Archive for the ‘Gene Therapy Research’ Category

Researcher: Genetics impacts everyone

BY AUDREY DWYER | FEBRUARY 02, 2012 7:20 AM

Popular genetics affects everyone.

That's the message of Spencer Wells, the director of the National Geographic Genographic Project, who described to University of Iowa students on Wednesday how genetic research uncovers hidden ties in society.

"It's a story about all of us," he said.

He is leading a global expedition to collect DNA samples from various indigenous human populations. These samples are being used to record history of human migrations that began in Africa and spread throughout the world.

"The average person doesn't think of genetics as being terribly relevant to her or him," he told The Daily Iowan. "I think what this study does is raise awareness about genetics to the average person who is not a genetics scientist."

Wells — who became curious in genetics when he was 10 years old in a biology lab with his mother — said the lecture was an opportunity to bring the excitement of genetics to students in all different areas of study.

He spoke at the Englert Theatre, 221 E. Washington St., about his research experience in roughly 80 countries.

In Wells' research, scientists are able to study how the Y chromosome, found in most male mammals, traces ancestral lineage.

Dan Eberl, the director of the UI's interdisciplinary Ph.D. program in genetics, said the program helps train students to be independent thinkers.

"This enables us to expose our students to a wide variety of studies; these ideas are really important," he said.

Though the number of students in the program has remained steady over the past few years, averaging roughly 45 students, Eberl said the program has expanded significantly through the numerous interdisciplinary programs.

John Manak, a UI assistant professor of genomics and genetics, said several projects underway in the genetics program examine ways to improve medicine.

Manak stressed the importance of Wells' study in his explanation of human ancestry. The study helps answer the question of human identity and origin simply by looking at DNA.

The UI initially had a basic genetics program, but as developments in the field grew over time, the university expanded opportunities for students. Genetics has become an interdisciplinary field at the university, with officials hiring additional faculty through cluster hiring.

Lily Paemka, a graduate student in genetics, said while she feels genetics is obviously important, giving the community an opportunity to listen to a well-known researcher such as Wells may inspire future generations.

"Hopefully, we will also catch the attention of promising future scientists and maybe even convert some," she said.

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Researcher: Genetics impacts everyone

SAN MARINO, Calif.--(BUSINESS WIRE)-- Viral Genetics, Inc. (Pink Sheets: VRAL) today posted to its website a President’s Letter to Shareholders that reviews the past year and looks ahead to what 2012 holds for the Company. Highlights of the President’s letter, including key updates on the Company’s important cancer study and biofuel testing programs, are below. In particular, in 2011 our Metabolic Disruption technology (MDT) additives successfully produced significant algal oil yield increases in independent testing at larger-scale production environments; and, though later than announced, three of the Company’s most promising pharmaceutical products – its therapies for treatment-resistant cancer with MDT compounds, its treatment of HIV/AIDS with APi1177, and its treatment of Lyme disease with VGV-L – are anticipated to commence or follow up on prior FDA reviews at various times in 2012, including one clinical trial.

“2011 was a year of tremendous growth for our companies, full of accomplishments and advancements across the board, which brought along with them an exciting set of new challenges. As we have since our founding, we continue to limit our full time personnel to conserve capital with management focusing on funding our growth, while our advisory board focuses on continually and successfully advancing our science. Possibly the single most important event in 2011 was the evolution of our new subsidiary, VG Energy, Inc., which added diverse new potential areas of business for us through our majority position in VG Energy, Inc. We believe this has added tremendous current and future potential value as our shareholders now, in a sense, own two companies with equally significant potential. Understandably, launching a new company brings with it new management and fund-raising challenges and goals to be met – challenges we spent much of the latter part of 2011 addressing, putting us closer to attaining those goals,” said Haig Keledjian, President of Viral Genetics and VG Energy.

