunkett's Biotech & Genetics Industry Almanac 2012: Biotech & Genetics Industry Market Research, Statistics, Trends & Leading Companies" to their offering.

A complete market research report, including forecasts and market estimates, technologies analysis and developments at innovative firms.

You will gain vital insights that can help you shape your own strategy for business development, product development and investments.

- How is the industry evolving?

- How is the industry being shaped by new technologies?

- How is demand growing in emerging markets and mature economies?

- What is the size of the market now and in the future?

- What are the financial results of the leading companies?

- What are the names and titles of top executives?

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Research and Markets: Plunkett's Biotech & Genetics Industry Almanac 2012: Biotech & Genetics Industry Market Research ...

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SAN MARINO, Calif.--(BUSINESS WIRE)--

Viral Genetics (VRAL) majority-owned subsidiary, VG Energy, has contracted with Eno Research Chemicals & Custom Synthesis Group for production of its LipidMax lipid enhancement compound, in sufficient capacity to meet demand from commercial and research end-users worldwide.

Orders for LipidMax can be placed at https://store.vgenergy.net/. Once approved for purchases, customers will be shipped LipidMax in 10g units. Additional information is also available at lipidmax@vgenergy.net.

LipidMax, the first product marketed by VG Energy, is a lipid-enhancement compound for use in the production of oils from algae, corn, palm, and other plants or plant-like organisms and is based on the Companys exclusively licensed Metabolic Disruption Technology (MDT).

Independent testing has shown that, when treated with LipidMax, the yields from several algae and algae-like species including Schizochytrium, Prymnesium parvum, and Chlamydomonas reinhardtii, have shown significant increases in oil (lipid) yields. Similar, if not stronger, results have been observed in palm and other oil-producing plants. The Company believes that LipidMax should generate oil-enhancing results in most other species of plants and plant-like organisms beyond those mentioned, and is continuing testing to validate and quantify this.

The oil yield increase is thought to provide a possible catalyst for changing the economic feasibility for algal-derived biofuels in the marketplace, making biofuels more cost-competitive, when compared to petroleum-based fuels. Similar cost-reduction effects in plant oils used as food, nutraceuticals and cosmetics should also result from productivity-enhancement.

The company joins a newly emerging category of businesses called intermediates1 in the biofuels and bio-chemical sectors. These products can be utilized in the production of an array of fuels, chemicals, flavors, fragrances and other end products. Intermediates constitute building blocks and intermediate steps upon which other processes and products are built, and as such can become integral to building the value chain in these rapidly growing bio-based industries.

VG Energys Chief Scientist, Dr. M. Karen Newell-Rogers, noted that the Eno Research Chemicals and Custom Synthesis Group is fully cGMP- and cGLP-compliant, has passed a rigorous set of internal testing protocols, and the product produced at the facility meets the companys standards for chemical consistency, purity and yield. When scaled up to commercially viable quantities, the LipidMax produced at this facility meets or exceeds the same quality standards we established using smaller research-grade batches at the Agrilife facilities. The process of commercial or industrial scale-up of a chemical such as our product can sometimes alter the ultimate activity of a compound, but LipidMax produced at scaled up production protocols has shown to match the results we observed during initial evaluations.

Haig Keledjian, Viral Genetics CEO said, This marks the transition to commercialization from a purely research based company and we are very pleased and excited to now commence sales of our LipidMax product to customers in the bio-fuels, and high quality edible and nutraceutical oil markets.

Mr. Keledjian continued, We expect that initial customers will be industrial laboratories and academic research institutions looking to establish and verify the economic advantages of LipidMax that we have demonstrated in our own and independent testing. As end users attain increased yields of usable oil in commercial size quantities, we anticipate a rapid and widespread awareness of LipidMax, leading to adoption of LipidMax in a host of industries worldwide including algal biofuel and palm oil, amongst others.

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Viral Genetics’ Subsidiary, VG Energy, Commencing Sales of LipidMax™

Recommendation and review posted by Bethany Smith

When Jessica Ainslie had her son Colton, she knew there was something wrong. Born prematurely, he weighed just 2 pounds, 9 ounces at birth, and he had to spend time in the neonatal intensive care unit before he could come home.

Thought to be out out of the woods, Colton then started developing breathing problems and was vomiting often, just a few months later.

It just kept getting worse. He wasnt eating a whole lot, and he couldnt keep anything down, Ainslie, from Peoria, Ariz., told FoxNews.com. We took him to the ER a couple times; they kept giving him fluids and sending him back home. But I knew there was something wrong with my kid. I had that mom gut feeling.

Multiple blood tests were done on Colton, but nothing definitive came up. Finally, one of Ainslies doctors said she was going to test for SCID, a possible diagnosis that made the new mom incredibly anxious.

For small children with severe combined immunodeficiency (SCID) more famously known as bubble boy syndrome disease and infection are a constant source of worry due to a weakened, or almost non-existent immune system. If left untreated, the condition is fatal in just one to two years.

Sure enough, Coltons blood work showed that he had ADA-deficient SCID, a form of SCID that affects 15 percent of SCID patients. While some treatments exist for those suffering from the disease, options are mostly limited to rare bone marrow matches or frequent drug injections that can last the entirety of the childs life. Though helpful, these treatments dont always work and can come with terrible side effects and high costs.

Devastated by the diagnosis, Ainslie was offered some hope when she was asked if they could Air Evac 10-month-old Colton to Dr. Donald Kohns office at UCLA, one of the leading doctors in ADA-deficient SCID. Now, after having participated in a new gene therapy study developed by Kohn, Colton and eventually his baby sister Abbygail are living normal lives, nearly SCID-free.

Be their own donor

Just about the time Colton was diagnosed, Kohn had been working on a novel gene therapy treatment for children with SCID. In collaboration with researchers from both the University of California at Los Angeles and that National Institute of Health, Kohn and his colleagues have spent 11 years creating and testing this new therapy, which is capable of restoring immune systems in children with ADA-deficient SCID.

What were doing with gene therapy is having the patient be their own donor, study author Kohn, a member of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA, told FoxNews.com. We insert the gene theyre missing and transport it back through their system.

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New Therapy for Bubble Babies

Recommendation and review posted by Bethany Smith

Public release date: 11-Sep-2012 [ | E-mail | Share ]

Contact: Kim Irwin kirwin@mednet.ucla.edu 310-435-9457 University of California - Los Angeles Health Sciences

UCLA stem cell researchers have found that a gene therapy regimen can safely restore immune systems to children with so-called "Bubble Boy" disease, a life threatening condition that if left untreated can be fatal within one to two years.

