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Calcutta News.Net
Monday 6th February, 2012 (IANS)

The environment ministry's Genetic Engineering Approval Committee (GEAC) ignored violation of law by the US-based company Monsanto which conducted trials of herbicide-tolerant, genetically modified (GM) maize across India without permission, an RTI reply revealed Monday.

The Right to Information (RTI) reply, to a query filed by an activist of Alliance for Sustainable and Holistic Agriculture (ASHA), revealed that GEAC did not take any action even when a scientist pointed out that planting of herbicide-tolerant GM maize was done without permission. GEAC is the apex body constituted by the ministry for approving GM foods in India.

"Monsanto's GM maize trials have been going on for several seasons now in various locations around the country. It took a scientist in one monitoring team to point out the fact that planting of the herbicide-tolerant GM maize took place without permission from competent authorities," said Kavitha Kuruganti, member of Coalition for a GM-Free India.

"What is more damning is that there is no evidence of any discussion or action by the regulators on this finding. This clearly demonstrates that the regulators are unconcerned about biosafety violations or contamination and are protecting and supporting offenders like Monsanto," she said.

According to ASHA, the GEAC has authorised Monsanto to conduct trials of herbicide tolerant and insect-resistant GM maize but the company conducted trials for only herbicide-tolerant GM maize.

This is also the first GM product of Monsanto in India in its own name and not in the name of associate companies like Mahyco.

"This appears to be a repetition of an earlier episode of herbicide tolerant cotton planted by Mahyco without permission. The GEAC, in that instance, found the clarifications submitted by Mahyco highly unsatisfactory and warned that any non-compliance in future would attract punitive actions," Kuruganti said.

The coalition demanded that the ministry fix accountability on Monsanto and take action against the regulators who repeatedly fail to check the violations of the corporations.

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Monsanto's violations in GM maize trials ignored: RTI reply

11-11-2011 10:58 New noninvasive tests that screen for genetic disease in a fetus can also tell the baby's sex in the seventh week. This could lead to gender selection, but doctors don't need to go along with it. Medscape expert commentator Dr. Arthur Caplan weighs in. View more Dr. Caplan videos on Medscape: medscape.com/index/section_10186_0

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Will New Tests Promote Abortion of an 'Undesired Sex' Fetus? - Video

Life Technologies this week named Alan Sachs as head of global research and development and Ronnie Andrews as president of medical sciences.

Sachs was previously the vice president of exploratory and translational sciences for Merck Research Laboratories, where he spent 10 years in various leadership roles, Life Tech said. Prior to that Sachs served an associate professor of biochemistry and molecular biology at the University of California, Berkeley, and as a Whitehead fellow at the Whitehead Institute for Biomedical Research.

Andrews joins Life Tech from GE Molecular Diagnostics, where he served as a segment leader following GE's 2010 acquisition of Clarient, where Andrews was CEO. Andrews has also held executive positions with Abbott Diagnostics, Roche Diagnostics, and Immucor.

Stephen O'Brien has left the National Cancer Institute's Laboratory of Genomic Diversity after 25 years to help launch a genome bioinformatics program at St. Petersburg University in Russia. O'Brien received a $5 million grant from the Russian Ministry of Education and Science last year under a program that aims to lure big-name researchers to Russia. Over the coming three years, O'Brien will spend at least four months per year in Russia working at the center, which is scheduled to open in May.

Saladax Biomedical said today that President and CEO Edward Erickson has resigned due to personal and family reasons, and that he will be replaced by Kevin Harter on an interim basis. Erickson will remain a member of the company's board of directors. Harter is a co-founder and senior VP of the Life Sciences Greenhouse, and he has served as executive chairman at Saladax.

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Genetic Technologies, Eurofins STA Labs Settle Infringement Dispute

Public release date: 6-Feb-2012
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Contact: Les Lang
llang@med.unc.edu
919-966-9366
University of North Carolina School of Medicine

CHAPEL HILL, N.C. ? UNC researchers have discovered how the genetic defect underlying one of the most common congenital heart diseases keeps the critical organ from developing properly. According to the new research, mutations in a gene called SHP-2 distort the shape of cardiac muscle cells so they are unable to form a fully functioning heart.

The study also shows that treatment with a drug that regulates cell shape rescues the cardiac defect, pointing to therapeutic avenues that could one day benefit Noonan syndrome patients. The results, which were produced in a frog model of the disease, appeared online January 25, 2012, in the journal Development.

Genetic studies have shown that SHP-2 plays a critical role in human physiology and disease. Interestingly, different mutations in different portions of SHP-2 result in three different diseases ? Noonan syndrome, a severe congenital heart disease; juvenile myelo-monocytic leukemia, a lethal form of cancer; and Leopard syndrome, a rare condition with skin, facial and cardiac abnormalities. This observation has intrigued a number of researchers, including senior study author Frank Conlon, PhD.

"I've wondered how it is that one mutation gives heart disease and doesn't affect your white blood cells, and another will wipe out your white blood cells and leave your heart alone," said Conlon, an associate professor of genetics and a member of the UNC McAllister Heart Institute. He and others have explored this mystery by creating transgenic animals -- fruit flies, mice, or in Conlon's case, frogs -- that possess a mutated form of SHP-2.

When Conlon and his team genetically engineered frogs to contain the very same defects seen in humans with Noonan syndrome, they found that the frogs did in fact develop cardiac defects. But when they created them with a mutation seen in humans with leukemia, there were no heart defects. The researchers then performed 3D modeling on the animals to assess the nature of the anatomical defects, and discovered that actin filaments ? proteins responsible for giving structure to the cardiac muscle cells -- were the ones affected.

Conlon and his collaborator Joan Taylor, PhD, an associate professor of pathology and laboratory medicine at UNC, then tested whether they could reverse the heart malformation using a drug called fausidil that had been shown to improve cardiac function in animal models of heart failure. The drug blocks a protein called ROCK that resides in the same neighborhood ? or pathway ? of intracellular processes as SHP-2.

The researchers dissolved the drug in the mutant frogs' water tank and found that it did correct the cardiac defects. Their findings connect the dots between Noonan syndrome's underlying genetic defect and the resulting cardiac malformations.

"The human mutations could have been linked to anything, proliferation or cell death, and what this study does is it links it to cell shape changes, which are mediated by this important molecule ROCK," said Conlon. "Our lab studies heart development and heart disease, so we are interested in how this one set of mutations specifically target that one organ. Why the heart? We still have to figure that out."

###

The research was funded in by the National Institutes of Health and the American Heart Association. Study co-authors from UNC were Yvette Langdon, PhD; Panna Tandon, PhD; Erika Paden; and Jennifer Duddy.

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'ROCK' off: Study establishes molecular link between genetic defect and heart malformation

Public release date: 6-Feb-2012
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Contact: David Sampson
jmdmedia@elsevier.com
215-239-3171
Elsevier Health Sciences

Philadelphia, PA, February 6, 2012 ? DNA sequencing to detect genetic mutations can aid in the diagnosis and selection of treatment for cancer. Current methods of testing DNA samples, Sanger sequencing and pyrosequencing, occasionally produce complex results that can be difficult or impossible to interpret. Scientists at the Johns Hopkins University School of Medicine have developed a free software program, Pyromaker, that can more accurately identify such complex genetic mutations.

Pyromaker is a web-based application that produces simulated pyrograms based on user input including the percentage of tumor and normal cells, the wild-type sequence, the dispensation order, and any number of mutant sequences. Pyromaker calculates the relative mutant and wild-type allele percentages and then uses these to generate the expected signal at each point in the dispensation sequence. The final result is a virtual trace of the expected pyrogram.

The researchers validated Pyromaker against actual pyrograms containing common mutations in the KRAS gene, which plays an important role in the pathogenesis of a variety of tumors. The actual pyrograms and virtual pyrograms were quantitatively identical for all mutations tested.

They then demonstrated that all codon 12 and 13 single and complex mutations generate unique pyrograms. However, some complex mutations were indistinguishable from single base mutations, indicating that complex mutations may be underreported. Working with two complex pyrograms that were difficult to interpret initially, the researchers identified five approaches to resolve them: Sanger sequencing alone, hypothesis testing with Pyromaker, Pyromaker iterative mutation re-creation, melting curve analysis, and TA cloning with Sanger sequencing.

Senior author James R. Eshleman, MD, PhD, Professor of Pathology and Oncology, Associate Director, Molecular Diagnostics Laboratory, Johns Hopkins University School of Medicine, explains, "User-directed hypothesis testing allows for generating virtual traces that can be compared to the actual data to clarify ambiguous results from pyrosequencing and the Sanger method. Alternatively, Pyromaker can quickly and efficiently test the possibilities that can explain a complicated polysequencing result." Both strategies were able to successfully identify the complex mutations.