“Concurrently with the launch of our VG Energy business and its rapid growth, after years of effort by our dedicated researchers and advisory team, our drug development programs really took off and bore fruit as we found ourselves in the exciting and enviable position of having three drug candidates nearing FDA review and clinical trial status. On top of that, our oncology trial at Scott and White went from being a relatively small, single-site, more traditional 'physician’s study' to potentially a dual-site, larger study consisting of upwards of several dozen patients with a second (or 'co-') primary investigator that may be a Phase 1 or Phase 2 study. These are all accomplishments we have strived towards for years and they mark a potential new foundation for the coming years’ successes. Long-time shareholders will know that we spent many years almost exclusively focused on HIV/AIDS and to a large extent we developed our resources – including personnel – with an eye to focusing on preclinical or lab research. Last year, however, we found ourselves quickly advancing in several new areas including cancer and Lyme disease, and moving quickly towards clinical testing, meaning we required new resources and personnel. As a result of this, as is common with drug programs, we experienced some delays. New initiatives and modifications took time to work themselves out, and we had to recruit new clinical advisors. Looking ahead to 2012, however, we have an expanded team of advisors to assist management: notably, in terms of new clinical advisors for our planned clinical trials and at the board level on the VG Energy side as we recently announced. We think these efforts position the Company and VG Energy well to face what could be the most important and positive year in our history,” said Haig Keledjian.

Biofuel Testing – VG Energy

In 2011 we began the process of conducting independent testing of our MDT additives in industrial-scale algae production environments. We originally expected to conclude portions of this testing, including “dose response testing” and scale-up studies, within 2-3 months. Following successful preliminary results in the summer of 2011 which were previously announced, we decided to transition to new testing facilities because we were not satisfied with the degree of protection afforded our intellectual property rights during the ongoing product development and validation process in the initial testing. Protection of our intellectual property rights in this and other areas is critical to the Company’s long-term success. Although we believe that existing testing is sufficient to support some commercial implementation, testing and product development is ongoing and expected to continue at both contracted testing facilities and by potential commercial partners as we develop and refine MDT applications in this and other areas.

“As many of our shareholders know, there are a lot of very exciting developments going on in the biofuel industry. At the same time, the industry is still evolving and processes and products that will emerge as successes are being vetted in terms of process improvements, algae strains, genetic modifications vs. process improvement, for example. In the end, this will be determined by economics borne out through testing. Establishing those economics through testing in actual production environments is exactly what we are focused on,” continued Mr. Keledjian.

“Compared to one year ago, we now have independent and ongoing testing validating our early belief in this technology in many areas and our decision to launch VG Energy and fund this research. This testing continues as we reach out to research collaborators and potential partners, while Dr. Newell Rogers’ team continues their own work advancing this technology. Our goal now is to locate those producers that would benefit from introducing our additives to their process, which is precisely the focus of much of the ongoing testing we are conducting with third parties. So we are working through the various scenarios with as many producers or potential producers as we can, while protecting our intellectual property rights in the process,” continued Mr. Keledjian. “We have encountered situations where a potential partner’s method for enhancing algae yields using their own technology turned out to be incompatible on a molecular level with ours. For instance, in one case genetic modifications to a potential partner’s yeast strain intended to enhance yields blocked uptake of our additives. Therefore, one of the key elements of our business development model is to determine the industry players whose approaches work best with ours, thereby determining companies with whom we want to partner and reach commercial scalability, and ultimately cash flow. While this testing will continue throughout the year and we cannot guarantee an outcome, early indications of interest leave us confident that we may secure a commercial partner before the year is out.”

