Cord Blood Stem Cell Therapy and Cord Blood Banking in Thailand UCB Cells
Cord blood refers to blood left in the umbilical cord after birth. More:http://stemcellthailand.org/cord-blood-stem-cell-therapy-ucb-banking/ Back in the day...

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Cord Blood Stem Cell Therapy and Cord Blood Banking in Thailand UCB Cells - Video

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The Doctors - Stem Cell Therapy For Red The Dog
Stemcellvet.co.uk offer adipose derived Stem Cell Therapy for pets in the UK. We treat cats and dogs predominantly for arthritis but there is also the potent...

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The Doctors - Stem Cell Therapy For Red The Dog - Video

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Dr Jamal A Khan holds PC for #39;Dentroitic Cell Therapy #39;

By: Bollywood Royal

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Dr Jamal A Khan holds PC for 'Dentroitic Cell Therapy' - Video

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Washington, Sept. 10 (ANI): Researchers have developed a therapy that could dramatically slow the onset and progression of the Lou Gehrig's disease.

The researchers, led by teams from The Research Institute at Nationwide Children's Hospital and the Ludwig Institute at the University of California, San Diego, found a survival increase of up to 39 percent in animal models with a one-time treatment, a crucial step toward moving the therapy into human clinical trials.

The therapy reduces expression of a gene called SOD1, which in some cases of familial amyotrophic lateral sclerosis (ALS) has a mutation that weakens and kills nerve cells called motor neurons that control muscle movement.

While many drug studies involve only one type of animal model, this effort included analysis in two different models treated before and after disease onset.

Brian Kaspar, PhD, a principal investigator in the Center for Gene Therapy at Nationwide Children's and a senior author on the research, said that they designed these rigorous studies using two different models of the disease with the experimenters blinded to the treatment and in two separate laboratories.

Ideally, a therapy would hit motor neurons and astrocytes equally hard. The best way to do that is to deliver the drug directly into the cerebrospinal fluid (CSF), which would reduce the amount of SOD1 suppression in cells outside the brain and reduce immune system exposure to AAV9-elements that would add weight to an argument for studying the drug in humans.

Injections directly into CSF cannot be done easily in mice, so the team took the study a crucial step further by injecting AAV9-SOD1-shRNA into the CSF of healthy nonhuman primates.

The results were just as the team hoped-the amount of gene expression dropped by as much as 90 percent in motor neurons and nearly 70 percent in astrocytes and no side effects were reported, laying the groundwork towards moving to human clinical trials.

The study has been published online in Molecular Therapy. (ANI)

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New therapy could help slow down progression of Lou Gehrig's disease

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Latest Diet & Weight Management News

FRIDAY, Sept. 6 (HealthDay News) -- Genetic testing for obesity risk does not discourage people from trying to lose weight -- instead, it may help reduce how much they blame themselves for their weight problems, according to a small new study.

Research has shown that genes influence a person's risk of becoming overweight and one gene, called FTO, appears to have the greatest effect. The "A" variant of the gene is associated with a greater risk of weight gain, while the "T" variant of the gene is associated with a lower risk.

One in two people has at least one copy of the A variant. People with two A variants -- one from their mother and one from their father -- are 70 percent more likely to become obese than those with two T variants, according to the study authors at University College London (UCL).

Researchers have access to a genetic test for FTO variants, but the test is not commercially available. Among experts, there's debate about how people would react to getting results of the FTO genetic test. Some believe that such knowledge would help motivate people to manage their weight, while others think it would make people feel there was nothing they could do about their weight.

In this study, researchers assessed how 18 people responded to having the FTO genetic test. The male and female participants, who ranged in weight from underweight to obese, were enthusiastic about getting their genetic test results, according to the study in a recent issue of the Journal of Genetic Counseling.

People who struggled with their weight said the knowledge was helpful because it reduced some of the emotional stress associated with weight control and eased some of the stigma and self-blame. None of the participants had a negative reaction to the genetic test result, nor did they say it made them feel like there was nothing they could do about their weight.

"These results are encouraging. Regardless of gene status or weight, all the volunteers recognized that both genes and behavior are important for weight control. The results indicate that people are unlikely to believe that genes are destiny and stop engaging with weight control once they know their FTO status," study leader Susanne Meisel said in a UCL news release.

"Although they knew that FTO's effect is only small, they found it motivating and informative. We are now doing a larger study to confirm whether more people react in the same way," Meisel added.

Heredity alone doesn't determine obesity, another expert noted.

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Obesity Gene Tests May Not Hamper Weight-Loss Efforts

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Rensselaer

Notions of the Capital Region as a scientific Smallbany frustrate Douglas Conklin.

In the University at Albany Cancer Research Center a 9-year-old building that the associate professor blithely termed "Joe Bruno pork" Conklin and his team have earned a patent for identifying a gene as a possible target for breast cancer drugs. The gene has been known as the cause of another disease an immune disorder affecting mostly men.