TA cloning and sequencing also provided unequivocal interpretation, but this method is labor intensive, risks plasmid contamination of the laboratory, may delay reporting, and is not routinely used in most clinical diagnostic laboratories.

"Although pyrosequencing and Sanger sequencing are both powerful tools to resolve most mutations, for certain complex cases, neither of them alone is enough to provide a definitive interpretation," notes Dr. Eshleman. "Additional methods, such as Pyromaker analysis or TA cloning and sequencing, allow one to definitively diagnose the variant allele. Pyromaker is available free online and can be accessed from any computer with internet access. Iterative Pyromaker analysis is the least expensive and fastest method to resolve these cases."

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Pyromaker has been made freely available at http://pyromaker.pathology.jhmi.edu.

The article is "A Virtual Pyrogram Generator to Resolve Complex Pyrosequencing Results," by G. Chen, M.T. Olson, A. O'Neill, A. Norris-Kirby, K. Beierl, S. Harada, M. Debeljak, K. Rivera-Roman, S. Finley, A. Stafford, C.D. Gocke, M-T. Lin, and J. R. Eshleman (doi: 10.1016/j.jmoldx.2011.12.001). The Journal of Molecular Diagnostics, Volume 14, Issue 2 (March 2012) published by Elsevier.

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New virtual tool may provide more accurate diagnosis of genetic mutations

julietvanree posted a photo:

This is a brindle argente winter white hamster. Normally argente doesn't occur in winter white hamsters, thus this is a hybrid color. It is also has two genes for black. In the case of brindle the genetic make up (in color in this case) of the individual cells differs. It is a form of mosaicism. (but not germeline, so it doesn't pass on to the babies). So some cells display as black colored and other ones as argente colored. The same happened with the eye color, black hamsters have black eyes and argente hamsters have red eyes. This is why one eye is red and one eye is black.

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Brindle argente hamster (odd eyed)

Washington, Feb 5 (ANI): Using a liquid laser, researchers have devised a better way to detect the slight genetic mutations that might make a person more vulnerable to a particular type of cancer or other diseases.

This work by University of Michigan researchers could advance understanding of the genetic basis of diseases.

It also has applications in personalized medicine, which aims to target drugs and other therapies to individual patients based on a thorough knowledge of their genetic information.

The researchers say their technique works much better than the current approach, which uses fluorescent dye and other biological molecules to find and bind to mutated DNA strands.

When a patrol molecule catches one of these rogues, it emits a fluorescent beacon. This might sound like a solid system, but it's not perfect. The patrol molecules tend to bind to healthy DNA as well, giving off a background glow that is only slightly dimmer than a positive signal.

"Sometimes, we can fail to see the difference," said Xudong Fan, an associate professor in the Department of Biomedical Engineering and principal investigator on the project.

"If you cannot see the difference in signals, you could misdiagnose. The patient may have the mutated gene, but you wouldn't detect it."

In the conventional fluorescence technique, the signal from mutated DNA might be only a few tenths of a percent higher than the background noise. With Fan's new approach it's hundreds of times brighter.

"We found a clever way to amplify the intrinsic difference in the signals," Fan said.

He did it with a bit of backtracking.

Liquid lasers, discovered in the late '60s, amplify light by passing it through a dye, rather than a crystal, as solid-state lasers do. Fan, who works at the intersection of biomedical engineering and photonics, has been developing them for the past five years.

In his unique set-up, the signal is amplified in a glass capillary called a "ring resonator cavity."

Last year, Fan and his research group found that they could employ DNA (the blueprints for life that reside in all cells) to modulate a liquid laser, or turn it on and off.

His group is one of just a few in the world to accomplish this, Fan said. At the time, they didn't have a practical application in mind. Then they had an epiphany.

"We thought, 'Let's look at the laser output. Can we see what's causing the different outputs and use it to detect differences in the DNA?'" Fan said.

"I had an intuition, and it turns out the output difference was huge," Fan added.

The journal editors named this a "hot paper" that "advances knowledge in a rapidly evolving field of high current interest."

The study has been published in German journal Angewandte Chemie. (ANI)

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Liquid lasers to make detection of cancer genes easier

16-01-2012 13:54 s2ep13

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Pony Genetics - Video

09-09-2011 23:32 http://www.infowars.com Pandora's Box has surely been opened. A dangerous genetic experiment has come out of the shadows, and the human-animal hybrids, chimeras and other transgenic clones it has yielded now threaten to endanger and irrevocably alter life as we know it. The controllers of elite-funded science and R

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Genetic Armageddon: Humanity's Greatest Threat - Video

Public release date: 3-Feb-2012
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Contact: Sara LaJeunesse
SDL13@psu.edu
814-863-4325
Penn State

A preference for fatty foods has a genetic basis, according to researchers, who discovered that people with certain forms of the CD36 gene may like high-fat foods more than those who have other forms of this gene.

The results help explain why some people struggle when placed on a low-fat diet and may one day assist people in selecting diets that are easier for them to follow. The results also may help food developers create new low-fat foods that taste better.

"Fat is universally palatable to humans," said Kathleen Keller, assistant professor of nutritional sciences, Penn State. "Yet we have demonstrated for the first time that people who have particular forms of the CD36 gene tend to like higher fat foods more and may be at greater risk for obesity compared to those who do not have this form of the gene. In animals, CD36 is a necessary gene for the ability to both detect and develop preferences for fat. Our study is one of the first to show this relationship in humans."

Keller and a tem of scientists from Penn State, Columbia University, Cornell University and Rutgers University examined 317 African-American males and females because individuals in this ethnic group are highly vulnerable to obesity and thus are at greatest risk for obesity-related diseases.

The team gave the participants Italian salad dressings prepared with varying amounts of canola oil, which is rich in long-chain fatty acids. The participants were then asked to rate their perceptions of the dressings' oiliness, fat content and creaminess on a scale anchored on the ends with "extremely low" and "extremely high."

The team also gave participants questionnaires aimed at understanding their food preferences. Participants rated how much they liked each food on a scale anchored with "dislike extremely" and "like extremely." Foods included on the questionnaire were associated with poor dietary intake and health outcomes, such as half-and-half, sour cream, mayonnaise, bacon, fried chicken, hot dogs, French fries, cheese, chips, cake, cookies and doughnuts. The researchers collected saliva samples from the participants to determine which forms of CD36 they had. From the saliva samples, they extracted DNA fragments and examined differences in the CD36 gene contained within the fragments.

They found that participants who had the "AA" form of the gene -- present in 21 percent of the population -- rated the salad dressings as creamier than individuals who had other forms of the gene. These individuals reported that the salad dressings were creamier regardless of how much fat was actually in them. The researchers also found that "AA" individuals liked salad dressings, half-and-half, olive oil and other cooking oils more than those who had other forms of the gene. The results are published in a recent issue of the journal Obesity.

"It is possible that the CD36 gene is associated with fat intake and therefore obesity through a mechanism of oral fat perception and preference," said Keller. "In other words, our results suggest that people with certain forms of the CD36 gene may find fat creamier and more enjoyable than others. This may increase their risk for obesity and other health problems."

According to Keller, having certain forms of a gene that help in the perception and enjoyment of fats in foods might once have been an advantage.

"Fats are essential in our diets," she said. "In our evolutionary history, people who were better able to recognize fats in foods were more likely to survive. Such forms of the gene, however, are less useful to us today as most of us no longer have to worry about getting enough fats in our diets."

In fact, she added, having such forms of a gene can be detrimental in today's world of fat-laden convenience foods.

"Our results may help explain why some people have more difficulty adhering to a low-fat diet than other people and why these same people often do better when they adopt high-fat, low-carbohydrate diets such as the Atkins diet," said Keller. "We hope these results will one day help people select diets that are easier for them to follow. We also think the results could help food developers create better tasting low-fat foods that appeal to a broader range of the population."

In the future, the team plans to expand the population they examine to include children.

"By the time we are adults it is very hard for us to change our eating behaviors," said Keller. "So if we can determine which children have forms of the CD36 gene, as well as other genes that are associated with greater liking of fats, we can help them develop healthier eating behaviors at a young age."

Keller also plans to incorporate novel techniques, such as functional magnetic resonance imaging (fMRI), to better understand why certain forms of the CD36 gene are linked to higher fat preferences.