In the 11-year study, researchers were able to test two therapy regimens for 10 children with ADA-deficient severe combined immunodeficiency (SCID). During the study, they refined their approach to include a light dose of chemotherapy to help remove many of the blood stem cells in the bone marrow that are not creating an enzyme called adenosine deaminase (ADA), which is critical for the production and survival of healthy white blood cells, said study senior Dr. Donald Kohn, a professor of pediatrics and of microbiology, immunology, and molecular genetics in Life Sciences and a member of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA.

The refined gene therapy and chemotherapy regimen proved superior to the other method tested in the study, restoring immune function to three of the six children who received it, Kohn said. Going forward, an even further refined regimen using a different type of virus delivery system will be studied in the next phase of the study, which already has enrolled eight of the 10 patients needed.

The study appears Aug. 30 in the advance online issue of the peer-reviewed journal Blood.

"We were very happy that in the human trials we were able to see a benefit in the patients after we modified the protocol," Kohn said. "Doctors treating ADA-deficient SCID have had too few options for too long, and we hope this will provide them with an efficient and effective treatment for this devastating disease."

Children born with SCID, an inherited immunodeficiency, are generally diagnosed at about six months. They are extremely vulnerable to infectious diseases and don't grow well. Chronic diarrhea, ear infections, recurrent pneumonia and profuse oral candidiasis commonly occur in these children. SCID cases occur in about 1 of 100,000 births

Currently, the only treatment for ADA-deficient SCID calls for injecting the patients twice a week with the necessary enzyme, Kohn said, a life-long process that is very expensive and often doesn't return the immune system to optimal levels. These patients also can undergo bone marrow transplants from matched siblings, but matches can be very rare.

About 15 percent of all SCID patients are ADA-deficient. Kohn and his team used a virus delivery system that he had developed in his lab in the 1990s to restore the gene that produces the missing enzyme necessary for a healthy immune system. To date, about 40 children with SCID have received gene therapy in clinical trials around the world, Kohn said.

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UCLA stem cell researchers use gene therapy to restore immune systems in 'bubble babies'

Recommendation and review posted by Bethany Smith

ScienceDaily (Sep. 11, 2012) UCLA stem cell researchers have found that a gene therapy regimen can safely restore immune systems to children with so-called "Bubble Boy" disease, a life threatening condition that if left untreated can be fatal within one to two years.

In the 11-year study, researchers were able to test two therapy regimens for 10 children with ADA-deficient severe combined immunodeficiency (SCID). During the study, they refined their approach to include a light dose of chemotherapy to help remove many of the blood stem cells in the bone marrow that are not creating an enzyme called adenosine deaminase (ADA), which is critical for the production and survival of healthy white blood cells, said study senior Dr. Donald Kohn, a professor of pediatrics and of microbiology, immunology, and molecular genetics in Life Sciences and a member of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA.

The refined gene therapy and chemotherapy regimen proved superior to the other method tested in the study, restoring immune function to three of the six children who received it, Kohn said. Going forward, an even further refined regimen using a different type of virus delivery system will be studied in the next phase of the study, which already has enrolled eight of the 10 patients needed.

The study appears Aug. 30 in the advance online issue of the peer-reviewed journal Blood.

"We were very happy that in the human trials we were able to see a benefit in the patients after we modified the protocol," Kohn said. "Doctors treating ADA-deficient SCID have had too few options for too long, and we hope this will provide them with an efficient and effective treatment for this devastating disease."

Children born with SCID, an inherited immunodeficiency, are generally diagnosed at about six months. They are extremely vulnerable to infectious diseases and don't grow well. Chronic diarrhea, ear infections, recurrent pneumonia and profuse oral candidiasis commonly occur in these children. SCID cases occur in about 1 of 100,000 births

Currently, the only treatment for ADA-deficient SCID calls for injecting the patients twice a week with the necessary enzyme, Kohn said, a life-long process that is very expensive and often doesn't return the immune system to optimal levels. These patients also can undergo bone marrow transplants from matched siblings, but matches can be very rare.

About 15 percent of all SCID patients are ADA-deficient. Kohn and his team used a virus delivery system that he had developed in his lab in the 1990s to restore the gene that produces the missing enzyme necessary for a healthy immune system. To date, about 40 children with SCID have received gene therapy in clinical trials around the world, Kohn said.

Two slightly different viral vectors were tested in the study, each modified to deliver healthy ADA genes into the bone marrow cells of the patients so the needed enzyme could be produced and make up for the cells that don't have the gene. Four of the 10 patients in the study remained on their enzyme replacement therapy during the gene therapy study. There were no side effects, but their immune systems were not sufficiently restored, Kohn said.

In the next six patients, the enzyme therapy was stopped and a small dose of chemotherapy was given before starting the gene therapy to deplete the ADA-deficient stem cells in their bone marrow. Of those patients, half had their immune systems restored. The human findings confirmed another study, also published recently in Blood by Kohn and UCLA colleague Dr. Denise Carbonaro-Sarracino, which tested the techniques in parallel, using a mouse model of ADA-deficient SCID.

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Stem cell researchers use gene therapy to restore immune systems in 'Bubble Boy' disease

Recommendation and review posted by Bethany Smith

Public release date: 11-Sep-2012 [ | E-mail | Share ]

Contact: Raymond MacDougall macdougallr@mail.nih.gov 301-402-0911 NIH/National Human Genome Research Institute

Researchers have demonstrated that a refined gene therapy approach safely restores the immune systems of some children with severe combined immunodeficiency (SCID). The rare condition blocks the normal development of a newborn's immune system, leaving the child susceptible to every passing microbe. Children with SCID experience chronic infections, which usually triggers the diagnosis. Their lifespan is two years if doctors cannot restore their immunity.

The findings from facilities including the National Institutes of Health, the University of California, Los Angeles (UCLA), and the Children's Hospital Los Angeles, are reported in the Sept. 11, 2012, advanced online issue of the journal Blood, the official journal of the American Society of Hematology.

In the 11-year study, the researchers tested a combination of techniques for gene therapy, arriving at one that produced normal levels of immune function for three patients.

"Doctors who treat patients with SCID have had limited treatment options for too long," said Dan Kastner, M.D., Ph.D., scientific director of the National Human Genome Research Institute (NHGRI), part of the NIH. "The research teams and the patients who have participated in the studies have together achieved an impressive advance toward a cure that is welcome news for both the scientific and patient communities."

Gene therapy is an experimental method for treating patients with genetic diseases. It is intended to integrate functioning genes among those naturally existing in the cells of the body to make up for faulty genes. Researchers in the current study tested a set of methods to improve outcomes for children with a particular form of SCID.