The patent is the result of years of effort casting a broad net to understand how breast cancer invades a woman's body, experimenting, watching and waiting until "the breast cancer cells tell us what's important to them," as Conklin put it.

The work is no different from that going on at research centers with international reputations, he said.

"It cheeses me off to no end, when somebody (local) says, 'We're collecting money for St. Jude's hospital,'" said Conklin, referring to the well-known children's cancer center in Memphis.

Conklin himself came to Albany by way of the Cold Spring Harbor Laboratory on Long Island, known for its groundbreaking work on DNA. (He does a mean impression of James Watson, the co-discoverer of DNA, who directed that lab.)

As blunt as he is in his opinions, Conklin is patient and plainspoken in explaining the complexities of breast cancer research conducted at his lab. His team of 10 scientists are engaged in multiple experiments connected by the common thread of breast cancer.

It was through manipulating the regulation of various genes turning one gene after another "off" to see how cells would function without it that they discovered breast cancer cells die when the Bruton's tyrosene kinase gene is silenced.

BTK is known for its role in X-linked agammaglobulinaemia, a rare immune deficiency disease that affects one in 200,000 newborns, according to the National Institutes of Health. A mutation in the gene destroys the body's immune system response, including the production of antibodies, making even slight infections dangerous. Because the BTK gene is on the X chromosome, women carry it and pass it along to children, but men are almost exclusively the victims.

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Quest to solve breast cancer

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Public release date: 9-Sep-2013 [ | E-mail | Share ]

Contact: Alison Barbuti alison.barbuti@manchester.ac.uk 44-016-127-58383 University of Manchester

Scientists at The University of Manchester and medical institutes in Italy have identified a gene variant that predisposes people to a special type of heart attack.

Their research, published in the International Journal of Cardiology could lead to the development of new drugs to treat the problem.

Dr Paolo Tammaro, who led the team, said: "Heart attacks happen when the blood supply to the heart is reduced by the narrowing or blocking of the coronary artery the vessel that supplies the heart with oxygen and nutrients. Often this is due to fatty deposits which narrow the vessel. However, in some people with perfectly clean arteries, the vessel suddenly constricts shutting off the blood supply. We have discovered that this process, known as vasospasm, can be associated with a rare variant of a particular gene."

Dr Enzo Emanuele, from the University of Pavia, who screened the patients, said: "We knew that this type of heart attack occurs in about 6% of patients and that many of them have a genetic predisposition, but we did not know the gene responsible. Now that it is identified it will be possible to predict who is at risk and to treat them accordingly."

The gene identified by the team encodes a protein termed KATP channel. This protein forms microscopic gated pores that allow potassium ions to move into and out of the cells, in this way giving rise to electrical impulses.

Dr Tammaro and research scientist Keith Smith, both based at the Faculty of Life Sciences at The University of Manchester, added: "These channels are abundant in the cells forming the wall of coronary arteries, and the electrical impulses they generate govern this artery's diameter. Due to the mutation we have identified, the KATP channel in the coronary artery can no longer fulfill this delicate process."

###

The team, whose work was supported by the BBSRC (Biotechnology and Biological Sciences Research Council), now plans to approach pharmaceutical companies with their findings, aiming to design novel drugs that could interact with this new target.

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A tiny channel and a large vessel: A new clue for heart attack

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HOLLYWOOD, Fla. -

Barbaree King began smoking when she was a teenager. She struggled for years to quit.

"At some time, I had quit for a couple of years and in a moment of weakness, I said, 'I'll just have one' and I did," she said.

King wondered why smoking cessation aids never seemed to help her, but researchers may now have an answer.

The U.S. National Institute on Drug Abuse found several genetic variations that may play a role in whether people will respond well to nicotine replacement therapy and the smoking cessation drug Bupropion. Researchers found 41 genetic variants linked to smokers who were able to quit using nicotine replacement therapy, including patches and gum, and 26 genes that could help people successfully quit with Bupropion.

"Some people will be able to quit without the medication. Some people are going to have a really tough time," said Dr. Mark Block, a lung specialist with Memorial Health Care System.

Block said the research may lead to more tailored treatment approaches.

"You don't want to give medication to people who aren't going to benefit from it and by the same token, you don't want to withhold it from people who are really going to benefit, so it's a nice way to target therapy based on genetics," he said.