"We plan to scan children while they are tasting high-fat foods and beverages so that we can see how their brains react to fats," she said. "By doing this, we may be able to develop foods that are perceived by the brain as palatable high-fat treats, even though in reality, they are low-fat and healthy."

###

Kathleen Keller was an assistant professor and research associate at Columbia University and the New York Nutrition Obesity Research Center when she conducted the research. Other authors on the paper include Columbia University graduate students Lisa Liang, Johannah Sakimura, Daniel May and Christopher van Belle; Cornell University undergraduate students Cameron Breen and Elissa Driggin; and Beverly Tepper, professor, Rutgers University. Also at Columbia were Patricia Lanzano, research coordinator; Liyong Deng, research technician; and Wendy Chung, assistant professor.

The National Institutes of Health funded this research.

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Gene related to fat preferences in humans found

23-11-2011 02:11 For instance, neural cells in the brain and spinal cord that have been damaged can be replaced by stem cells. In the treatment of cancer, cells partially damaged by radiation or chemotherapy can be replaced with new healthy stem cells that adapt to the affected area, whether it be part of the brain, heart, liver, lungs, or wherever. Dead cells of almost any kind, no matter the type of injury or disease, can be replaced with new healthy cells thanks to the amazing flexibility of stem cells.

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stem cell therapy mexico, Successfully Results - Video

Public release date: 2-Feb-2012
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Contact: Steve Yozwiak
syozwiak@tgen.org
602-343-8704
The Translational Genomics Research Institute

PHOENIX, Ariz. ? Feb. 2, 2012 ? Combination drug therapy may be needed to combat non-small cell lung cancer (NSCLC), according to a study by the Translational Genomics Research Institute (TGen) and Van Andel Research Institute (VARI).

The study, "STAT3 is Activated by JAK2 Independent of Key Oncogenic Driver Mutation in Non-Small Cell Lung Carcinoma," was published online today, Feb. 2, 2012, by the Public Library of Science (PLoS) ONE.

The study found that in NSCLC ? the most common form of lung cancer ? that the STAT3 gene is activated in some NSCLC cell lines by the JAK2 protein. This signaling can play a crucial role in tumor-cell behavior that may not be effectively inhibited by drugs that selectively target these mutations, the study concluded.

"This suggests that there may be a potential role for combination therapy, so you have a better chance of knocking out select NSCLC tumors driven by STAT3-JAK2, or keeping it at bay," said Dr. Glen Weiss, Co-Unit Head of TGen's Lung Cancer Research Laboratory and Director of Thoracic Oncology at Virginia G. Piper Cancer Center Clinical Trials at Scottsdale Healthcare, a partnership between TGen and Scottsdale Healthcare that treats cancer patients with promising new drugs.

The JAK2 protein can activate the gene called STAT3, part of a family of genes that provide instructions for making proteins that are part of the essential chemical signaling pathways that control growth and development in cells. STAT3 has been found to be overactive in cases of several types of cancer, including breast, prostate, pancreas, leukemia and lymphoma.

In laboratory tests involving seven NSCLC cell lines, the TGen-VARI study found that STAT3 was activated in some cell lines by JAK2, independent of key oncogenic, or potentially cancer-causing, genes.

"JAK2-STAT3 signaling plays crucial roles in tumor-cell behavior that may not be effectively inhibited by drugs that selectively target these mutations," said Dr. Jeff MacKeigan, Head of VARI's Laboratory of Systems Biology. VARI is TGen's affiliate in Grand Rapids, Mich.

This study, funded by a TGen-VARI integration grant, should benefit future lung cancer research because of the study's clinically annotated tissue microarray, MacKeigan said.

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About Van Andel Institute

Established by Jay and Betty Van Andel in 1996, Van Andel Institute (VAI) is an independent research and educational organization based in Grand Rapids, Mich., dedicated to preserving, enhancing and expanding the frontiers of medical science, and to achieving excellence in education by probing fundamental issues of education and the learning process. Van Andel Education Institute (VAEI) is dedicated to strengthening science education and preparing and motivating individuals to pursue science or science-related professions. Van Andel Research Institute (VARI), the research arm of VAI, is dedicated to probing the genetic, cellular and molecular origins of cancer, Parkinson's and other diseases and working to translate those findings into effective therapies. This is accomplished through the work of over 200 researchers in 18 on-site laboratories and in collaborative partnerships that span the globe. VARI is affiliated with the Translational Genomics Research Institute, (TGen), of Phoenix, Arizona. For more information, visit: http://www.vai.org.

Media Contact:
Joe Gavan
Vice President, Communications and External Relations
(616) 234-5390
joe.gavan@vai.org

About TGen

The Translational Genomics Research Institute (TGen) is a Phoenix, Arizona-based non-profit organization dedicated to conducting groundbreaking research with life changing results. Research at TGen is focused on helping patients with diseases such as cancer, neurological disorders and diabetes. TGen is on the cutting edge of translational research where investigators are able to unravel the genetic components of common and complex diseases. Working with collaborators in the scientific and medical communities, TGen believes it can make a substantial contribution to the efficiency and effectiveness of the translational process. TGen is affiliated with the Van Andel Research Institute in Grand Rapids, Michigan. For more information, visit: http://www.tgen.org.

Press Contact:
Steve Yozwiak
TGen Senior Science Writer
602-343-8704
syozwiak@tgen.org

About The Virginia G. Piper Cancer Center at Scottsdale Healthcare

The Virginia G. Piper Cancer Center at Scottsdale Healthcare in Scottsdale, Ariz. offers comprehensive cancer care and research through Phase I clinical trials, diagnosis, treatment, prevention and support services in collaboration with leading scientific researchers and community oncologists. Scottsdale Healthcare is the nonprofit parent organization of the Virginia G. Piper Cancer Center at Scottsdale Healthcare, Scottsdale Healthcare Research Institute, Scottsdale Healthcare Osborn Medical Center, Scottsdale Healthcare Shea Medical Center and Scottsdale Healthcare Thompson Peak Hospital. For more information, visit http://www.shc.org.

Press Contact:
Keith Jones
Public Relations Director, Virginia G. Piper Cancer Center
480-323-1383
kjones@shc.org

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Combination drug therapy urged to battle lung cancer

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Celexa or Lexapro - Video

* Shire (Stuttgart: A0MMAG - news) to pay $13 mln upfront, plus milestones

* Sangamo shares rise more than 25 percent (Adds analyst comment, share price)

Feb 1 (Reuters) - Pharmaceutical company Shire said on Wednesday it would collaborate with Sangamo BioSciences (Hamburg: GBY.HM - news) to develop treatments for hemophilia and other inherited diseases based on Sangamo's gene regulation and modification technology.

The news, seen as a vote of confidence in Sangamo's experimental gene-disrupting technique, sent shares of the Richmond (NZSE: RHD.NZ - news) , California-based company up more than 25 percent.

Shire is buying the rights to the U.S. company's proprietary technology to target four genes, which the company said it hoped could lead to therapies for haemophilia A and B. Shire also acquired the right to designate three additional gene targets.

Sylvie Grégoire, president of Shire's Human Genetic Therapies business, said: "While still early in the clinical development process, this DNA-binding protein technology is aligned with our focus of developing new treatments."

The British company is paying Sangamo $13 million in an upfront payment, followed by development and commercial payments and royalties on product sales.

After the deal was announced, Piper Jaffray (Berlin: PJR.BE - news) upgraded Sangamo to "neutral" from "underweight," and raised its price target on the shares to $4 from $2.

Shares of Sangamo were up 92 cents at $4.37 in midday trading on Nasdaq (Nasdaq: ^NDX - news) .

Genetic disease are an important therapeutic area for Shire, and the group has found success with drugs to treat the rare Gaucher's and Fabry's diseases. (Reporting by Paul Sandle and Deena Beasley. Editing by Gunna Dickson)

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UPDATE 2-Shire partners Sangamo in gene therapy for hemophilia

By Maureen Salamon
HealthDay Reporter

WEDNESDAY, Feb. 1 (HealthDay News) -- Treating stroke patients with stem cells taken from their own bone marrow appears to safely help them regain some of their lost abilities, two small new studies suggest.

Indian researchers observed mixed results in the extent of stroke patients' improvements, with one study showing marked gains in daily activities, such as feeding, dressing and movement, and the other study noting these improvements to be statistically insignificant. But patients seemed to safely tolerate the treatments in both experiments with no ill effects, study authors said.

"The results are encouraging to know but we need a larger, randomized study for more definitive conclusions," said Dr. Rohit Bhatia, a professor of neurology at the All India Institute of Medical Sciences in New Delhi, and author of one of the studies. "Many questions -- like timing of transplantation, type of cells, mode of transplantation, dosage [and] long-term safety -- need answers before it can be taken from bench to bedside."