Scott and White Cancer Study

It is now being determined whether to commence with this study as an expanded Phase 1 or Phase 2 physician’s- initiated study with a second test site at a second hospital in addition to Texas A&M University Health Sciences Center-affiliated Scott and White Hospital. We originally expected to begin enrolling patients in the summer of 2011 for a physician’s IND (Investigational New Drug) study to be carried out exclusively at Scott and White. We also indicated that we expected this study to focus on certain types of cancer, including, amongst others, a form of brain cancer called glioblastoma. Following new interest from a potential co-primary investigator at a possible new test site – including potential expansion of the study to a more robust clinical trial under a more advanced protocol design involving more patients and other types of cancer – enrollment was delayed to accommodate finalization of the new developments including institutional reviews that are now underway. The study, which is funded in part by a grant of $1.5 million to Scott and White, will require approximately 6 to 8 weeks of treatment and 12 months of follow up and is expected to begin as soon as reviews are concluded at the new institution and, subsequently, the FDA. We currently believe this study will begin by the second quarter of 2012, possibly sooner. This study will test compounds that are part of our Metabolic Disruption (MDT) platform in combination with existing cancer treatments on patients with drug resistant forms of various types of cancers, most likely starting with ovarian cancer.

Additional details on both of these topics are available in the 2012 Letter to Shareholders at this link: http://www.viralgenetics.com/investors/2012-Letter-to-Shareholders.pdf.

Other Highlights

HIV/AIDS Program – APi1177

As a result of our pre-IND communication with the FDA in 2011, we initiated a search for and recently completed the securing of a manufacturer to produce GLP (Good Laboratory Practices) quality APi1177 for use in pharmacology, toxicology, and virology studies, and certain assay development work required to submit a full IND. We have identified contractors to carry out the preclinical testing and assays required and we intend to commence with the preclinical studies and assays once we are satisfied with the GLP product which we are now working at concluding. This progression will also accelerate several of our other programs as the molecule being used is substantially similar.

New Intellectual Property – DCA patents

In December 2011, a patent falling within our licensed MDT portfolio was awarded that is the first issued patent covering the use of dichloroacetic acid (“DCA”) in the treatment of cancer. We believe that this patent is “foundational” to the use and study of DCA for cancer treatment, an area many other companies and research entities, both in the US and internationally, have been increasingly studying. We intend to seek potential clinical trial or licensing opportunities for this patent this year. There are currently six FDA approved clinical trials in motion that have incorporated DCA into their drug regimen.

Other High Value Oils – VG Energy

In addition to the biofuel testing update above, we are pursuing other potential partnering opportunities with both commercial and research entities for a variety of uses of MDT additives in high value oils used in food, animal feed, cosmetics and nutraceuticals. The business and product development process for this area of VG Energy’s focus is similar to the biofuel process in that we are conducting testing with existing and potential producers to determine the fit of our compounds to their production methods. We believe it is possible for us to secure one or more commercial partners by the end of this year.

Lyme Disease

We have recently entered into an agreement with a physician associated with one of the leading medical centers in the country to act as the “clinical lead” for this drug program. This doctor will complete the clinical portions of the pre-IND including an outline of the clinical trial protocol, as well as possibly serve as primary investigator for the planned clinical trial of our Lyme disease compound. Other than the clinical portions (those dealing with use of the drug on humans, mostly in a clinical trial) the pre-IND for this study is ready to submit and we expect to do so imminently. Once we have finalized arrangements with the physician and his institution, we expect to be able to add more detail on these developments.

Multiple Sclerosis, Staphylococcus, Streptococcus and Sepsis

We continue to perform preclinical testing of these drug candidate compounds, and hope to be in a position to submit pre-INDs for each of them this year. We are also working at securing research partners, including clinical leads for these programs.

Fund Raising

Our goal is to raise $2,000,000 to $3,000,000 to achieve our 2012 goals which includes the budget of VG Energy. It is expected that this will be in the form of sales of equity or debt securities of the Company and/or VG Energy. We are also exploring raising funds by possibly commercial partnering and licensing with various third parties, and we will also continue to sponsor or support applications for grant funding of research towards the development of our products.

Annual Report

We recently filed our quarterly report for the period ending September 30, 2011 and we are now working to complete the 2011 annual report by late March or early April. The Company has recommitted to making its periodic reports available on a timely basis and intends to issue a monthly Letter to Shareholders going forward.