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Research may lead to 'smoking gene'

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Home Mail News Sports Finance Weather Games Groups Answers Flickr More omg! Shine Movies Music TV Health Shopping Travel Autos Homes Mobile Yahoo! News Search News Search Web Sign In Mail Help Account Info Help Suggestions Yahoo! Home Video Photos GMA Year in Review Odd Comics Travel Opinion Trending Now Who Knew? Weather The Upbeat U.S. U.S. Video GMA Education Religion Crimes and Trials Local Contributor Network Year In Review World World Video Middle East Europe Latin America Africa Asia Canada Australia/Antarctica Business Video Exclusives Today's Markets Stocks Personal Finance Marketplace Entertainment Video Clinton Concert Celebrity TV Movies Music Fashion Books Arts Theater Dear Abby Comics Odd News Sports Video NFL MLB NBA NCAAF NCAAB Soccer Cycling NHL Tennis Golf Boxing Motor Sports MMA Olympics Tech Gadgets Wireless Apple Social Media Security Open Source Gaming Apps This Could Be Big Upgrade Your Life Politics Remake America The Issues Women and Politics Press Releases Video Science Science Video Weather News Space / Astronomy Pets Dinosaurs / Fossils Biotech Energy Green Health Video Weight Loss Cancer Sexual Health Medications/Drugs Parenting/Kids Seniors/Aging Diseases/Conditions Blogs The Sideshow Katie's Take Power Players This Could Be Big Newsmakers Trending Now The Upbeat Who Knew? Nightline Fix Beyond the Headline Local Popular Search Keyword News Search

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Rare, inherited mutation leaves children susceptible to acute lymphoblastic leukemia

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SAINT PAUL, Minn.--(BUSINESS WIRE)--

The first published research on the groundbreaking use of a modified gene-editing system to produce horn-free dairy cattle was released this week in Proceedings of the National Academy of Sciences (PNAS). PNAS is the official journal of the National Academies of Sciences and is among the world's most-cited multidisciplinary scientific publications.

Drs. Scott Fahrenkrug, Perry Hackett and their team at Recombinetics, a Minnesota-based global innovator in genome editing, authored Efficient nonmeiotic allele introgression in livestock using custom endonucleases, a new paper detailing an important new approach that will not only make hornless dairy cattle a reality, but accelerate the genetic improvement of livestock for food production and the development of regenerative medicines.

For some time now, explains Fahrenkrug, CEO of Recombinetics, farmers have practiced selective breeding for desirable DNA variation with the intention of influencing livestock traits. In this paper, we have shown for the first time that its possible to bypass decades of breeding by introgressing genetic variants directly into livestock genomes using targeted nucleases, without the use of any transgenic DNA. Our team used TALENs and other sequence-specific DNA scissors to custom-engineer and modify several genes of interest in pigs, cows and goats. Recombinetics uses its proprietary genome-editing technologies to accelerate the breeding of natural characteristics in livestock to enhance their health and welfare, and advance worldwide food production and safety.

The group demonstrated that a sequence associated with horns in dairy cattle could be converted to a natural beef cattle variant that is hornless, providing a strategy to improve animal welfare by genetic, instead of physical or chemical dehorning.

Targeted genetic improvement can save numerous generations and decades of selective breeding. The technology promises to rapidly enhance protein production in indigenous livestock breeds and to introduce natural disease resilience traits into breeds and species that dont already have them. The paper also reports the introgression of precise variants from warthogs into the swine genome to protect against the highly-contagious and lethal African Swine Fever Virus; and the copying of a natural sequence into the goat genome to increase the frequency of twinning, helping enhance food security for small farmers in the developing world.

Recombinetics also applies its genome-editing solutions and TALEN technologies to create large animal models for human disease research accelerate the development of therapeutic compounds, medical devices and protocols.

About Recombinetics

A private company founded in 2008, Recombinetics has emerged as a global leader in proprietary gene repair and gene-editing technology. Breakthrough scientific research including the development of TALEN technologies has resulted in global exclusive rights in the biomedical, animal agriculture and livestock vertical markets.

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First Published Research Shows Success with Targeted Gene-Editing to Accelerate Genetic Improvement in Dairy Cattle

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Public release date: 9-Sep-2013 [ | E-mail | Share ]

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

New Rochelle, NY, September 9, 2013Studies have shown that caffeine users can become dependent on or addicted to caffeine and may have difficulty reducing their consumption, as can occur with other drugs of dependence. A comprehensive review of the current evidence on caffeine dependence is presented in an article in Journal of Caffeine Research, a peer-reviewed publication from Mary Ann Liebert, Inc., publishers. The article is available free on the Journal of Caffeine Research website at http://www.liebertpub.com/jcr.

Steven Meredith and Roland Griffiths, Johns Hopkins University School of Medicine (Baltimore, MD), Laura Juliano, American University (Washington, DC), and John Hughes, University of Vermont (Burlington), reviewed the published research on caffeine dependence. In the article "Caffeine Use Disorder: A Comprehensive Review and Research Agenda" they describe the prevalence of caffeine dependence, clinically relevant indicators of functional impairment among caffeine users, and the criteria for making a diagnosis of caffeine use disorder.

The authors propose an agenda for future research that would include clinical, epidemiologic, and genetic investigations to lead to a better understanding of the clinical signs and the prevalence of caffeine dependence, as well as the risk factors and best approaches for treating caffeine addiction.