The studies are scheduled to be presented Wednesday and Thursday at the American Stroke Association's annual meeting in New Orleans.

Stem cells -- unspecialized cells from bone marrow, umbilical cord blood or human embryos that can change into cells with specific functions -- have been explored as potential therapies for a host of diseases and conditions, including cancer and strokes.

In one of the current studies, 120 moderately affected stroke patients ranging from 18 to 75 years old were split into two groups, with half infused intravenously with stem cells harvested from their hip bones and half serving as controls. About 73 percent of the stem cell group achieved "assisted independence" after six months, compared with 61 percent of the control group, but the difference wasn't considered statistically significant.

In the other study, presented by Bhatia, 40 patients whose stroke occurred between three and 12 months prior were also split into two groups, with half receiving stem cells, which were dissolved in saline and infused over several hours. When compared to controls, stroke patients receiving stem cell therapy showed statistically significant improvements in feeding, dressing and mobility, according to the study. On functional MRI scans, the stem cell recipients also demonstrated an increase in brain activity in regions that control movement planning and motor function.

Neither study yielded adverse effects on patients, which could include tumor development.

But Dr. Matthew Fink, chief of the division of stroke and critical care neurology at New York-Presbyterian Hospital/Weill Cornell Medical Center, said that the therapy's safety is the only thing the two studies seemed to demonstrate.

"The thing to keep in mind is that these are really phase one trials," said Fink, also a professor of neurology at Weill Cornell Medical College. "I'm concerned that people get the idea that now stem cell treatment is available for stroke, and that's not the case."

Fink noted that the cells taken from study participants' hip bones can only be characterized as "bone marrow aspirates" since the authors didn't prove that actual stem cells were extracted.

"They haven't really analyzed if they're stem cells and what they turn into when they go into circulation," he added. "The best way to look at this is, it's very preliminary . . . when patients come to me to talk about it, I'm going to tell them it's years away before we know if this is going to work."

Studies presented at scientific conferences should be considered preliminary until published in a peer-reviewed medical journal.

Copyright © 2012 HealthDay. All rights reserved.

SOURCES: Rohit Bhatia, M.D., professor, neurology, All India Institute of Medical Sciences, New Delhi; Matthew Fink, M.D., professor of neurology, Weill Cornell Medical College, and chief, division of stroke and critical care neurology, New York-Presbyterian Hospital/Weill Cornell Medical Center, New York City; abstracts from American Stroke Association, annual meeting, Feb. 1-2, 2012, New Orleans

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Stem Cell Therapy Shows Promise for Stroke, Studies Say

This is one of the first examples in infectious disease of where an individual's genetic profile can determine which drug will work best for them – the idea of personalised medicine that is gradually becoming familiar in cancer medicine.

The scientists found that people generate an immune response to tuberculosis that is 'too much', 'too little' or 'just right', according to what versions they have of the LTA4H gene.

The findings indicate that patients are likely to benefit from different drug treatments depending on their LTA4H gene profile.

Furthermore, the researchers show that steroids used as part of the standard treatment for the most severe form of tuberculosis, TB meningitis, only benefit some patients.

The results of the study, part-funded by the Wellcome Trust, are published in the journal Cell.

Tuberculosis is a major cause of death worldwide, with an estimated 9.4 million cases and 1.7 million deaths in 2009. The disease is caused by Mycobacterium tuberculosis bacteria and differs according to where the infection takes hold. Most TB affects the lungs, but around 40% of cases involve disease elsewhere. In perhaps 1% of cases, TB affects the brain. This form of the disease, TB meningitis, is the most serious. It is hard to diagnose and treat, and even with treatment it is often fatal.

The standard treatment for TB meningitis involves a range of antibiotics to try and kill the bacteria, and the steroid dexamethasone to dampen inflammation – the body's response to tuberculosis infection that can be almost as much of a problem.

The new study combines work in zebrafish at the University of Washington, Seattle to identify genes and biological pathways involved in the immune response to TB, with clinical research work in collaboration with Pham Ngoc Thach Hospital, the Hospital for Tropical Diseases and the Oxford University Clinical Research Unit in Vietnam.

The scientists identified a gene in zebrafish associated with susceptibility to tuberculosis, which controlled the balance of the inflammatory response. Variations in the DNA code in this gene could alter different biological pathways, leading either to too much inflammation or too little. Both too much and too little inflammation were problems, allowing the tuberculosis bacteria to thrive and multiply.

The researchers showed that blocking the appropriate biological pathway with drugs could restore just the right level of inflammatory response.

The researchers based in Vietnam then went back to samples from a previous clinical trial in over 500 patients with TB meningitis. They showed changes at a single position in the human LTA4H gene were associated with treatment response.

Only those having LTA4H genes that led to too much inflammation benefitted from the use of the steroid dexamethasone.

There is some suggestion that the steroid could have an adverse effect for those whose LTA4H genes already lead them to have a reduced inflammatory response, though the result is not statistically significant.

'It's like a "Goldilocks" gene. Depending on what versions of the LTA4H gene you have inherited, you could see an inflammatory response to tuberculosis that is "too much", "too little", or "just right",' explains Dr Sarah Dunstan Head of Human Genetics of Oxford University Vietnam. 'You are likely to benefit most from a treatment tailored to your own genes.'

Dr Guy Thwaites of King's College London and who lead the clinical study in Vietnam on a Wellcome Trust Fellowship says: 'This is a fundamental discovery. It is now possible to think about the use of simple but rapid genetic tests to determine how people will respond to tuberculosis infection and whether they would benefit from steroids.'

'The findings could apply much more widely than just in TB meningitis, or other forms of tuberculosis,' adds Dr Thwaites. 'Since the inflammation pathways governed by the LTA4H gene are central to many infections, there could be implications for many diseases.'

'This study highlights the power of really good clinical research supported through Wellcome Trust Fellowships and linked with some of the very best scientists in the world in Vietnam and the USA, which can bring immediate benefits to patients and also point the way to develop better, more targeted drugs to treat people with tuberculosis in the future,' says Professor Jeremy Farrar who leads the Oxford University Clinical Research Unit in Vietnam. 'The idea that a patient's genes can determine what treatment they will benefit from is pretty novel outside of cancer. Nothing like this has been seen before in infectious disease. Now we need to see if we can use this to help patients with this devastating disease'

More information: 'Host genotype-specific therapies can optimise the inflammatory response to mycobacterial infections', by David Tobin et al., Cell (2012).

Provided by King's College London (news : web)

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'Goldilocks' gene could determine best treatment for tuberculosis patients

Public release date: 2-Feb-2012
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Contact: Katherine Barnes
katherine.barnes@kcl.ac.uk
44-020-784-83076
King's College London

'Goldilocks' gene could determine best treatment for TB patients Tuberculosis patients may receive treatments in the future according to what version they have of a single 'Goldilocks' gene, says an international research team from Oxford University, King's College London, Vietnam and the USA.

This is one of the first examples in infectious disease of where an individual's genetic profile can determine which drug will work best for them ? the idea of personalised medicine that is gradually becoming familiar in cancer medicine.

The scientists found that people generate an immune response to tuberculosis that is 'too much', 'too little' or 'just right', according to what versions they have of the LTA4H gene.

The findings indicate that patients are likely to benefit from different drug treatments depending on their LTA4H gene profile.

Furthermore, the researchers show that steroids used as part of the standard treatment for the most severe form of tuberculosis, TB meningitis, only benefit some patients.

The results of the study, part-funded by the Wellcome Trust, are published in the journal Cell.

Tuberculosis is a major cause of death worldwide, with an estimated 9.4 million cases and 1.7 million deaths in 2009. The disease is caused by Mycobacterium tuberculosis bacteria and differs according to where the infection takes hold. Most TB affects the lungs, but around 40% of cases involve disease elsewhere. In perhaps 1% of cases, TB affects the brain. This form of the disease, TB meningitis, is the most serious. It is hard to diagnose and treat, and even with treatment it is often fatal.

The standard treatment for TB meningitis involves a range of antibiotics to try and kill the bacteria, and the steroid dexamethasone to dampen inflammation ? the body's response to tuberculosis infection that can be almost as much of a problem.

The new study combines work in zebrafish at the University of Washington, Seattle to identify genes and biological pathways involved in the immune response to TB, with clinical research work in collaboration with Pham Ngoc Thach Hospital, the Hospital for Tropical Diseases and the Oxford University Clinical Research Unit in Vietnam.