About Viral Genetics, Inc.

San Marino, California-based Viral Genetics discovers drug therapies from two platform technologies based on over 60 patents: Metabolic Disruption (MDT) and Targeted Peptides (TPT). Founded in 1994, the biotech company is researching treatments for HIV/AIDS, Lyme Disease, Strep, Staph and drug resistant cancer. A majority-owned subsidiary, VG Energy (www.vgenergy.net), is dedicated to exploring biofuel and agricultural applications for the MDT platform. For more information, visit http://www.viralgenetics.com.

About VG Energy

VG Energy Inc. is an alternative energy and agricultural biotech company that is a majority-owned subsidiary of Viral Genetics Inc. Using its Metabolic Disruption Technology (MDT), Viral Genetics' cancer research led to discoveries with major consequences in a wide variety of other industries, including production of biofuel and vegetable oils. VG Energy holds the exclusive worldwide license to the MDT patent rights for use in the increase of production of various plant-derived oils from algae and seeds. Application of MDT technology to the biofuel industry could potentially allow it to overcome its major obstacle in the area of production efficiency: namely, an increase in production yields leading to feasible economic returns on investment, allowing renewable biodiesel to be competitive with fossil fuels. For more information, please visit http://www.vgenergy.net.

SAFE HARBOR FOR FORWARD-LOOKING STATEMENTS:

This news release contains forward-looking statements that involve risks and uncertainties associated with financial projections, budgets, milestone timelines, clinical trials, regulatory approvals, and other risks described by Viral Genetics, Inc. from time to time in its periodic reports, including statements about its VG Energy, Inc. subsidiary. None of Viral Genetics' drug compounds are approved by the US Food and Drug Administration or by any comparable regulatory agencies elsewhere in the world, nor are any non-pharmaceutical products of VG Energy, Inc. commercialized. While Viral Genetics believes that the forward-looking statements and underlying assumptions reasonable, any of the assumptions could be inaccurate, including, but not limited to, the ability of Viral Genetics to establish the efficacy of any of its drug therapies in the treatment of any disease or health condition, the development of studies and strategies leading to commercialization of those drug compounds in the United States, the obtaining of funding required to carry out the development plan, the completion of studies and tests including clinical trials on time or at all, the successful outcome of such studies or tests, or the successful commercialization of VG Energy, Inc.’s non-pharmaceutical products. Therefore, there can be no assurance that the forward-looking statements included in this release will prove to be accurate. In light of the significant uncertainties inherent in the forward-looking statements included herein, the forward-looking statements should not be regarded as a representation by Viral Genetics or any other person that the objectives and plans of Viral Genetics will be achieved.

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Viral Genetics Inc. Issues 2011 Year in Review and 2012 Outlook

01-02-2012 05:22 Specific challenges of avant-garde therapies Authorities/sponsors: being concomitantly on a learning curve Translational research: key success factors Case study: SAF-301

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Entering into the clinic with an intracerebral gene therapy product / Karen Aiach, Project Manager, - Video

Public release date: 31-Jan-2012
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Contact: Phil Sahm
phil.sahm@hsc.utah.edu
801-581-2517
University of Utah Health Sciences

SALT LAKE CITY -- A team of scientists from the University of Utah and the University of California at San Francisco has discovered that the mutation of a gene encoding a ketone body transporter triggers accumulation of fat and other lipids in the livers of zebrafish. This discovery, published in the Feb. 1, 2012, issue of Genes & Development, reveals that transport of ketone bodies out of the liver is a critical step in energy metabolism during fasting. It also provides a new approach for studying the development of fatty liver disease in humans.