"Caffeine-related problems are increasingly being seen as clinically important by addiction professionals," says Jack E. James, PhD, Editor-in-Chief of Journal of Caffeine Research. "The article by Dr. Steven Meredith and colleagues is timely in helping to clarify the dimensions of caffeine dependence problems, while also providing direction for future research in this neglected area."

###

About the Journal

Journal of Caffeine Research: The International Multidisciplinary Journal of Caffeine Science is a quarterly journal published in print and online that covers the effects of caffeine on a wide range of diseases and conditions, including mood disorders, neurological disorders, cognitive performance, cardiovascular disease, and sports performance. The Journal explores all aspects of caffeine science including the biochemistry of caffeine; its actions on the human body; benefits, dangers, and contraindications; and caffeine addiction and withdrawal, across all stages of the human life span from prenatal exposure to end-of-life. Tables of content and a sample issue may be viewed on the Journal of Caffeine Research website at http://www.liebertpub.com/jcr.

About the Publisher

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More research urgently needed on caffeine

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TORONTO, Sept. 9, 2013 /CNW/ - Scientists at the Centre for Addiction and Mental Health (CAMH) and University Health Network (UHN) have found a new link between early-onset Parkinson's disease and a piece of DNA missing from chromosome 22. The findings help shed new light on the molecular changes that lead to Parkinson's disease.

The study appears online today in JAMA Neurology.

Among people aged 35 to 64 who were missing DNA from a specific part of chromosome 22, the research team found a marked increase in the number of cases of Parkinson's disease, compared to expected rates of Parkinson's disease in the general population from the same age group.

The deletion, which occurs when a person is born with about 50 genes missing on one chromosome 22, is associated with 22q11.2 deletion syndrome. People with this condition may have heart or other birth defects, learning or speech difficulties, and some develop schizophrenia. It occurs in an estimated 1 in 2,000 to 4,000 births, but is believed to be under-diagnosed.

"22q11.2 deletion syndrome has been fairly well studied in childhood and adolescence, but less is known about its effects as people age," said Dr. Anne Bassett, Director of CAMH's Clinical Genetics Research Program and Director of the Dalglish Family Hearts and Minds Clinic at UHN, the world's first clinic dedicated to adults with 22q11.2 deletion syndrome. A few cases of patients with the syndrome who had Parkinson's disease symptoms had been previously reported, which suggested that the two conditions might be linked.

Parkinson's disease is one of the most common neurodegenerative disorders worldwide, typically affecting people over the age of 65. Earlier onset of Parkinson's disease, before age 50, is rare and has been associated with several other genetic changes that are not on chromosome 22.

The researchers studied 159 adults with 22q11.2 deletion syndrome to discover how many had been clinically diagnosed with Parkinson's disease. For three individuals with the deletion and Parkinson's disease who were deceased, brain tissue was also examined.

"Through a post-mortem examination, we were able to show that all three patients had a loss of neurons that was typical of that seen in Parkinson's disease. The examination also helped to show that the symptoms of Parkinson's disease were not related to side effects of the medications commonly used to treat schizophrenia," added Dr.Rasmus Kiehl, neuropathologist in UHN's Laboratory Medicine Program, who co-authored the report with CAMH graduate student Nancy Butcher. The team also found that Parkinson's disease in 22q11.2 deletion syndrome is associated with abnormal accumulations of protein called Lewy bodies in the brain in some, but not all cases, just as in another genetic form of Parkinson's disease.

The findings highlight the complexity of clinical care when both Parkinson's disease and 22q11.2 deletion syndrome are present. "Our results may inform best practices in the clinic in these cases," said Dr. Bassett, Senior Scientist in CAMH's Campbell Family Mental Health Research Institute.

Because patients with 22q11.2DS who have schizophrenia are often prescribed anti-psychotic medications, they may experience side-effects such as tremors and muscle stiffness, similar to symptoms of Parkinson's disease.

Link:
Early-onset Parkinson's disease linked to genetic deletion

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Guido Pontecorvo - Professor of Genetics 1955 to 1968 University of Glasgow.
Guido Pontecorvo (1907-1999), who liked to be known by his nickname, Ponte, was the University #39;s first Professor of Genetics, 1955 to 1968, and has been desc...

By: University of Glasgow

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Guido Pontecorvo - Professor of Genetics 1955 to 1968 University of Glasgow. - Video

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Let #39;s Play Panzer Dragoon Saga [Part 17] - Ancient Genetics
We #39;re bound to find some interesting facts in this massive place...

By: Zergem

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Let's Play Panzer Dragoon Saga [Part 17] - Ancient Genetics - Video

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NASHVILLE, Tenn., Sept. 9, 2013 /PRNewswire/ -- NextGxDx Inc., which provides an online genetic testing marketplace for healthcare professionals and hospitals, today announced an agreement with genetic testing laboratory Cancer Genetics, Inc. (CGIX), to offer Cancer Genetics' genomic-based, proprietary oncology tests and services through the NextGxDx platform.