The scientists identified a gene in zebrafish associated with susceptibility to tuberculosis, which controlled the balance of the inflammatory response. Variations in the DNA code in this gene could alter different biological pathways, leading either to too much inflammation or too little. Both too much and too little inflammation were problems, allowing the tuberculosis bacteria to thrive and multiply.

The researchers showed that blocking the appropriate biological pathway with drugs could restore just the right level of inflammatory response.

The researchers based in Vietnam then went back to samples from a previous clinical trial in over 500 patients with TB meningitis. They showed changes at a single position in the human LTA4H gene were associated with treatment response.

Only those having LTA4H genes that led to too much inflammation benefitted from the use of the steroid dexamethasone.

There is some suggestion that the steroid could have an adverse effect for those whose LTA4H genes already lead them to have a reduced inflammatory response, though the result is not statistically significant.

'It's like a "Goldilocks" gene. Depending on what versions of the LTA4H gene you have inherited, you could see an inflammatory response to tuberculosis that is "too much", "too little", or "just right",' explains Dr Sarah Dunstan Head of Human Genetics of Oxford University Vietnam. 'You are likely to benefit most from a treatment tailored to your own genes.'

Dr Guy Thwaites of King's College London and who lead the clinical study in Vietnam on a Wellcome Trust Fellowship says: 'This is a fundamental discovery. It is now possible to think about the use of simple but rapid genetic tests to determine how people will respond to tuberculosis infection and whether they would benefit from steroids.'

'The findings could apply much more widely than just in TB meningitis, or other forms of tuberculosis,' adds Dr Thwaites. 'Since the inflammation pathways governed by the LTA4H gene are central to many infections, there could be implications for many diseases.'

'This study highlights the power of really good clinical research supported through Wellcome Trust Fellowships and linked with some of the very best scientists in the world in Vietnam and the USA, which can bring immediate benefits to patients and also point the way to develop better, more targeted drugs to treat people with tuberculosis in the future,' says Professor Jeremy Farrar who leads the Oxford University Clinical Research Unit in Vietnam. 'The idea that a patient's genes can determine what treatment they will benefit from is pretty novel outside of cancer. Nothing like this has been seen before in infectious disease. Now we need to see if we can use this to help patients with this devastating disease'

###

For more information please contact:

Dr Sarah Dunstan of the Oxford University Clinical Research Unit in Vietnam on: 84-90-810-7807 or sdunstan@oucru.org

Dr Guy Thwaites of King's College London on: 07818-040689 or guy.thwaites@btinternet.com

Professor Jeremy Farrar of the Oxford University Clinical Research Unit in Vietnam on: 84-83-836-2225 or jfarrar@oucru.org

Or the University of Oxford press office on 44-1865-280530 or press.office@admin.ox.ac.uk

Notes to Editors

* The paper 'Host genotype-specific therapies can optimise the inflammatory response to mycobacterial infections' by David Tobin and colleagues is to be published in the journal Cell with the embargo of 17:00 UK time / 12:00 noon US Eastern time on Thursday 2 February 2012.

* The Wellcome Trust is a global charitable foundation dedicated to achieving extraordinary improvements in human and animal health. It supports the brightest minds in biomedical research and the medical humanities. The Trust's breadth of support includes public engagement, education and the application of research to improve health. It is independent of both political and commercial interests. http://www.wellcome.ac.uk

* King's College London is one of the top 30 universities in the world (2011/12 QS World University Rankings), and the fourth oldest in England. A research-led university based in the heart of London, King's has nearly 23,500 students (of whom more than 9,000 are graduate students) from nearly 140 countries, and some 6,000 employees. King's is in the second phase of a ?1 billion redevelopment programme which is transforming its estate.

King's has an outstanding reputation for providing world-class teaching and cutting-edge research. In the 2008 Research Assessment Exercise for British universities, 23 departments were ranked in the top quartile of British universities; over half of our academic staff work in departments that are in the top 10 per cent in the UK in their field and can thus be classed as world leading. The College is in the top seven UK universities for research earnings and has an overall annual income of nearly ?450 million.

King's has a particularly distinguished reputation in the humanities, law, the sciences (including a wide range of health areas such as psychiatry, medicine, nursing and dentistry) and social sciences including international affairs. It has played a major role in many of the advances that have shaped modern life, such as the discovery of the structure of DNA and research that led to the development of radio, television, mobile phones and radar. It is the largest centre for the education of healthcare professionals in Europe; no university has more Medical Research Council Centres.

King's College London and Guy's and St Thomas', King's College Hospital and South London and Maudsley NHS Foundation Trusts are part of King's Health Partners. King's Health Partners Academic Health Sciences Centre (AHSC) is a pioneering global collaboration between one of the world's leading research-led universities and three of London's most successful NHS Foundation Trusts, including leading teaching hospitals and comprehensive mental health services. For more information, visit: http://www.kingshealthpartners.org.

* Oxford University's Medical Sciences Division is one of the largest biomedical research centres in Europe, with over 2,500 people involved in research and more than 2,800 students. The University is rated the best in the world for medicine, and it is home to the UK's top-ranked medical school.

From the genetic and molecular basis of disease to the latest advances in neuroscience, Oxford is at the forefront of medical research. It has one of the largest clinical trial portfolios in the UK and great expertise in taking discoveries from the lab into the clinic. Partnerships with the local NHS Trusts enable patients to benefit from close links between medical research and healthcare delivery.

A great strength of Oxford medicine is its long-standing network of clinical research units in Asia and Africa, enabling world-leading research on the most pressing global health challenges such as malaria, TB, HIV/AIDS, Dengue and Influenza. Oxford is also renowned for its large-scale studies which examine the role of factors such as smoking, alcohol and diet on cancer, heart disease and other conditions.

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'Goldilocks' gene could determine best treatment for TB patients

Public release date: 1-Feb-2012
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Contact: Vicki Cohn
vcohn@liebertpub.com
914-740-2100
Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY -- A variety of innovative products and technologies that promote healing of difficult, painful, and potentially life-threatening acute and chronic wounds are described in the premier issue of Advances in Wound Care, a bimonthly online publication from Mary Ann Liebert, Inc. (http://www.liebertpub.com) and an Official Journal of the Wound Healing Society. The issue is available free online at http://www.liebertpub.com/wound

Several Technology Reports highlight products such as a negative pressure device that delivers a continuous subatmospheric pressure level to the wound bed to promote healing. Advanced dressings described in the reports can absorb fluid produced by the wound, cushion the surrounding area, and provide continuous cleansing to accelerate healing, reduce pain, and control swelling. Also featured are biological therapies that may include the delivery of growth factors, bioengineered cells, or components of the patient's own cells to stimulate the healing process.

"Thanks to the Wound Healing Society, Advances in Wound Care is a peer-reviewed forum where the essence of latest advances in science contributed by world-experts meets practical solutions in wound care," says Editor-in-Chief Chandan K. Sen, PhD, Professor of Surgery and Director of the Comprehensive Wound Center at The Ohio State University Medical Center.

###

Advances in Wound Care is a bimonthly online journal that reports the latest scientific discoveries, translational research, and clinical developments in acute and chronic wound care. Each issue provides a digest of the latest research findings, innovative wound care strategies, industry product pipeline, and developments in biomaterials and skin and tissue regeneration to optimize patient outcomes. The broad scope of applications covered includes limb salvage, chronic ulcers, burns, trauma, blast injuries, surgical repair, skin bioengineering, dressings, anti-scar strategies, diabetic ulcers, ostomy, bedsores, biofilms, and military wound care. Complete tables of content and a sample issue may be viewed online (http://www.liebertpub.com/wound).

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

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

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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

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New high-tech wound care products speed healing of ulcers, burns, injuries and surgical wounds

02-11-2011 12:51 Selena shares her family's experience with Lynch syndrome. This workshop is part of a genomics curriculum for practicing healthcare providers developed by the Genomic Medicine Institute at El Camino Hospital, Genetic Alliance, and the National Coalition for Health Professional Education in Genetics. This workshop, the second in a 10-part series, covered genetic-testing technology; selecting appropriate genetic tests; ordering tests; pre- and post-test counseling; test costs; interpreting test results.