"This is a highly rewarding study for those of us in the clinic and lab," said Fabio Candotti, M.D., a senior author and a senior investigator in NHGRI's Genetics and Molecular Biology Branch. "Not only have we realized an important advancement in gene therapy, but we have seen a renewal of health in our patients."

While rare, SCID became widely known because of the remarkable boy-in-the-bubble story of the 1970s. The story was based in part on a boy named David Vetter, who lived for 13 years in a plastic isolation unit to protect him from infections. He died following an unsuccessful bone marrow transplant that doctors had hoped would repair his immune system.

SCID has many causes. In one type, a gene that produces the adenosine deaminase (ADA) enzyme becomes mutated and fails to produce the normal enzyme. Without ADA, a chemically altered form of adenosine, one of DNA's building blocks, accumulates in rapidly dividing bone marrow cells, killing them and destroying the immune system in the process. Normal bone marrow makes healthy white blood cells, or lymphocytes, which are the key players in the immune response that reacts against harmful bacteria and destroys cells infected by viruses. ADA deficiency accounts for some 15 percent of SCID cases.

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NIH researchers restore children's immune systems with refinements in gene therapy

Recommendation and review posted by Bethany Smith

Public release date: 11-Sep-2012 [ | E-mail | Share ]

Contact: Claire Gwayi-Chore cgwayi-chore@hematology.org 202-776-0544 American Society of Hematology

By including chemotherapy as a conditioning regimen prior to treatment, researchers have developed a refined gene therapy approach that safely and effectively restores the immune system of children with a form of severe combined immunodeficiency (SCID), according to a study published online today in Blood, the Journal of the American Society of Hematology (ASH).

SCID is a group of rare and debilitating genetic disorders that affect the normal development of the immune system in newborns. Infants with SCID are prone to serious, life-threatening infections within the first few months of life and require extensive treatment for survival beyond infancy.

Adenosine deaminase (ADA) deficiency, which accounts for approximately 15 percent of all SCID cases, develops when a gene mutation prohibits the production of ADA, an enzyme that breaks down toxic molecules that can accumulate to harmful levels and kill lymphocytes, the specialized white blood cells that help make up the immune system. In its absence, infants with ADA-deficient SCID lack almost all immune defenses and their condition is almost always fatal within two years if left untreated. Standard treatment for ADA-deficient SCID is a hematopoietic stem cell transplant (HSCT) from a sibling or related donor; however, finding a matched donor can be difficult and transplants can carry significant risks. An alternate treatment method, enzyme replacement therapy (ERT), involves regular injections of the ADA enzyme to maintain the immune system and can help restore immune function; however, the treatments are extremely expensive and painful for the young patients and the effects are often only temporary.

Given the limitations of HSCT and ERT, in the 1990s researchers began investigating the efficacy of gene therapy for ADA-deficient SCID. They discovered that they could "correct" the function of a mutated gene by adding a healthy copy into the cells of the body that help fight infectious diseases. Since then, there have been significant advances in gene therapy for SCID, yet successful gene therapy in patients with ADA-deficient SCID has been seen in only a small series of children due to the difficulty of introducing a healthy ADA gene into bone marrow stem cells and to engraft these cells back into the patients.

"Although the basic steps of gene therapy for patients with SCID have been known for a while, technical and clinical challenges still exist and we wanted to find an optimized gene therapy protocol to restore immunity for young children with ADA-deficient SCID," said Fabio Candotti, MD, one of the study's senior authors, senior investigator in the Genetics and Molecular Biology Branch of the National Human Genome Research Institute at the National Institutes of Health, and chair of the ASH Scientific Committee on Immunology and Host Defense.

To determine whether an enhanced gene therapy approach would improve immunity in children with ADA-deficient SCID, the teams of Dr. Candotti and Donald B. Kohn, MD, director of the Human Gene Medicine Program at the University of California, Los Angeles (UCLA), Professor of Pediatrics and of Microbiology, Immunology, and Molecular Genetics, and a member of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA, conducted a clinical trial in 10 patients with the disorder. For the first time, Drs. Candotti and Kohn and their team of investigators compared two different retroviral vectors, MND-ADA and GCsapM-ADA, to transport normal ADA genes into the young patients' bone marrow stem cells as well as two different treatment plans in preparation for receiving gene therapy. Following therapy, investigators found that more bone marrow stem cells were marked with the MND-ADA vector, demonstrating its superiority over the GCsapM-ADA vector.

The investigators also sought to determine whether providing a low dose of chemotherapy prior to gene therapy, known as a pre-transplant conditioning regimen, would successfully deplete the young patients' bone marrow stem cells and make room for gene-corrected stem cells. In four patients, gene therapy was performed without chemotherapy, and the patients remained on ERT throughout the entire procedure to evaluate the efficiency of ERT combined with gene therapy. While these patients did not experience any adverse effects, they also did not experience a significant increase in their levels of the ADA enzyme. They also maintained low absolute lymphocyte counts (ALC) and minimal immune system function, leading the researchers to believe that ERT may weaken the therapy's effect by diluting the number of gene-corrected lymphocytes.

The remaining six patients were treated with the chemotherapy drug busulfan prior to gene therapy and ERT was discontinued prior to the gene therapy procedure. A significant increase in ADA was observed in all six patients; half of them remain off of ERT with partial immune reconstitution findings that support results from prior trials in Italy and the United Kingdom using chemotherapy prior to gene therapy and discontinuting ERT. While the ALC of all six patients declined sharply in the first few months due to combined effects of busulfan administration and ERT withdrawal, their counts increased from six to 24 months, even in the three patients that remained off of ERT. After adjusting the chemotherapy dosage, investigators were able to determine an optimal level for enhancing the efficacy of the gene-therapy-corrected cells with minimal toxicity.

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Researchers improve gene therapy technique for children with immune disorder

Recommendation and review posted by Bethany Smith

ScienceDaily (Sep. 11, 2012) By including chemotherapy as a conditioning regimen prior to treatment, researchers have developed a refined gene therapy approach that safely and effectively restores the immune system of children with a form of severe combined immunodeficiency (SCID), according to a study published online September 11 in Blood, the Journal of the American Society of Hematology (ASH).

SCID is a group of rare and debilitating genetic disorders that affect the normal development of the immune system in newborns. Infants with SCID are prone to serious, life-threatening infections within the first few months of life and require extensive treatment for survival beyond infancy.