"Genetic testing within oncology is evolving at a tremendous rate," said NextGxDx CEO Mark Harris, PhD, MBA. "Our newest partner, Cancer Genetics, provides our growing marketplace with a robust catalog of more than 100 regulatory approved oncology testing products and solutions for easy search, comparison and ordering."

Cancer Genetics is an emerging leader in DNA-based cancer diagnostics and services for some of the most prestigious medical institutions in the world. The company is focused on transforming diagnosis and disease management for the most complex and difficult-to-treat cancers, including hematologic, urogenital, and gynecological malignancies.

"Our team takes tremendous pride in our focus on personalizing the diagnosis for cancer patients," said Panna Sharma, CEO of Cancer Genetics, Inc. "The NextGxDx platform supports our mission by enhancing our market reach while allowing us to focus on delivering critical genomic information through our clinical trial services and proprietary testing where patients and their physicians need it mostto diagnose, monitor and inform cancer treatment."

About NextGxDxNextGxDx, Inc. provides an online genetic testing marketplace that offers healthcare professionals and hospitals the ability to access up-to-date listings of all genetic tests from CLIA-certified laboratories, view pertinent information about each test, order tests online, and manage results electronically within the HIPAA-compliant portal.By providing clinicians with a one-stop-shop to search, compare and order genetic tests, NextGxDx reduces the time and costs associated with the ordering of genetic tests.For more information, visit http://www.NextGxDx.com.

About Cancer GeneticsCancer Genetics, Inc. is an emerging leader in DNA-based cancer diagnostics that personalizes the diagnosis and prediction of treatment outcomes for difficult to diagnose cancers. These cancers include hematological, urogenital and HPV-associated cancers. The Company's comprehensive range of oncology-focused tests and laboratory services provide critical genomic information to healthcare professionals, cancer centers, and to biopharma companies. Through its CLIA certified and CAP accredited state-of-the-art reference lab, Cancer Genetics servicessome of the most prestigious medical institutions in the world and has strong research collaborations with major cancer centers such as Memorial Sloan-Kettering, The Cleveland Clinic, Mayo Clinic and the National Cancer Institute. For further information, please seewww.cancergenetics.com.

Media Contact: Erin George 615-946-9914 erin@lovell.com

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NextGxDx Adds Cancer Genetics, Inc. to Genetic Testing Platform

Recommendation and review posted by Bethany Smith

In late August, Amgen agreed to buy Onyx Pharmaceuticals in one of the worst-kept M&A secrets of the year. Amgen paid 50% more than Onyx's pre-rumor trading price, suggesting there may be other biotech companies similarly undervalued. Seattle Genetics (NASDAQ: SGEN) , a biotech collaborating with some of the largest drug companies on cancer research, may be on that list.

Biotechnology is one of the most M&A-friendly industriesThe cost to develop and the failure rate of new drugs are high. Because of this, fledgling biotechs often turn to venture capital and partner with major drug companies to finance development

Seattle Genetics currently has just one drug on the market, Adcetris, which was approved in 2011 to treat Hodgkin's lymphoma and anaplastic large-cell lymphoma. The drug serves as a showcase for the company's antibody-drug conjugates, or ADCs -- complex molecules delivering payloads directly to cancerous cells without the collateral damage associated with traditional chemotherapy.

As a result of Adcetris winning 70% of the market share for its approved indications, major drug companies including Bayer, Roche's Genentech, Takeda's Millennium, AbbVie (NYSE: ABBV) , and Pfizer (NYSE: PFE) have inked lucrative deals with Seattle Genetics to gain access to its ADC portfolio.

Those deals mean big money for Seattle Genetics, totaling as much as $3.5 billion in future milestone payments plus royalties from any drugs that become commercialized.

Seattle Genetics' big plans for Adcetris Adcetris was the first new Hodgkin's treatment approved in 30 years when it got the nod from the FDA in 2011. The drug has generated nearly $70 million in revenue in the first half of this year, and the company hopes it can build a billion-dollar franchise around the drug by expanding its label.

As part of that goal, Seattle Genetics is in phase 2 trials for Adcetris as a front line treatment for large B-cell lymphoma and is currently in phase 3 trials studying Adcetris as a replacement for Bleomycin in the most common chemotherapy cocktail used in lymphoma patients. The company is also studying Adcetris as a stand-alone first line treatment for Hodgkin's as well. If successful, an expanding patient pool could move Adcetris closer to $1 billion blockbuster status and that could prove intriguing to many of Seattle Genetics' big pharma partners.

Catching the eye of the biggest drugmakersSeattle is currently working with cancer research powerhouse Genentech onnine different programs. Those programs include ADC research targeting ovarian and prostate cancer, from which positive early stage data was presented at ASCO this past summer. If those early successes continue, SeattleGenetics could earn up to $900 million in milestones from Genentech, as well as future royalties.