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Workshop 2: Fundamentals of Genetic Testing Part I - Selena Martinez - Video

26-01-2012 09:21 Jared Taylor, editor of American Renaissance, explains the biological basis of race. Sources: Weiss, Rick, and Justin Gillis. "Teams Finish Mapping Human DNA." Washington Post 27 June 2000: A1. Print. Edwards, AWF "Human Genetic Diversity: Lewontin's Fallacy." BioEssays 25.8 (2003): 798-801. Web. http://www.goodrumj.com Lewontin, Richard C. "The Apportionment of Human Diversity." Evolutionary Biology 6 (1972): 391-98. Print. Risch, Niel J. et al. "Genetic Structure, Self-Identified Race/Ethnicity, and Confounding in Case-Control Association Studies." American Journal of Human Genetics 76.2 (2005): 268-75. Web. http://www.ncbi.nlm.nih.gov Ousley, Stephen D. "Understanding Race and Human Variation: Why Forensic Anthropologists Are Good at Identifying Race." American Journal of Physical Anthropology 139 (2009): 68-76. Web. onlinelibrary.wiley.com Sauer, Norman J. "Forensic Anthropology and the Concept of Race: If Races Don't Exist, Why Are Forensic Anthropologists So Good at Identifying Them?" Social Science Medicine 34.2 (1992): 107-11. Print. Norton, Cherry. "Hidden Black Ancestry Linked to Rise in Sickle Cell Blood Disorder." Independent. 23 Oct. 1999. Web. http://www.independent.co.uk Motulsky, Arno G. "Frequency of Sickling Disorders in US Blacks." New England Journal of Medicine 288 (1973): 31-33. Print. "Hemochromatosis." PubMed Health. 12 Apr. 2010. Web. http://www.ncbi.nlm.nih.gov Parker, Heidi G et al. "Genetic Structure of the Purebred Domestic Dog." Science 304 (2004): 1160-164. Print ...

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The Reality of Race - Video

23-12-2011 02:33 KXAN Medical Minute -- Texas Oncology http://www.texasoncology.com

More here:
Medical advice from Dr. Sandbach - Genetic Testing - Video

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

Vertex Pharmaceuticals Incorporated (Nasdaq: VRTX) announced today that the U.S. Food and Drug Administration (FDA) has approved KALYDECOTM (ivacaftor), the first medicine to treat the underlying cause of cystic fibrosis (CF), a rare, genetic disease. KALYDECO (kuh-LYE-deh-koh) is approved for people with CF ages 6 and older who have at least one copy of the G551D mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Approximately 1,200 people in the United States, or 4 percent of those with CF, are believed to have this mutation. KALYDECO was granted approval in approximately three months, making it one of the fastest FDA approvals ever and marking the second approval of a new medicine from Vertex in less than a year. The company has established a financial assistance and patient support program to help get KALYDECO to eligible patients for whom it is prescribed. KALYDECO was discovered as part of a collaboration with Cystic Fibrosis Foundation Therapeutics, Inc., the nonprofit drug discovery and development affiliate of the Cystic Fibrosis Foundation.

KALYDECO carton, bottle, and pills (Photo: Business Wire)

Vertex is ready to support the introduction of KALYDECO and will begin shipping it to pharmacies in the United States this week. The company will host a conference call for investors and media today, January 31, 2012, at 12:15 p.m. ET to provide more information on KALYDECO availability, price and the financial assistance and patient support program.

"More than 13 years ago we set out to change the lives of people with cystic fibrosis by developing new medicines that address the underlying cause of this rare and devastating disease," said Jeffrey Leiden, M.D., Ph.D., Vertex's incoming President and Chief Executive Officer. "KALYDECO represents a major advance in the treatment of cystic fibrosis for people with a specific type of this disease. But our work isn't done. With the ongoing support of doctors, patients and the Cystic Fibrosis Foundation, we're making progress toward our ultimate goal of developing additional medicines to help many more people with cystic fibrosis."

The approval of KALYDECO was based on data from two Phase 3 studies of people with CF who have at least one copy of the G551D mutation. Those who were treated with KALYDECO experienced significant and sustained improvements in lung function as well as other disease measures, including weight gain and certain quality of life measurements, compared to those who received placebo. People who took KALYDECO also experienced significantly fewer pulmonary exacerbations, which are periods of worsening in the signs and symptoms of the disease that often require treatment with antibiotics and hospital visits. Fewer people in the KALYDECO treatment groups discontinued treatment due to adverse events than in the placebo groups. The majority of adverse events associated with KALYDECO were mild to moderate. Adverse events commonly observed in those taking KALYDECO included headache, upper respiratory tract infection (common cold), stomach pain and diarrhea.

"Advances in cystic fibrosis treatment have helped manage symptoms of the disease, however people with cystic fibrosis still have a hard time staying healthy and being active," said Bonnie Ramsey, M.D., Director of the Center for Clinical and Translational Research at Seattle Children's Research Institute and principal investigator for one of the Phase 3 KALYDECO trials. "KALYDECO is a fundamental shift in the way cystic fibrosis is treated. In people with a specific genetic mutation, KALYDECO helped them breathe more easily, gain weight and generally feel better."

"Together, we're changing the lives of people with cystic fibrosis," said Robert J. Beall, Ph.D., President and CEO of the Cystic Fibrosis Foundation. "We now have a medicine that treats the underlying cause of the disease in people with the G551D mutation. KALYDECO also provides us with a roadmap for exploring additional targeted approaches to treatment for all people with cystic fibrosis."

Cystic fibrosis is a rare, life-threatening genetic disease for which there is no cure. CF is caused by defective or missing CFTR proteins resulting from mutations in the CFTR gene. CFTR proteins act as channels at the cell surface that control the flow of salt and water across the cells. When the defective CFTR protein does not work properly at the cell surface, abnormally thick, sticky mucus builds up in the lungs. The digestive tract and a number of other organs are also affected. KALYDECO, an oral medicine known as a CFTR potentiator, helps the CFTR protein function more normally once it reaches the cell surface. KALYDECO targets the abnormal CFTR protein channels and opens them to allow chloride ions to move into and out of the cell, which helps thin the mucus so it can hydrate and protect the airways, and keeps them from getting clogged and then infected.

Because KALYDECO targets a specific genetic mutation, a person's genotype should be known before this new medicine is prescribed. Genetic testing is widely available and FDA-cleared tests are available for people with CF whose genotype is unknown. According to the 2010 Cystic Fibrosis Foundation's Patient Registry, nearly 92 percent of people with CF have already had their CF mutations identified.

KALYDECO by itself works in a subset of people with CF, but research is ongoing to explore a similar targeted approach using a combination of medicines, including KALYDECO, to treat the most common form of the disease.

Helping People with CF Get KALYDECO

The people who work at Vertex understand that medicines can only help patients who can get them. To that end, the company offers a comprehensive financial assistance and patient support program. A specially-trained and dedicated Vertex team will provide one-on-one support to help eligible patients who are prescribed KALYDECO understand their insurance benefits and the resources that are available to help them.

For eligible patients, the program also includes the following:

Free Medicine Program: Vertex will provide KALYDECO for free to people who do not have insurance and have an annual household income of $150,000 or less; and Co-Pay Assistance Program: For patients with commercial insurance plans that cover KALYDECO and who are enrolled in the Guidance and Patient Support, or GPS, program, there will be a minimal out-of-pocket obligation after which Vertex will help cover co-pay or co-insurance costs up to 30 percent of the list price of the medicine. There is no income limit to be eligible for this program.

Some patients are not eligible for company co-pay support because they have Medicare or Medicaid coverage or live in Massachusetts. There are independent non-profit copay assistance foundations that may be able to help those patients with their out-of-pocket costs.

More information about this program is available by calling 1-877-7-KALYDECO (877-752-5933) or visiting http://www.VertexGPS.com.

About KALYDECO

KALYDECO is the first treatment to target the underlying cause of CF. The Phase 3 studies evaluated KALYDECO in people with CF ages 6 and older who had at least one copy of the G551D mutation. PERSIST, a Phase 3, open-label, 96-week extension study, is underway to evaluate the long-term safety and durability of treatment with KALYDECO. This ongoing study enrolled people who completed 48 weeks of treatment in either Phase 3 study (placebo and KALYDECO treatment groups) and met other eligibility criteria. KALYDECO will be taken as one 150-mg tablet twice daily (every 12 hours).

Vertex retains worldwide rights to develop and commercialize KALYDECO. In October 2011, Vertex submitted a marketing authorization application to the European Medicines Agency (EMA) for KALYDECO and has received agreement from the EMA for accelerated assessment in Europe. The EMA regulatory review is ongoing.

Indication and Important Safety Information

KALYDECO is a prescription medicine used for the treatment of cystic fibrosis (CF) in patients ages 6 years and older who have a certain mutation in their CF gene called the G551D mutation.