Nonalcoholic fatty liver disease (NAFLD), or abnormally high accumulation of lipids in the liver, is the most common cause of chronic liver disease worldwide. Lipids are a broad group of molecules that include fats, triglycerides, and cholesterol. In some people, NAFLD causes no complications, but in others, excess fat in the liver can lead to inflammation or development of scar tissue, resulting in permanent liver damage or even liver failure. NAFLD may also increase the risk of heart disease in people who are overweight or obese. The increasing prevalence of NAFLD in the United States is due, in large part, to the obesity epidemic and it is estimated that more than 6 million U.S. children already have fatty liver disease.

"Currently, there are a limited number of treatment options for decreasing excess fat in the liver and there are no methods for reversing damage to liver tissue due to NAFLD," says Amnon Schlegel, M.D., Ph.D., investigator in the University of Utah Molecular Medicine program, assistant professor of internal medicine at the University of Utah School of Medicine, and senior author on the study. "By identifying and characterizing novel genes that regulate accumulation of lipids in the liver, we may be able to gain new insight into the physiological processes that lead to NAFLD."

Previous research has shown that many of the proteins known to control lipid metabolism in humans are also present in zebrafish. Schlegel and his colleagues began by identifying a zebrafish mutant known as red moon (rmn), which developed abnormal lipid accumulation in liver cells, without evidence of associated liver inflammation or liver damage, when exposed to fasting conditions. Schlegel and his colleagues then used a molecular genetic technique called positional cloning to isolate the gene disrupted by the rmn mutation. They found that the rmn mutation inactivated slc16a6a, a gene thought to encode a protein required in the transport of nutrients during fasting.

"Until now, the activity of the Slc16a6a protein has not been functionally characterized in any organism," says Schlegel, who's also an adjunct assistant professor of biochemistry at the U medical school. "Our studies indicate that Slc16a6a is a protein involved in the transport of ?-hydroxybutyrate."

?-hydroxybutyrate is a ketone body, a compound that is produced in the liver when blood glucose is low and fatty acids are broken down for energy. During periods of fasting, most body tissues can use fatty acids as an energy source, but the brain relies on ?-hydroxybutyrate and other ketone bodies for fuel. Schlegel and his colleagues discovered that, in rmn mutants deprived of nutrition, loss of Slc16a6a function disabled secretion of ketone bodies from liver cells and increased lipid accumulation in the liver. They also found that introducing the human form of the SLC16A6 protein into rmn mutant livers restored ketone body secretion.

"Our research has uncovered a previously unrecognized, but critical step, in the complicated physiology of fasting," says Schlegel. "We still don't know whether altered fasting liver metabolism influences the development of NAFLD, but knowing that Slc16a6a is required for secretion of ketone bodies from liver cells during fasting may have implications for our understanding and treatment of other medical conditions where ketone bodies play a role. These include uncontrolled type 1 diabetes, obesity, and childhood metabolic disorders caused by defects in fatty acid metabolism."

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Gene mutation is linked to accumulation of fat, other lipids in liver

Experts who made an unprecedented recommendation that bird-flu researchers hold back some details of their work justified the controversial decision on Tuesday, saying that the experiments were akin to the 1940s work on nuclear weapons or the first attempts at genetic engineering in the 1970s.

Members of the National Science Advisory Board for Biosecurity said that bioterrorists or rogue governments could use details of the experiments to make a global weapon of catastrophic potential.

“We found the potential risk of public harm to be of unusually high magnitude,” they wrote in a statement published jointly in the rival journals Science and Nature.

The decision, they said, is too big for the scientific community to make on its own. “Physicists faced a similar situation in the 1940s with nuclear-weapons research, and it is inevitable that other scientific disciplines will also do so.”

Since it started spreading in 2003, H5N1 bird flu has killed 344 of the 583 people it is known to have infected--a mortality rate of 59 percent. This compares to a 2.5 percent fatality rate for the 1918 flu, which killed tens of millions of people, or 30 percent for smallpox before it was eliminated in 1979. Luckily, H5N1 doesn’t infect people easily, but it spreads rapidly through flocks of chickens, infects ducks with barely a symptom, and appears to be carried by migrating wild birds. All flu viruses mutate, and most flu experts fear it is only a matter of time before H5N1 either evolves or mixes up with another flu virus to make a form that can easily infect people.