Seattle Geneticsalso hastwo ADC trials ongoing with AbbVie -- the drug company spun off from Abbott Labs earlier this year. AbbVie expanded its relationship with Seattle Geneticslast fall in order to gain access to its auristatins, paying $25 million in upfront fees, offering milestone payments of up to $220 million per target, and royalties equal to mid-to-high single-digit percentages of commercialized drugs.

Not to be left out, Pfizeris also conducting research using Seattle Genetics' ADCs, inking a deal in 2011 that could be worth as much as $200 million in milestone payments. Pfizer also agreed to a collaboration deal with Seattle Genetics' ADC competitor CytomX Therapeutics worth more than $600 million this past June.

The rest is here:
Is Seattle Genetics an Acquisition Target?

Recommendation and review posted by Bethany Smith

RUTHERFORD, N.J., Sept. 9, 2013 (GLOBE NEWSWIRE) -- Cancer Genetics, Inc. (CGIX), an emerging leader in DNA-based cancer diagnostics that personalizes the diagnosis and prediction of treatment outcomes for difficult to diagnose cancers, today announced executives from the company will participate at the following investor conferences in September:

The company's investor presentation will be made available in the Investor Relations section of the CGI website.

About Cancer Genetics:

Cancer Genetics, Inc. is an emerging leader in DNA-based cancer diagnostics that personalizes the diagnosis and prediction of treatment outcomes for difficult to diagnose cancers. These cancers include hematological, urogenital and HPV-associated cancers. The Company's comprehensive range of oncology-focused tests and laboratory services provide critical genomic information to healthcare professionals, cancer centers, and biopharma companies. Through its CLIA certified and CAP accredited state-of-the-art reference lab, Cancer Genetics services some of the most prestigious medical institutions in the world and has strong research collaborations with major cancer centers such as Memorial Sloan-Kettering, The Cleveland Clinic, Mayo Clinic and the National Cancer Institute. For further information, please see http://www.cancergenetics.com.

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Cancer Genetics Announces Upcoming Investor Conference Schedule

Recommendation and review posted by Bethany Smith

Public release date: 9-Sep-2013 [ | E-mail | Share ]

Contact: Gina Bericchia Gina.Bericchia@NationwideChildrens.org 614-355-0495 Nationwide Children's Hospital

Studies of a therapy designed to treat amyotrophic lateral sclerosis (ALS) suggest that the treatment dramatically slows onset and progression of the deadly disease, one of the most common neuromuscular disorders in the world. The researchers, led by teams from The Research Institute at Nationwide Children's Hospital and the Ludwig Institute at the University of California, San Diego, found a survival increase of up to 39 percent in animal models with a one-time treatment, a crucial step toward moving the therapy into human clinical trials.

The therapy reduces expression of a gene called SOD1, which in some cases of familial ALS has a mutation that weakens and kills nerve cells called motor neurons that control muscle movement. While many drug studies involve only one type of animal model, this effort included analysis in two different models treated before and after disease onset. The in-depth study could vault the drug into human clinical trials, said Brian Kaspar, PhD, a principal investigator in the Center for Gene Therapy at Nationwide Children's and a senior author on the research, which was published online Sept. 6 in Molecular Therapy.

"We designed these rigorous studies using two different models of the disease with the experimenters blinded to the treatment and in two separate laboratories," said Dr. Kaspar, who collaborated on the study with a team led by Don Cleveland, PhD, at the University of California, San Diego. "We were very pleased with the results, and found that the delivery approach was successful in a larger species, enabling us to initiate a clinical translational plan for this horrible disease."

There currently is no cure for ALS, also called Lou Gehrig's disease. The Centers for Disease Control and Prevention estimates there are about 5,000 new cases in the U.S. each year, mostly in people age 50 to 60. Although the exact cause of ALS is unknown, more than 170 mutations in the SOD1 gene have been found in many patients with familial ALS, which accounts for about 2 percent of all cases.

SOD1 provides instructions for making an enzyme called superoxide dismutase, which is found throughout the body and breaks down toxic molecules that can be damaging to cells. When mutated, the SOD1 gene yields a faulty version of the enzyme that is especially harmful to motor neurons. One of the mutations, which is found in about half of all familial ALS patients, is particularly devastating, with death usually coming within 18 months of diagnosis. SOD1 has also been implicated in other types of ALS, called sporadic ALS, which means the therapy could prove beneficial for larger numbers of patients suffering with this disease.

Earlier work by Dr. Kaspar and others found that they could halt production of the mutated enzyme by blocking SOD1 expression, which in turn, they suspected, would slow ALS progression. To test this hypothesis, the researchers would not only need to come up with an approach that would block the gene, but also figure out how to specifically target cells implicated in the disease, which include motor neurons and glial cells. What's more, the therapy would preferably be administered noninvasively instead of direct delivery via burr holes drilled into the skull.