Adenosine deaminase (ADA) deficiency, which accounts for approximately 15 percent of all SCID cases, develops when a gene mutation prohibits the production of ADA, an enzyme that breaks down toxic molecules that can accumulate to harmful levels and kill lymphocytes, the specialized white blood cells that help make up the immune system. In its absence, infants with ADA-deficient SCID lack almost all immune defenses and their condition is almost always fatal within two years if left untreated. Standard treatment for ADA-deficient SCID is a hematopoietic stem cell transplant (HSCT) from a sibling or related donor; however, finding a matched donor can be difficult and transplants can carry significant risks. An alternate treatment method, enzyme replacement therapy (ERT), involves regular injections of the ADA enzyme to maintain the immune system and can help restore immune function; however, the treatments are extremely expensive and painful for the young patients and the effects are often only temporary.

Given the limitations of HSCT and ERT, in the 1990s researchers began investigating the efficacy of gene therapy for ADA-deficient SCID. They discovered that they could "correct" the function of a mutated gene by adding a healthy copy into the cells of the body that help fight infectious diseases. Since then, there have been significant advances in gene therapy for SCID, yet successful gene therapy in patients with ADA-deficient SCID has been seen in only a small series of children due to the difficulty of introducing a healthy ADA gene into bone marrow stem cells and to engraft these cells back into the patients.

"Although the basic steps of gene therapy for patients with SCID have been known for a while, technical and clinical challenges still exist and we wanted to find an optimized gene therapy protocol to restore immunity for young children with ADA-deficient SCID," said Fabio Candotti, MD, one of the study's senior authors, senior investigator in the Genetics and Molecular Biology Branch of the National Human Genome Research Institute at the National Institutes of Health, and chair of the ASH Scientific Committee on Immunology and Host Defense.

To determine whether an enhanced gene therapy approach would improve immunity in children with ADA-deficient SCID, the teams of Dr. Candotti and Donald B. Kohn, MD, director of the Human Gene Medicine Program at the University of California, Los Angeles (UCLA), Professor of Pediatrics and of Microbiology, Immunology, and Molecular Genetics, and a member of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA, conducted a clinical trial in 10 patients with the disorder. For the first time, Drs. Candotti and Kohn and their team of investigators compared two different retroviral vectors, MND-ADA and GCsapM-ADA, to transport normal ADA genes into the young patients' bone marrow stem cells as well as two different treatment plans in preparation for receiving gene therapy. Following therapy, investigators found that more bone marrow stem cells were marked with the MND-ADA vector, demonstrating its superiority over the GCsapM-ADA vector.

The investigators also sought to determine whether providing a low dose of chemotherapy prior to gene therapy, known as a pre-transplant conditioning regimen, would successfully deplete the young patients' bone marrow stem cells and make room for gene-corrected stem cells. In four patients, gene therapy was performed without chemotherapy, and the patients remained on ERT throughout the entire procedure to evaluate the efficiency of ERT combined with gene therapy. While these patients did not experience any adverse effects, they also did not experience a significant increase in their levels of the ADA enzyme. They also maintained low absolute lymphocyte counts (ALC) and minimal immune system function, leading the researchers to believe that ERT may weaken the therapy's effect by diluting the number of gene-corrected lymphocytes.

The remaining six patients were treated with the chemotherapy drug busulfan prior to gene therapy and ERT was discontinued prior to the gene therapy procedure. A significant increase in ADA was observed in all six patients; half of them remain off of ERT with partial immune reconstitution -- findings that support results from prior trials in Italy and the United Kingdom using chemotherapy prior to gene therapy and discontinuting ERT. While the ALC of all six patients declined sharply in the first few months due to combined effects of busulfan administration and ERT withdrawal, their counts increased from six to 24 months, even in the three patients that remained off of ERT. After adjusting the chemotherapy dosage, investigators were able to determine an optimal level for enhancing the efficacy of the gene-therapy-corrected cells with minimal toxicity.

This study is the first to detail comparisons of ADA-deficient SCID patient outcomes between those treated with gene therapy who have not received pre-transplant conditioning while continuing to receive ERT with those receiving pre-transplant conditioning without the administration of ERT. This study is also the first to compare two different viral vectors to transport normal ADA genes into patient bone marrow.

"We were very happy that in this trial we were able to see a benefit in the patients after we modified the protocol," said Dr. Kohn. "Doctors treating ADA-deficient SCID have had too few options for too long, and we hope this will provide them with an efficient and effective treatment for this devastating disease."

Read the rest here:
Gene therapy technique for children with immune disorder improved

Recommendation and review posted by Bethany Smith

ScienceDaily (Sep. 11, 2012) UCLA stem cell researchers have found that a gene therapy regimen can safely restore immune systems to children with so-called "Bubble Boy" disease, a life threatening condition that if left untreated can be fatal within one to two years.

In the 11-year study, researchers were able to test two therapy regimens for 10 children with ADA-deficient severe combined immunodeficiency (SCID). During the study, they refined their approach to include a light dose of chemotherapy to help remove many of the blood stem cells in the bone marrow that are not creating an enzyme called adenosine deaminase (ADA), which is critical for the production and survival of healthy white blood cells, said study senior Dr. Donald Kohn, a professor of pediatrics and of microbiology, immunology, and molecular genetics in Life Sciences and a member of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA.

The refined gene therapy and chemotherapy regimen proved superior to the other method tested in the study, restoring immune function to three of the six children who received it, Kohn said. Going forward, an even further refined regimen using a different type of virus delivery system will be studied in the next phase of the study, which already has enrolled eight of the 10 patients needed.

The study appears Aug. 30 in the advance online issue of the peer-reviewed journal Blood.

"We were very happy that in the human trials we were able to see a benefit in the patients after we modified the protocol," Kohn said. "Doctors treating ADA-deficient SCID have had too few options for too long, and we hope this will provide them with an efficient and effective treatment for this devastating disease."

Children born with SCID, an inherited immunodeficiency, are generally diagnosed at about six months. They are extremely vulnerable to infectious diseases and don't grow well. Chronic diarrhea, ear infections, recurrent pneumonia and profuse oral candidiasis commonly occur in these children. SCID cases occur in about 1 of 100,000 births

Currently, the only treatment for ADA-deficient SCID calls for injecting the patients twice a week with the necessary enzyme, Kohn said, a life-long process that is very expensive and often doesn't return the immune system to optimal levels. These patients also can undergo bone marrow transplants from matched siblings, but matches can be very rare.

About 15 percent of all SCID patients are ADA-deficient. Kohn and his team used a virus delivery system that he had developed in his lab in the 1990s to restore the gene that produces the missing enzyme necessary for a healthy immune system. To date, about 40 children with SCID have received gene therapy in clinical trials around the world, Kohn said.