“A pandemic, or the deliberate release of a transmissible highly pathogenic influenza A/H5N1 virus, would be an unimaginable catastrophe for which the world is currently inadequately prepared,” the NSABB wrote.

Usually, when viruses acquire the ability to infect easily, they also become less lethal. So scientists are keen to find out what an H5N1 virus that could easily infect people might look like. If it transmits easily from one person to another, does it give up some of its killing power?

Two labs took a big step toward this goal last year, one in the Netherlands and one at the University of Wisconsin. They engineered forms of H5N1 that ferrets could easily pass to one another--ferrets being the closest thing in the animal world to humans when it comes to getting flu. The good news was that vaccines and drugs both worked against the new strain.

One team sent its findings to Science to be published, while the other submitted its results to Nature. The usual process would have been for the journals to ask other flu and genetics experts to critique the papers, and then they would publish them so other researchers could try to replicate the findings, adding to the world’s knowledge about H5N1, how to watch for dangerous changes, and how to make drugs and vaccines to protect people.

The flu community was atwitter about the pending news, and the potential consequences alarmed the NSABB, which was set up after the 2001 anthrax attacks and which includes heavyweight experts on bioterrorism such as Paul Keim of Northern Arizona University and Mike Osterholm of the University of Minnesota, as well as genetics experts like Claire Fraser-Liggett of the University of Maryland. They asked the two labs to hold off last year until the scientific community could agree on a way to make sure the information got into the right hands--and not into the wrong hands. The experts and the journals have agreed to wait for the time being, and the World Health Organization has set up a meeting in February in Geneva that includes experts from the two teams.

To say the decision frightened and irritated the scientific community would be an understatement. Almost everybody who is anybody in the world of viral research, bioterrorism, and scientific freedom has weighed in--most recently in eight letters to The New York Times.

Keim wrote a separate explanation for the online journal mBio, published by the American Society for Microbiology. “I carefully considered how restricting the information would compromise scientific research progress and even how it would hinder public health efforts to prevent such a horrific pandemic,” Keim wrote. “The short-term negative consequences of restricting experimental details seemed small in contrast to the large consequences of facilitating the replication of these experiments by someone with nefarious intent…. Publishing a detailed experimental protocol on how to produce a highly transmissible H5N1 virus in a highly regarded scientific journal is a very bad idea.”

Dr. Robert Webster of St. Jude Children’s Research Hospital in Memphis, Tenn., a pioneer in influenza research who doesn’t serve on the NSABB, agreed.  “It has been argued that suppression of information serves no purpose, as the information will inevitably be ‘leaked.’ Although this viewpoint is likely correct, I do not believe we should publish the detailed methods of preparing transmissible H5N1,” Webster wrote in a separate commentary in mBio. But he said that the research itself must continue. “While bioterrorism is of real concern, nature has the potential to do much greater damage,” Webster pointed out.

Vincent Racaniello, a microbiologist at Columbia University College of Physicians and Surgeons, disagreed. “Bioterrorists do not want to carry out an experiment; they want to instill terror,” he wrote in mBio. “Science has always worked best when information is freely accessible. Fear has clouded the NSABB’s vision. We cannot allow fear to limit our ability to address medical problems.”

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Flu Work Akin to Nuclear-Bomb Experiments, Board Says

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ScienceDaily (Jan. 31, 2012) — A report from investigators at the Massachusetts General Hospital (MGH) Cancer Center has defined the role of a recently identified gene abnormality in a deadly form of lung cancer. Tumors driven by rearrangements in the ROS1 gene represent 1 to 2 percent of non-small-cell lung cancers (NSCLC), the leading cause of cancer death in the U.S. The researchers show that ROS1-driven tumors can be treated with crizotinib, which also inhibits the growth of tumors driven by an oncogene called ALK, and describe the remarkable response of one patient to crizotinib treatment.