Dr. Kaspar's team accomplished the second part of this challenge in 2009, when they discovered that adeno-associated virus serotype 9 (AAV9) could cross the blood-brain barrier, making it an ideal transport system for delivering genes and RNA interference strategies designed to treat disease.

In this new work, funded by the National Institutes of Health, the researchers blocked human SOD1, using a technology known as short hairpin RNA, or shRNA. These single strands of RNA are designed in the lab to seek out specific sequences found in the human SOD1 gene, latch onto them and block gene expression.

Original post:
Therapy slows onset and progression of Lou Gehrig's disease, study finds

Recommendation and review posted by Bethany Smith

Newswise Studies of a therapy designed to treat amyotrophic lateral sclerosis (ALS) suggest that the treatment dramatically slows onset and progression of the deadly disease, one of the most common neuromuscular disorders in the world. The researchers, led by teams from The Research Institute at Nationwide Childrens Hospital and the Ludwig Institute at the University of California, San Diego, found a survival increase of up to 39 percent in animal models with a one-time treatment, a crucial step toward moving the therapy into human clinical trials.

The therapy reduces expression of a gene called SOD1, which in some cases of familial ALS has a mutation that weakens and kills nerve cells called motor neurons that control muscle movement. While many drug studies involve only one type of animal model, this effort included analysis in two different models treated before and after disease onset. The in-depth study could vault the drug into human clinical trials, said Brian Kaspar, PhD, a principal investigator in the Center for Gene Therapy at Nationwide Childrens and a senior author on the research, which was published online Sept. 6 in Molecular Therapy.

We designed these rigorous studies using two different models of the disease with the experimenters blinded to the treatment and in two separate laboratories, said Dr. Kaspar, who collaborated on the study with a team led by Don Cleveland, PhD, at the University of California, San Diego. We were very pleased with the results, and found that the delivery approach was successful in a larger species, enabling us to initiate a clinical translational plan for this horrible disease.

There currently is no cure for ALS, also called Lou Gehrigs disease. The Centers for Disease Control and Prevention estimates there are about 5,000 new cases in the U.S. each year, mostly in people age 50 to 60. Although the exact cause of ALS is unknown, more than 170 mutations in the SOD1 gene have been found in many patients with familial ALS, which accounts for about 2 percent of all cases.

SOD1 provides instructions for making an enzyme called superoxide dismutase, which is found throughout the body and breaks down toxic molecules that can be damaging to cells. When mutated, the SOD1 gene yields a faulty version of the enzyme that is especially harmful to motor neurons. One of the mutations, which is found in about half of all familial ALS patients, is particularly devastating, with death usually coming within 18 months of diagnosis. SOD1 has also been implicated in other types of ALS, called sporadic ALS, which means the therapy could prove beneficial for larger numbers of patients suffering with this disease.

Earlier work by Dr. Kaspar and others found that they could halt production of the mutated enzyme by blocking SOD1 expression, which in turn, they suspected, would slow ALS progression. To test this hypothesis, the researchers would not only need to come up with an approach that would block the gene, but also figure out how to specifically target cells implicated in the disease, which include motor neurons and glial cells. Whats more, the therapy would preferably be administered noninvasively instead of direct delivery via burr holes drilled into the skull.

Dr. Kaspars team accomplished the second part of this challenge in 2009, when they discovered that adeno-associated virus serotype 9 (AAV9) could cross the blood-brain barrier, making it an ideal transport system for delivering genes and RNA interference strategies designed to treat disease.

In this new work, funded by the National Institutes of Health, the researchers blocked human SOD1, using a technology known as short hairpin RNA, or shRNA. These single strands of RNA are designed in the lab to seek out specific sequences found in the human SOD1 gene, latch onto them and block gene expression.

In one of the mouse models used in the study, ALS develops earlier and advances more quickly. In the other, the disease develops later and progresses more slowly. All of the mice received a single injection of AAV9-SOD1-shRNA before or after disease onset.

Results showed that in the rapid-disease-progressing model, mice treated before disease onset saw a 39 percent increase in survival compared to control treated mice. Strikingly, in mice treated at 21 days of age, disease progression was slowed by 66 percent. Perhaps more surprising was the finding that even after symptoms surfaced in these models, treatment still resulted in a 23 percent increase in survival and a 36 percent reduction in disease progression. In the slower-disease-onset model, treatment extended survival by 22 percent and delayed disease progression by 38 percent.

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Therapy Slows Onset and Progression of Lou Gehrig's Disease

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Neuromuscular Energising Therapy (NET): Spinal Cord Injury

By: Charles King

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Neuromuscular Energising Therapy (NET): Spinal Cord Injury - Video

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NET: Spinal Cord Injury

By: Charles King

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NET: Spinal Cord Injury - Video

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Stem Cell Therapy For Pets
Stemcellvet.co.uk offer adipose derived Stem Cell Therapy for pets in the UK. We treat cats and dogs predominantly for arthritis but there is also the potent...