Two slightly different viral vectors were tested in the study, each modified to deliver healthy ADA genes into the bone marrow cells of the patients so the needed enzyme could be produced and make up for the cells that don't have the gene. Four of the 10 patients in the study remained on their enzyme replacement therapy during the gene therapy study. There were no side effects, but their immune systems were not sufficiently restored, Kohn said.

In the next six patients, the enzyme therapy was stopped and a small dose of chemotherapy was given before starting the gene therapy to deplete the ADA-deficient stem cells in their bone marrow. Of those patients, half had their immune systems restored. The human findings confirmed another study, also published recently in Blood by Kohn and UCLA colleague Dr. Denise Carbonaro-Sarracino, which tested the techniques in parallel, using a mouse model of ADA-deficient SCID.

Read more here:
Stem cell researchers use gene therapy to restore immune systems in 'Bubble Boy' disease

Recommendation and review posted by simmons

Public release date: 11-Sep-2012 [ | E-mail | Share ]

Contact: Kim Irwin kirwin@mednet.ucla.edu 310-435-9457 University of California - Los Angeles Health Sciences

UCLA stem cell researchers have found that a gene therapy regimen can safely restore immune systems to children with so-called "Bubble Boy" disease, a life threatening condition that if left untreated can be fatal within one to two years.

In the 11-year study, researchers were able to test two therapy regimens for 10 children with ADA-deficient severe combined immunodeficiency (SCID). During the study, they refined their approach to include a light dose of chemotherapy to help remove many of the blood stem cells in the bone marrow that are not creating an enzyme called adenosine deaminase (ADA), which is critical for the production and survival of healthy white blood cells, said study senior Dr. Donald Kohn, a professor of pediatrics and of microbiology, immunology, and molecular genetics in Life Sciences and a member of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA.

The refined gene therapy and chemotherapy regimen proved superior to the other method tested in the study, restoring immune function to three of the six children who received it, Kohn said. Going forward, an even further refined regimen using a different type of virus delivery system will be studied in the next phase of the study, which already has enrolled eight of the 10 patients needed.

The study appears Aug. 30 in the advance online issue of the peer-reviewed journal Blood.

"We were very happy that in the human trials we were able to see a benefit in the patients after we modified the protocol," Kohn said. "Doctors treating ADA-deficient SCID have had too few options for too long, and we hope this will provide them with an efficient and effective treatment for this devastating disease."

Children born with SCID, an inherited immunodeficiency, are generally diagnosed at about six months. They are extremely vulnerable to infectious diseases and don't grow well. Chronic diarrhea, ear infections, recurrent pneumonia and profuse oral candidiasis commonly occur in these children. SCID cases occur in about 1 of 100,000 births

Currently, the only treatment for ADA-deficient SCID calls for injecting the patients twice a week with the necessary enzyme, Kohn said, a life-long process that is very expensive and often doesn't return the immune system to optimal levels. These patients also can undergo bone marrow transplants from matched siblings, but matches can be very rare.

About 15 percent of all SCID patients are ADA-deficient. Kohn and his team used a virus delivery system that he had developed in his lab in the 1990s to restore the gene that produces the missing enzyme necessary for a healthy immune system. To date, about 40 children with SCID have received gene therapy in clinical trials around the world, Kohn said.

Continued here:
UCLA stem cell researchers use gene therapy to restore immune systems in 'bubble babies'

Recommendation and review posted by simmons

Public release date: 10-Sep-2012 [ | E-mail | Share ]

Contact: Bill Seiler bseiler@umm.edu 410-328-8919 University of Maryland Medical Center

Baltimore, MD September 10, 2012 Researchers at the University of Maryland School of Medicine, who are exploring novel ways to treat serious heart problems in children, have conducted the first direct comparison of the regenerative abilities of neonatal and adult-derived human cardiac stem cells. Among their findings: cardiac stem cells (CSCs) from newborns have a three-fold ability to restore heart function to nearly normal levels compared with adult CSCs. Further, in animal models of heart attack, hearts treated with neonatal stem cells pumped stronger than those given adult cells. The study is published in the September 11, 2012, issue of Circulation.

"The surprising finding is that the cells from neonates are extremely regenerative and perform better than adult stem cells," says the study's senor author, Sunjay Kaushal, M.D., Ph.D., associate professor of surgery at the University of Maryland School of Medicine and director, pediatric cardiac surgery at the University of Maryland Medical Center. "We are extremely excited and hopeful that this new cell-based therapy can play an important role in the treatment of children with congenital heart disease, many of whom don't have other options."

Dr. Kaushal envisions cellular therapy as either a stand-alone therapy for children with heart failure or an adjunct to medical and surgical treatments. While surgery can provide structural relief for some patients with congenital heart disease and medicine can boost heart function up to two percent, he says cellular therapy may improve heart function even more dramatically. "We're looking at this type of therapy to improve heart function in children by 10, 12, or 15 percent. This will be a quantum leap in heart function improvement."

Heart failure in children, as in adults, has been on the rise in the past decade and the prognosis for patients hospitalized with heart failure remains poor. In contrast to adults, Dr. Kaushal says heart failure in children is typically the result of a constellation of problems: reduced cardiac blood flow; weakening and enlargement of the heart; and various congenital malformations. Recent research has shown that several types of cardiac stem cells can help the heart repair itself, essentially reversing the theory that a broken heart cannot be mended.

Stem cells are unspecialized cells that can become tissue- or organ-specific cells with a particular function. In a process called differentiation, cardiac stem cells may develop into rhythmically contracting muscle cells, smooth muscle cells or endothelial cells. Stem cells in the heart may also secrete growth factors conducive to forming heart muscle and keeping the muscle from dying.

To conduct the study, researchers obtained a small amount of heart tissue during normal cardiac surgery from 43 neonates and 13 adults. The cells were expanded in a growth medium yielding millions of cells. The researchers developed a consistent way to isolate and grow neonatal stem cells from as little as 20 milligrams of heart tissue. Adult and neonate stem cell activity was observed both in the laboratory and in animal models. In addition, the animal models were compared to controls that were not given the stem cells.

Dr. Kaushal says it is not clear why the neonatal stem cells performed so well. One explanation hinges on sheer numbers: there are many more stem cells in a baby's heart than in the adult heart. Another explanation: neonate-derived cells release more growth factors that trigger blood vessel development and/or preservation than adult cells.