KALYDECO is not for use in people with CF due to other mutations in the CF gene. It is not effective in CF patients with two copies of the F508del mutation (F508del/F508del) in the CF gene.

It is not known if KALYDECO is safe and effective in children under 6 years of age.

KALYDECO should not be used with certain medicines, including the antibiotics rifampin and rifabutin; seizure medications (phenobarbital, carbamazepine, or phenytoin); and the herbal supplement St. John's Wort.

KALYDECO can cause serious side effects. High liver enzymes in the blood have occurred in patients taking KALYDECO. Regular assessment is recommended.

The most common side effects associated with KALYDECO include headache; upper respiratory tract infection (common cold) including sore throat, nasal or sinus congestion, and runny nose; stomach (abdominal) pain; diarrhea; rash; nausea; and dizziness.

These are not all the possible side effects of KALYDECO. Patients should tell their healthcare providers about any side effect that bothers them or doesn't go away.

Please see full Prescribing Information for KALYDECO at http://www.KALYDECO.com.

Conference Call for Media and Investors

Vertex will host a conference call and webcast today, January 31, 2012 at 12:15 p.m. ET to provide more information about today's approval, the price of KALYDECO and Vertex's new financial assistance and patient support program. The conference call will be webcast live and a link to the webcast may be accessed from the ‘Events & Presentations' page of Vertex's website at http://www.vrtx.com.

To listen to the live call on the telephone, dial 1-877-250-8889 (United States and Canada) or 1-720-545-0001 (International). To ensure a timely connection, it is recommended that users register at least 15 minutes prior to the scheduled webcast.

The conference ID number for the live call and replay is 48426093.

The call will be available for replay via telephone commencing January 31, 2012 at 3:00 p.m. ET running through 5:00 p.m. ET on February 7, 2012. The replay phone number for the United States and Canada is 1-855-859-2056. The international replay number is 1-404-537-3406.

Following the live webcast, an archived version will be available on Vertex's website until 5:00 p.m. ET on February 14, 2012. Vertex is also providing a podcast MP3 file available for download on the Vertex website at http://www.vrtx.com.

About Cystic Fibrosis

Cystic fibrosis is a rare, life-threatening genetic disease affecting approximately 30,000 people in the United States and 70,000 people worldwide. Today, the median predicted age of survival for a person with CF is approximately 38 years but the median age of death remains in the mid-20s. There are more than 1,800 known mutations in the CFTR gene. Some of these mutations, which can be determined by a genetic, or genotyping test, lead to CF by creating non-working or too few CFTR proteins at the cell surface. The absence of working CFTR proteins results in poor flow of salt and water across cell membranes in a number of organs, including the lungs. This leads to the buildup of abnormally thick, sticky mucus that can cause chronic lung infections and progressive lung damage.

In some people, CFTR proteins are present at the cell surface but do not work properly. One type of this dysfunction is known as the G551D mutation. Approximately 4 percent of those with CF, or about 1,200 people in the United States, are believed to have this mutation. An estimated 1,000 people in Europe have the G551D mutation.

In people with the most common mutation in the CFTR gene, F508del, the CFTR protein does not reach the cell surface in normal amounts and the CFTR proteins that reach the surface do not work correctly. Nearly 90 percent of people with CF have at least one copy of the F508del mutation; approximately half of those with CF have two copies. KALYDECO is not effective in CF patients who have two copies of the F508del mutation in the CFTR gene.

Vertex's Ongoing CF Research and Development Program

KALYDECO has been approved by the FDA for people with CF ages 6 and older who have at least one copy of the G551D mutation. Vertex is planning to begin additional studies this year to evaluate KALYDECO in children with CF as young as 2 years old and in people with CF who have the R117H mutation or gating mutations that were not evaluated in the previous Phase 3 studies.

Enrollment is ongoing in the second part of a Phase 2 clinical trial of combination regimens of KALYDECO and VX-809, a CFTR corrector, in people with the most common mutation in CF, known as F508del. In addition, the company plans to begin Phase 2 development of VX-661, a second CFTR corrector, in the first quarter of 2012.

Collaborative History with Cystic Fibrosis Foundation Therapeutics, Inc. (CFFT)

Vertex initiated its CF research program in 1998 as part of a collaboration with CFFT, the nonprofit drug discovery and development affiliate of the Cystic Fibrosis Foundation. This collaboration was expanded to support the accelerated discovery and development of Vertex's CFTR modulators.

About the Cystic Fibrosis Foundation

The Cystic Fibrosis Foundation is the world's leader in the search for a cure for cystic fibrosis. The Foundation funds more CF research than any other organization and nearly every CF drug available today was made possible because of Foundation support. Based in Bethesda, Md., the Foundation also supports and accredits a national care center network that has been recognized by the National Institutes of Health as a model of care for a chronic disease. The CF Foundation is a donor-supported nonprofit organization. For more information, visit http://www.cff.org.

About Vertex

Vertex creates new possibilities in medicine. Our team discovers, develops and commercializes innovative therapies so people with serious diseases can lead better lives.

Vertex scientists and our collaborators are working on new medicines to cure or significantly advance the treatment of hepatitis C, cystic fibrosis, rheumatoid arthritis, epilepsy and other life-threatening diseases.

Founded more than 20 years ago in Cambridge, MA, we now have ongoing worldwide research programs and sites in the U.S., U.K. and Canada. Today, Vertex has more than 2,000 employees around the world, and Science magazine named Vertex number one on its 2011 list of Top Employers in the life sciences.

Special Note Regarding Forward-Looking Statements

This press release contains forward-looking statements, as defined in the Private Securities Litigation Reform Act of 1995, as amended, including statements regarding (i) Vertex being ready to support the introduction of KALYDECO and beginning to ship it to pharmacies this week; (ii) Vertex's financial assistance and patient support programs; (iii) the progress Vertex is making toward its ultimate goal of developing additional medicines to help many more people with cystic fibrosis; (iv) the roadmap provided by KALYDECO for exploring additional targeted approaches to treatment for all people with cystic fibrosis; (v) the ongoing research to explore a targeted approach using a combination of medicines, including KALYDECO, to treat the most common form of the disease and (vi) planned additional clinical trials of KALYDECO in children as young as 2 years old and people with CF who have the R117H mutation and gating mutations that were not evaluated in previous Phase 3 clinical trials. While the company believes the forward-looking statements contained in this press release are accurate, there are a number of factors that could cause actual events or results to differ materially from those indicated by such forward-looking statements. Those risks and uncertainties include, among other things, risks related to the commercialization of KALYDECO and development of additional medicines to treat cystic fibrosis and the other risks listed under Risk Factors in Vertex's annual report and quarterly reports filed with the Securities and Exchange Commission and available through Vertex's website at http://www.vrtx.com. Vertex disclaims any obligation to update the information contained in this press release as new information becomes available.

(VRTX-GEN)

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Main Category: Genetics
Also Included In: Bones / Orthopedics
Article Date: 02 Feb 2012 - 10:00 PST

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According to a study published in the online version of the journal The Oncologist, a genetic variation that increases the risk of individuals who take bisphosphonates, developing serious necrotic jaw bone lesions, has been identified by researchers at the Columbia University College of Dental Medicine.

Bisphosphonates are a common class of osteoclastic inhibitors that work by attaching to calcium in the bone and inhibiting osteoclasts, bone cells that disintegrate the bone's mineral structure. The finding opens the door for a genetic screening test to determine which individuals can take these medications safely.

At present, approximately 3 million women in the U.S. take oral bisphosphonates for the treatment or prevention of osteoporosis. Furthermore, each year, thousands of cancer patients are given intravenous bisphosphonates to prevent excess calcium (hypercalcemia) from gathering in the blood and to control the spread of bone cancer.

Lead researcher of the study, Athanasios I. Zavras, DMD, MS,DMSc, associate professor of Dentistry and Epidemiology and Director of the Division of Oral Epidemiology & Biostatistics at the Columbia University College of Dental Medicine, explained:

"These drugs have been widely used for years and are generally considered safe and effective. But the popular literature and blogs are filled with stories of patients on prolonged bisphosphonate therapy who were trying to control osteoporosis or hypercalcemia only to develop osteonecrosis of the jaw."

Often, osteonecrosis of the jaw (ONJ) results in painful and difficult-to-treat bone lesions, which can ultimately result in entire jaw loss. Among individuals taking bisphosphonates, ONJ usually occurs in those who go through invasive dental procedures or those with dental disease.

At present, figures on the incidence of ONJ in individuals taking oral bisphosphonates are unreliable. According to the American College of Rheumatology, estimates vary from 1 in 1,000 to 1 in 100,000 patients each year of exposure to the drug. Approximately 5% to 10% of cancer patients taking intravenous bisphosphonates are affected by ONJ.