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Stem Cell Therapy - Cosmetic Surgery PH Beaufaces
Stem Cell Therapy at Beaufaces Cosmetic Surgery Center Manila, Philippines For more info visit http://www.cosmeticsurgeryph.com/ Or email us at info@cosmetic...

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There is no doubt that parents of persons with autism will exhaust all possible means to look for ways to improve the lives of their children. Some will even look for the ''cure'' at all costs literally, especially if they can afford it.

The buzz word for possible autism cure these last few years is stem cell therapy, a medical intervention that involves extracting the body's repair cells and injecting them back to the body to replace old cells. The controversies about this therapy as autism ''cure'' include its high cost.

Angels Talk recently asked parent members of Autism Society Philippines the following question: If money was not an issue, will you consider stem cell therapy for your child with autism? Some were willing to take the chance while others were either cautious of trying ''cures'' that still need to be validated, or consider their children's autism as a gift. Here are some of their sentiments.

''Yes, I would. Whatever will help my nine-year old Sean, I will take the chance. I accept Sean and his condition but not everyone is accepting of autism. If stem cell therapy will give Sean a chance to enjoy life like an average kid, then I will pursue this.'' - JASMINE NADJA PINUGU, a parent who represents the views of 22 other respondents

''No. I would not subject my child to a treatment that has questionable therapeutic claims and safety issues. What we read in the news now are anecdotal reports from celebrity parents that include endorsement of a certain clinic or doctor. Our son Jorel, is doing well trying to adapt in the ''normal'' world. We would rather spend the money for his job or independent living training later on.'' - MENCHIE ALEGRE

''Not at this time but I am open to the possibility. I attended Dr. Samuel Bernal's talk on this topic at Medical City early this year and even this expert is not making claims that stem cell can ''cure'' autism. They are still doing further studies. I have also not heard about the results on the six children who've undergone the test for it. The procedure is quite scary and there will surely be side effects. Until such time that the procedure becomes less invasive, I will not agree to have this procedure done to my child. I appreciate though the efforts of all the people trying to find solution to improve the lives of our children. I pray that God may guide them well.'' - OLIVE MEDINA

''NO! I love him for what he is and he was born unique. Autism is not an illness; all special children need love, support and understanding from family, friends and especially our society. Special children are God's gift to society, to help us be humble, happy and content of what we have.'' - BERNADETTE TABARES

''No, I have two autistic sons and I have learned to respect their condition as God allowed it. I asked God for wisdom in rearing them and I enjoy their company. They showered me with so much attention and love. After 20 years of searching for solution for my two boys to act normal and be able to conform to the norms of society, I have witnessed that each one of us also have abnormalities. Being with them at all given time is the best treatment. Integrating them in all house activities boost their self-esteem.''- LOURY JACOB

''Autism is not the problem. Only ACCCEPTANCE can CURE AUTISM.'' - WHENG DOLLENTE

''What is the point of compelling your child to be someone he is not?'' - GERARD ATIENZA

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Will you consider stem cell therapy for your child with autism?

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Knowing whether you have the "obesity gene" doesn't seem to be a deterrent against weight loss, according to a new study.

Plus, researchers said, the knowledge could actually help to reduce self-blame for obesity.

"Regardless of gene status or weight, all the volunteers recognized that both genes and behavior are important for weight control," study researcher Susanne Meisel, of the Health Behaviour Research Centre at the University College London, said in a statement. "The results indicate that people are unlikely to believe that genes are destiny and stop engaging with weight control once they know their FTO [obesity gene] status. Although they knew that FTO's effect is only small, they found it motivating and informative. We are now doing a larger study to confirm whether more people react in the same way."

While a gene test for FTO -- which has two variants, one that is linked with high risk of weight gain and one that is with low risk -- is not yet commercially available, researchers are able to conduct it. The Journal of Genetic Counseling study noted that "about 37 percent of the Caucasian population carries one higher-risk (A) allele of the commonest obesity associated FTO variant (rs9939609), and 16 percent carry two (AA); conferring a 20 percent higher lifetime risk of becoming obese than those who carry none."

For the study, researchers tested 18 study participants to see whether they had the weight gain-linked FTO gene variant, and then interviewed them to see how they felt about their status.

They found that study participants who experienced weight struggles considered it helpful to know their gene status. They also said that they didn't think knowing their status made them feel like they were helpless in losing weight, and in fact made them feel less emotionally stressed about their weight.

People with normal weight who had the gene variant "described the result as a 'little warning bell' that would help them to be more conscious of their weight and monitor weight gain in the future," researchers wrote in the study. "Participants struggling with weight control described reassurance and relief of stigma, guilt or self-blame as benefits of receiving the test result. No one expressed a fatalistic attitude, nor was there evidence for a false sense of immunity to weight gain."

What do you think? How would knowing whether you had the "obesity gene" make you feel about your own weight loss journey?

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Knowing Obesity Gene Status Doesn't Make People Feel Helpless In Losing Weight, Study Suggests

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