"This research provides an important link in our quest to understand how stem cells function and how they can best be applied to cure disease and correct medical deficiencies," says E. Albert Reece, M.D., Ph.D., M.B.A., vice president for medical affairs, University of Maryland; the John Z. and Akiko K. Bowers Distinguished Professor; and dean, University of Maryland School of Medicine. "Sometimes simple science is the best science. In this case, a basic, comparative study has revealed in stark terms the powerful regenerative qualities of neonatal cardiac stem cells, heretofore unknown."

Read more here:
University of Maryland study: Neonatal heart stem cells may help mend kids' broken hearts

Recommendation and review posted by Bethany Smith

MULTIMEDIA ALERT: Video resources, including an interview with Dr. Crawford, are available for journalists at the Mayo Clinic News Network.

Newswise JACKSONVILLE, Fla. More than a cancer-causing gene is needed to trigger pancreatic cancer, a study led by Mayo Clinic has found. A second factor creates a perfect storm that allows tumors to form, the researchers say. The study, published in the Sept. 10 issue of Cancer Cell, overturns the current belief that a mutation in the KRAS oncogene is enough to initiate pancreatic cancer and unrestrained cell growth.

The findings uncover critical clues on how pancreatic cancer develops and why few patients benefit from current therapies. The findings also provide ideas about how to improve treatment and prevention of pancreatic cancer.

The research team, led by Howard C. Crawford, Ph.D., a cancer biologist at Mayo Clinics campus in Florida, and Jens Siveke, M.D., at Technical University in Munich, Germany, found that for pancreatic cancer to form, mutated KRAS must recruit a second player: the epidermal growth factor receptor, or EGFR.A third genetic participant known as Trp53 makes pancreatic tumors very difficult to treat, the study showed.

The scientists also found that EGFR was required in pancreatic cancer initiated by pancreatic inflammation known as pancreatitis.

We believe the perfect storm needed to trigger pancreatic cancer include KRAS mutations and inflammation in the organ, which then work synergistically to turn on EGFR, says Dr. Crawford.

The bottom line is, without EGFR, tumors dont form and that was never known before this study, he says. We also think that inflammation in the pancreas has a big impact on turning on EGFR.

The researchers discovered that when they blocked EGFR activity, the mice studied were protected against developing chronic pancreatitis and pancreatic cancer.

They further found that in mice that had lost expression of the TP53 tumor suppressor a situation that mirrors up to 60 percent of human pancreatic cancer cases tumors escape the dependency on EGFR for initiation and continued growth of pancreatic cancer, Dr. Crawford says.

Pancreatic cancer is a highly lethal disease; no drug has been able to target the mutant KRAS protein. The study suggests some patients, such as those with chronic pancreatitis, may be good candidates for treatment with EGFR inhibitors to fight or prevent pancreatic cancer, Dr. Crawford says.

Read the original here:
Cancer-Causing Gene Alone Doesn't Trigger Pancreatic Cancer

Recommendation and review posted by Bethany Smith

Cardiac stem cells from newborns show stronger regenerative ability than adult stem cells

BALTIMORE, Sept. 10, 2012 /PRNewswire-USNewswire/ -- Researchers at the University of Maryland School of Medicine, who are exploring novel ways to treat serious heart problems in children, have conducted the first direct comparison of the regenerative abilities of neonatal and adult-derived human cardiac stem cells. Among their findings: cardiac stem cells (CSCs) from newborns have a three-fold ability to restore heart function to nearly normal levels compared with adult CSCs. Further, in animal models of heart attack, hearts treated with neonatal stem cells pumped stronger than those given adult cells. The study is published in the September 11, 2012, issue of Circulation.

"The surprising finding is that the cells from neonates are extremely regenerative and perform better than adult stem cells," says the study's senor author, Sunjay Kaushal, M.D., Ph.D., associate professor of surgery at the University of Maryland School of Medicine and director, pediatric cardiac surgery at the University of Maryland Medical Center. "We are extremely excited and hopeful that this new cell-based therapy can play an important role in the treatment of children with congenital heart disease, many of whom don't have other options."

Dr. Kaushal envisions cellular therapy as either a stand-alone therapy for children with heart failure or an adjunct to medical and surgical treatments. While surgery can provide structural relief for some patients with congenital heart disease and medicine can boost heart function up to two percent, he says cellular therapy may improve heart function even more dramatically. "We're looking at this type of therapy to improve heart function in children by 10, 12, or 15 percent. This will be a quantum leap in heart function improvement."

Heart failure in children, as in adults, has been on the rise in the past decade and the prognosis for patients hospitalized with heart failure remains poor. In contrast to adults, Dr. Kaushal says heart failure in children is typically the result of a constellation of problems: reduced cardiac blood flow; weakening and enlargement of the heart; and various congenital malformations. Recent research has shown that several types of cardiac stem cells can help the heart repair itself, essentially reversing the theory that a broken heart cannot be mended.

Stem cells are unspecialized cells that can become tissue- or organ-specific cells with a particular function. In a process called differentiation, cardiac stem cells may develop into rhythmically contracting muscle cells, smooth muscle cells or endothelial cells. Stem cells in the heart may also secrete growth factors conducive to forming heart muscle and keeping the muscle from dying.

To conduct the study, researchers obtained a small amount of heart tissue during normal cardiac surgery from 43 neonates and 13 adults. The cells were expanded in a growth medium yielding millions of cells. The researchers developed a consistent way to isolate and grow neonatal stem cells from as little as 20 milligrams of heart tissue. Adult and neonate stem cell activity was observed both in the laboratory and in animal models. In addition, the animal models were compared to controls that were not given the stem cells.

Dr. Kaushal says it is not clear why the neonatal stem cells performed so well. One explanation hinges on sheer numbers: there are many more stem cells in a baby's heart than in the adult heart. Another explanation: neonate-derived cells release more growth factors that trigger blood vessel development and/or preservation than adult cells.

Go here to see the original:
University of Maryland Study Suggests Neonatal Cardiac Stem Cells May Help Mend Children's Broken Hearts

Recommendation and review posted by Bethany Smith

London, Sep 10:

Ladies, you may not have to depend upon painful Botox injections and expensive cosmetic surgery for long to look young.

A British firm is trialling a new natural method which involves injecting the patients own stem cells to restore skins youthful elasticity.

Researchers believe they will spur the growth of new skin cells, called fibroblasts, which make the elastic ingredient collagen which is produced in large quantities when we are young, but declines as we age, the Daily Mail reported.

The company Pharmacells, based in Glasgow, plans to begin clinical trials in 12 months, using stem cells harvested from a blood sample from the patients.