According to prior investigations, genetic factors play a significant role in predisposing patients to ONJ. Dr. Zavras and his team conducted genome-wide examination of 30 individuals who have developed ONJ while taking bisphosponates and compared them with several disease free individuals who used bisphosphonates.

Results showed that individuals who has a small variation in the RBMS3 gene were 5.8 times more likely to develop ONJ than individuals without the variation. The researchers also identified small variations in two other genes that may contribute to ONJ risk - IGFBP7 and ABCC4.

Dr. Zavras, explained:

"Our ultimate goal is to develop a pharmacogenetic test that personalizes risk assessment for ONJ, a test that you could give to people before they start to use bisphosphonates.

Those who are positive for this genetic variation would select some other treatment, while those who are negative could take these medications with little fear of developing ONJ."

Dr. Zavras, continued:

"At the moment, many women discontinue or avoid treatment for serious osteoporosis because they are afraid of losing their jaw bones. There even are reports of dentists who have refused to perform certain invasive procedures in patients taking bisphosphonates. So there is a great need for a pharmacogenetic screening test to determine which patients are really at risk for ONJ."

The researchers explain that additional studies are required in order to determine if the RBMS3 gene variation is seen in other racial groups, as the current investigation only examined Caucasians.

The study was supported by the National Institute of Dental and Craniofacial Research.

Written by Grace Rattue
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

Visit our genetics section for the latest news on this subject. “Genomewide Pharmacogenetics of Bisphosphonate-Induced Osteonecrosis of the Jaw: The Role of RBMS3” Paola Nicoletti et al.
The Oncologist, First Published Online January 20, 2012; doi: 10.1634/theoncologist.2011-0202

Source: Columbia University Medical Center

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Osteoporosis Drug Complications Linked To Genetic Factors

SAN DIEGO, Feb. 2, 2012 /PRNewswire/ -- Sequenom, Inc. (NASDAQ: SQNM - News), a life sciences company providing innovative genetic analysis solutions, today announced that a new publication of an independent multi-center study on Sequenom Center for Molecular Medicine's MaterniT21™ laboratory-developed test (LDT) appears today in the online issue of Genetics in Medicine. The study demonstrated the LDT can detect fetal trisomy 21, 18 and 13 with high accuracy from a maternal blood sample and will be published in the March issue. The full results of the study can be found online at http://journals.lww.com/geneticsinmedicine/.

"Together with the previously published results on the test's ability to detect trisomy 21 with high accuracy, this publication provides further evidence that this valuable non-invasive technology can identify nearly all cases of T18 and T13, as well as T21, at a low false positive rate," said Harry F. Hixson, Jr., Ph.D., Chairman and CEO, Sequenom, Inc. "This research continues to validate the use of our MaterniT21 LDT as a valuable tool in the care of pregnant women who are at high risk for fetal aneuploidy."  

The published results represent a large international, multi-center study conducted at 27 prenatal diagnostic centers. Participating sites collected and processed maternal plasma samples from 4,664 pregnant women at high risk for fetal aneuploidy undergoing diagnostic testing in the late first and early second trimester. The results of a blinded testing of 212 pregnancies with trisomy 21 and their 1,484 matched controls were previously published in Genetics in Medicine. During that same testing period, blinded samples from pregnancies with trisomy 18 and trisomy 13 and their controls were also tested. Inclusion criteria were the same as for the earlier study of trisomy 21. 

A total of sixty-two trisomy 18 and twelve trisomy 13 pregnancies along with their matched controls (including the trisomy 21 cases and matched controls) were tested using the MaterniT21 LDT. When unblinded, the detection rate for trisomy 18 was 100 percent and for trisomy 13, was 91.7 percent, with false positive rates of 0.28 and 0.97 percent, respectively. 

The research was led by Jacob Canick, PhD, and Glenn Palomaki, PhD, of the Division of Medical Screening and Special Testing in the Department of Pathology and Laboratory Medicine at Women & Infants Hospital and The Warren Alpert Medical School of Brown University, and included scientists at Sequenom Center for Molecular Medicine, San Diego, CA, and an independent academic laboratory at the University of California at Los Angeles. The MaterniT21 test is available exclusively through Sequenom CMM as a testing service to physicians.

An estimated 1,330 cases of trisomy 18 and 600 cases of trisomy 13 are expected at term among the estimated 4.25 million pregnancies in the United States each year.

About Sequenom

Sequenom, Inc. (NASDAQ: SQNM - News) is a life sciences company committed to improving healthcare through revolutionary genetic analysis solutions. Sequenom develops innovative technology, products and diagnostic tests that target and serve discovery and clinical research, and molecular diagnostics markets. The company was founded in 1994 and is headquartered in San Diego, California. Sequenom maintains a Web site at http://www.sequenom.com to which Sequenom regularly posts copies of its press releases as well as additional information about Sequenom. Interested persons can subscribe on the Sequenom Web site to email alerts or RSS feeds that are sent automatically when Sequenom issues press releases, files its reports with the Securities and Exchange Commission or posts certain other information to the Web site.

About Sequenom CMM

Sequenom Center for Molecular Medicine® (Sequenom CMM), a CAP accredited and CLIA-certified molecular diagnostics laboratory, is developing a broad range of diagnostics with a focus on prenatal diseases and conditions. These laboratory-developed tests provide beneficial patient management options for obstetricians, geneticists and maternal fetal medicine specialists. Sequenom CMM is changing the landscape in genetic disorder diagnostics using proprietary cutting edge technologies.

Forward-Looking Statement

Except for the historical information contained herein, the matters set forth in this press release, including statements regarding the use of the MaterniT21 test as a valuable tool in the care of pregnant women, expectations regarding the future performance, utility, and impact of the test, the Company's commitment to improving healthcare through revolutionary genetic analysis solutions, and Sequenom CMM changing the landscape in genetic disorder diagnostics, are forward-looking statements within the meaning of the "safe harbor" provisions of the Private Securities Litigation Reform Act of 1995. These forward-looking statements are subject to risks and uncertainties that may cause actual results to differ materially, including the risks and uncertainties associated with market demand for and acceptance and use by customers of new tests such as the MaterniT21 LDT, reliance upon the collaborative efforts of other parties, the Company's financial position, its ability to position itself for product launches and growth and develop and commercialize new technologies and products, particularly new technologies such as noninvasive prenatal diagnostics, laboratory developed tests, and genetic analysis platforms, the Company's ability to manage its existing cash resources or raise additional cash resources, competition, intellectual property protection and intellectual property rights of others, government regulation particularly with respect to diagnostic products and laboratory developed tests, obtaining or maintaining regulatory approvals, litigation involving the Company, and other risks detailed from time to time in the Company's most recently filed Quarterly Report on Form 10-Q and Annual Report on Form 10-K for the year ended December 31, 2010, and other documents subsequently filed with or furnished to the Securities and Exchange Commission. These forward-looking statements are based on current information that may change and you are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date of this press release. All forward-looking statements are qualified in their entirety by this cautionary statement, and the Company undertakes no obligation to revise or update any forward-looking statement to reflect events or circumstances after the issuance of this press release.

(Logo:  http://photos.prnewswire.com/prnh/20040415/SQNMLOGO)

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Study Published In Genetics In Medicine Demonstrates Sequenom CMM MaterniT21 Test Accurately Detects Two Additional ...

Signal Genetics, a closely held cancer testing company, agreed to buy ChipDX LLC to add diagnostic products in development for lung, breast and colon cancers.

The acquisition also adds closely held ChipDX’s technology to enable for remote interpretation of tests, New York-based Signal said today. Financial details weren’t disclosed.

Signal makes a prognostic test for multiple myeloma called MyPRS Plus, and will use its sales team to bring ChipDX’s products to market, the company said. ChipDX’s BreastGeneDX, ColonGeneDX and LungGeneDX products are designed to determine patients’ cancer risk levels.

“The acquisition of the intellectual property and patents of ChipDX dramatically expands and enhances our oncology pipeline,” Signal Chief Executive Officer Joe Hernandez said in a statement. “The addition of ChipDX’s bioinformatics capabilities drastically reduces our time to market with novel molecular tests designed to facilitate better patient outcomes at a lower cost profile.”

To contact the reporter on this story: Meg Tirrell in New York at mtirrell@bloomberg.net

To contact the editor responsible for this story: Reg Gale at rgale5@bloomberg.net

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Signal Genetics Agrees to Purchase ChipDX to Gain Cancer Diagnostics