They believe the procedure could be commercially available in just three years, potentially revolutionising the market for anti-ageing treatments.

By using the bodys own cells, it is billed as a more natural approach to reducing the signs of ageing than Botox, a chemical which freezes the facial muscles to smooth wrinkles.

The company has licensed the technology to harvest a new type of stem cell called a blastomere-like stem cell (CORR) which is found circulating in the blood.

Like other types of stem cells, it is unspecialised and can develop into many other types of cell in the human body such as a liver, brain or skin cell.

The advantage of this particular one it is available in very large doses from one blood sample.

Originally posted here:
Soon a stem cell jabs to end wrinkles

Recommendation and review posted by Bethany Smith

British firm is trialling new method by injecting patient's own stem cells to restore skin's youthful elasticity

By Tamara Cohen

PUBLISHED: 10:40 EST, 9 September 2012 | UPDATED: 02:12 EST, 10 September 2012

Scientists will begin clinical trials in 12 months, using stem cells harvested from a blood sample from the patients

Scientists are working on a new weapon in the war against wrinkles.

There are not many things women have not tried in the quest for a youthful complexion from lotions and potions to Botox and cosmetic surgery.

But a British firm is trialling a new method which involves injecting the patients own stem cells to restore skins youthful elasticity.

Researchers believe they will spur the growth of new skin cells, called fibroblasts, which make the elastic ingredient collagen which is produced in large quantities when we are young, but declines as we age.

The company Pharmacells, based in Glasgow, plan to begin clinical trials in 12 months, using stem cells harvested from a blood sample from the patients.

They believe the procedure could be commercially available in just three years, potentially revolutionising the market for anti-ageing treatments.

Read the original post:
Could this stem cell cure for wrinkles end the endless hunt for the perfect skin cream?

Recommendation and review posted by Bethany Smith

TORONTO, Sept. 10, 2012 /CNW/ - Sigmacon Skin Sciences announced it is the exclusive Canadian distributor of Stemulation, a luxury skin care line that uses the healing power of human stem cells to combat wrinkles and other signs of aging.

Stemulation is based on the science that stem cells can be effectively used for skin rejuvenation, tissue repair and wound healing. A research team of specialists spent two years capturing growth factors from adult human skin cells, which they turned into an active ingredient and the basis for Stemulation products. These growth factors stimulate collagen and the reproduction of new skin cells to reduce wrinkles, eliminate sun spots and smooth scars and fine lines. It truly is a groundbreaking (and technology-backed) new way to achieve younger-looking skin!

The Stemulation line includes a serum, cleanser, exfoliant and face and body creams. The line will be sold through select doctors, estheticians and medical spas.

ABOUT Sigmacon Skin Sciences is the national distributor of a comprehensive set of performance skin care products with dedicated product specialists and trainings all across Canada. Our product lines include professional treatments, sun protection products and results-oriented home care. Sigmacon is also the distributor of advanced medical and aesthetic devices. Visit http://www.skinsciences.ca to learn more.

Image with caption: "The Future of Skin Care: Stemulation Facial Serum and Boost Crme used over 1 year. (CNW Group/Sigmacon Skin Sciences)". Image available at: http://photos.newswire.ca/images/download/20120910_C3135_PHOTO_EN_17420.jpg

Link:
Introducing Canadians to a whole new way to treat aging skin: Stemulation

Recommendation and review posted by Bethany Smith

Public release date: 10-Sep-2012 [ | E-mail | Share ]

Contact: Kevin Punsky punsky.kevin@mayo.edu 904-953-2299 Mayo Clinic

JACKSONVILLE, Fla. More than a cancer-causing gene is needed to trigger pancreatic cancer, a study led by Mayo Clinic has found. A second factor creates a "perfect storm" that allows tumors to form, the researchers say. The study, published in the Sept. 10 issue of Cancer Cell, overturns the current belief that a mutation in the KRAS oncogene is enough to initiate pancreatic cancer and unrestrained cell growth.

The findings uncover critical clues on how pancreatic cancer develops and why few patients benefit from current therapies. The findings also provide ideas about how to improve treatment and prevention of pancreatic cancer.

The research team, led by Howard C. Crawford, Ph.D., a cancer biologist at Mayo Clinic's campus in Florida, and Jens Siveke, M.D., at Technical University in Munich, Germany, found that for pancreatic cancer to form, mutated KRAS must recruit a second player: the epidermal growth factor receptor, or EGFR.A third genetic participant known as Trp53 makes pancreatic tumors very difficult to treat, the study showed.

The scientists also found that EGFR was required in pancreatic cancer initiated by pancreatic inflammation known as pancreatitis.

"We believe the perfect storm needed to trigger pancreatic cancer include KRAS mutations and inflammation in the organ, which then work synergistically to turn on EGFR," says Dr. Crawford.

"The bottom line is, without EGFR, tumors don't form and that was never known before this study," he says. "We also think that inflammation in the pancreas has a big impact on turning on EGFR."

The researchers discovered that when they blocked EGFR activity, the mice studied were protected against developing chronic pancreatitis and pancreatic cancer.

They further found that in mice that had lost expression of the TP53 tumor suppressor a situation that mirrors up to 60 percent of human pancreatic cancer cases tumors escape the dependency on EGFR for initiation and continued growth of pancreatic cancer, Dr. Crawford says.

View post:
Cancer-causing gene alone doesn't trigger pancreatic cancer, Mayo-led study finds

Recommendation and review posted by Bethany Smith

Public release date: 10-Sep-2012 [ | E-mail | Share ]

Contact: Nicole Fawcett nfawcett@umich.edu 734-764-2220 University of Michigan Health System

This press release is available in Portuguese.

ANN ARBOR, Mich. Two different genetic mutations cooperate to induce adrenal cancer, according to a new study from researchers at the University of Michigan Comprehensive Cancer Center and University of Sao Paulo in Brazil.

The finding provides new clues to this rare and deadly cancer type, and researchers hope it will lead to better treatments by targeting both mutations.

About 600 Americans are diagnosed with adrenal cancer per year. It is typically diagnosed in late stages when there is nearly no chance of survival beyond five years.

"Because adrenal cancer is so rare, it has been challenging to find enough patients who can provide tissue samples for research. Only through collaboration can we do this," says senior study author Gary Hammer, M.D., Ph.D., the Millie Schembechler Professor of Adrenal Cancer at the University of Michigan Comprehensive Cancer Center.

The partnership between U-M and Sao Paulo has allowed researchers to collect tissue samples from 118 people with benign or cancerous adrenal tumors.

"Our goal is to understand these tumors and the genes that are critical lynchpins so that we can develop treatments that extend patients' lives," Hammer says.

By studying both benign and cancerous adrenal tissue samples, the researchers found aberrations in two genetic pathways: beta-catenin and insulin-like growth factor 2, or IGF-2. The benign tumors had a high percentage of mutations in beta-catenin, but IGF2 up-regulation was rare. On the other hand, most of the adrenal cancers exhibited IGF-2 up-regulation. Cancers that also had beta-catenin mutation were associated with high-grade disease and worse survival, compared to tumors with only IGF-2 up-regulation.

The rest is here:
Researchers find 2 gene mutations drive adrenal cancer

Recommendation and review posted by Bethany Smith

ScienceDaily (Sep. 10, 2012) Two different genetic mutations cooperate to induce adrenal cancer, according to a new study from researchers at the University of Michigan Comprehensive Cancer Center and University of Sao Paulo in Brazil.

The finding provides new clues to this rare and deadly cancer type, and researchers hope it will lead to better treatments by targeting both mutations.

About 600 Americans are diagnosed with adrenal cancer per year. It is typically diagnosed in late stages when there is nearly no chance of survival beyond five years.

"Because adrenal cancer is so rare, it has been challenging to find enough patients who can provide tissue samples for research. Only through collaboration can we do this," says senior study author Gary Hammer, M.D., Ph.D., the Millie Schembechler Professor of Adrenal Cancer at the University of Michigan Comprehensive Cancer Center.

The partnership between U-M and Sao Paulo has allowed researchers to collect tissue samples from 118 people with benign or cancerous adrenal tumors.

"Our goal is to understand these tumors and the genes that are critical lynchpins so that we can develop treatments that extend patients' lives," Hammer says.

By studying both benign and cancerous adrenal tissue samples, the researchers found aberrations in two genetic pathways: beta-catenin and insulin-like growth factor 2, or IGF-2. The benign tumors had a high percentage of mutations in beta-catenin, but IGF2 up-regulation was rare. On the other hand, most of the adrenal cancers exhibited IGF-2 up-regulation. Cancers that also had beta-catenin mutation were associated with high-grade disease and worse survival, compared to tumors with only IGF-2 up-regulation.

The researchers additionally tested this finding experimentally by inducing individual or combined mutations in beta-catenin and IGF-2 in the mouse adrenal. The mice developed cancer only when both mutations were present.

Results of the study appear in the September issue of the American Journal of Pathology.

The next step is to develop treatments that block both beta-catenin and IGF2.

Read more:
Two gene mutations drive adrenal cancer

Recommendation and review posted by Bethany Smith

ScienceDaily (Sep. 10, 2012) More than a cancer-causing gene is needed to trigger pancreatic cancer, a study led by Mayo Clinic has found. A second factor creates a "perfect storm" that allows tumors to form, the researchers say. The study, published in the Sept. 10 issue of Cancer Cell, overturns the current belief that a mutation in the KRAS oncogene is enough to initiate pancreatic cancer and unrestrained cell growth.

The findings uncover critical clues on how pancreatic cancer develops and why few patients benefit from current therapies. The findings also provide ideas about how to improve treatment and prevention of pancreatic cancer.

The research team, led by Howard C. Crawford, Ph.D., a cancer biologist at Mayo Clinic's campus in Florida, and Jens Siveke, M.D., at Technical University in Munich, Germany, found that for pancreatic cancer to form, mutated KRAS must recruit a second player: the epidermal growth factor receptor, or EGFR.A third genetic participant known as Trp53 makes pancreatic tumors very difficult to treat, the study showed.

The scientists also found that EGFR was required in pancreatic cancer initiated by pancreatic inflammation known as pancreatitis.

"We believe the perfect storm needed to trigger pancreatic cancer include KRAS mutations and inflammation in the organ, which then work synergistically to turn on EGFR," says Dr. Crawford.

"The bottom line is, without EGFR, tumors don't form -- and that was never known before this study," he says. "We also think that inflammation in the pancreas has a big impact on turning on EGFR."

The researchers discovered that when they blocked EGFR activity, the mice studied were protected against developing chronic pancreatitis and pancreatic cancer.

They further found that in mice that had lost expression of the TP53 tumor suppressor -- a situation that mirrors up to 60 percent of human pancreatic cancer cases -- tumors escape the dependency on EGFR for initiation and continued growth of pancreatic cancer, Dr. Crawford says.

Pancreatic cancer is a highly lethal disease; no drug has been able to target the mutant KRAS protein. The study suggests some patients, such as those with chronic pancreatitis, may be good candidates for treatment with EGFR inhibitors to fight or prevent pancreatic cancer, Dr. Crawford says.

"The clinical implications of this study are exciting. It suggests that pancreatic cancer patients with normal p53 activity, as well as patients with chronic pancreatitis, may be good candidates for treatment with EGFR inhibitors," Dr. Crawford says.

See the rest here:
Cancer-causing gene alone doesn’t trigger pancreatic cancer, research finds

Recommendation and review posted by Bethany Smith

CPG manufacturers may be on the cusp of monumental change as voters in California contemplate a hotly contested ballot initiative to require labeling of genetically modified foods.

Food marketers will face tough choices should the measure pass, as about 70% of processed foods sold in supermarkets contain GM ingredients like corn and soy. Some estimate that 100,000 or more foods sold in California contain some level of GE ingredients and would therefore be affected.

The mandate would be limited to the Golden State, but the implications for companies that choose not to move away from GM ingredients in advance of the July 1, 2014, deadline could be as far-reaching as consumer awareness spreads.

While the government deems genetically modified organisms safe, Californians want to judge for themselves. A Pepperdine University poll found that if the election were held last month, Californians would pass the proposition by a 3-1 margin.

To avoid the partially produced with genetic engineering label and possible consumer backlash, suppliers will likely reformulate product with more costly non-GE foods or organic ingredients, just as theyve done in countries where genetic modification disclosure is required.

Read more: Prop 37 Battle Rages in California

A recent study commissioned by the No on 37, Stop the Deceptive Food Labeling Scheme campaign, of which the Grocery Manufacturers Association is a chief sponsor, bears this out.

It projects that reformulations to non-GE and organic ingredients, which by law cannot be genetically modified, will be the most likely course taken by food producers.

Read more: California GMO Bill Is Top Priority for GMA

Retailers might also adjust their sourcing policies to gain consumer favor by incorporating more organic foods and those that have been verified under the Non-GMO Project and labeled with its seal.

See the original post:
Mandatory GM Labeling Would Require Major Change

Recommendation and review posted by Bethany Smith