"ROS1 encodes a protein that is important for cell growth and survival, and deregulation of ROS1 through chromosomal rearrangement drives the growth of tumors," says Alice Shaw, MD, PhD, of the MGH Cancer Center -- co-lead author of the paper which has been published online in the Journal of Clinical Oncology. "This finding is important because we have drugs that inhibit ROS1 and could lead to the sort of dramatic clinical response we describe in this paper."

The current findings add ROS1 to the list of genes known to drive NSCLC growth when altered -- a list that includes KRAS, mutations of which account for about 25 percent of cases; EGFR, accounting for 10 to 15 percent; and ALK, rearranged in about 4 percent. Altogether, known cancer-causing genetic changes have been found in a little more than half of NSCLC tumors. Originally identified in brain tumors, ROS1 rearrangement previously had been identified in one NSCLC patient and one NSCLC cell line. The current study was designed to determine the frequency of ROS1 rearrangement in NSCLC and to define the characteristics of patients with ROS1-rearranged tumors.

The investigators screened tumor samples from more than 1,000 NSCLC patients treated at the MGH, Vanderbilt University, the University of California at Irvine, and Fudan University in Shanghai, China. ROS1 rearrangement was identified in 18 tumor samples, for a prevalence of 1.7 percent; ALK rearrangements were identified in 31 samples, with no samples showing alterations in both genes. Patients with ROS1-positive tumors tended to be younger, never to have smoked and to have a type of lung cancer called adenocarcinoma -- characteristics very similar to those of ALK-positive patients.

An earlier MGH study of an experimental ALK inhibitor had found the drug suppressed the growth of a ROS1-positive cell line in addition to ALK-positive cell lines, suggesting that ROS1-positive tumors might be sensitive to the ALK-inhibitor crizotinib. This observation led corresponding author John Iafrate, MD, PhD, and his team to develop a diagnostic test that could identify ROS1-positive tumors. Around the time that test became clinically available, a lung cancer patient whose tumor had not responded to drugs targeting EGFR mutations was referred to the MGH Cancer Center for genetic testing. His tumor was negative for ALK but later proved to harbor a ROS1 rearrangement, and he was enrolled in an extension of the crizotinib clinical trial first reported in the October 28, 2010, New England Journal of Medicine.

"When he enrolled in the trial last April, this patient was extremely sick -- with significant weight loss and very low oxygen levels -- and was barely able to walk," says Shaw. "Within a few days of starting crizotinib, he felt better; and by the time we scanned his chest at seven weeks, the tumors had essentially disappeared from his lungs." Nine months after starting crizotinib therapy, this patient continues to do well. Additional ROS1-positive patients have been enrolled in this trial at MGH, at UC Irvine and at the University of Colorado.

Shaw is an assistant professor of Medicine and Iafrate is an associate professor of Pathology at Harvard Medical School. Co-lead authors are Kristin Bergethon, MGH Pathology, and Sai-Hong Ignatius Ou, MD, PhD, University of California at Irvine. The study was supported by grants from the National Institutes of Health and from Pfizer, which received FDA approval for crizotinib in August 2011.

Additional co-authors are Ryohei Katayama, Eugene Mark, Julie Batten, Eunice Kwak, Jeffrey Clark, Jeffrey Engelman, and Mari Mino Kenudson, MGH Cancer Center; Christina Siwak-Tapp, University of California at Irvine; Keith D. Wilner, Pfizer; Christine Lovly, Nerina McDonald, Pierre Massion, Adriana Gonzalez, David Carbone, and William Pao, Vanderbilt University Medical Center; Pierre Massion, Nashville Veterans Affairs Medical Center; Rong Fang and Hongbin Ji, Shanghai Institutes for Biological Sciences; and Haiquan Chen, Shanghai Medical College, Fudan University.

Massachusetts General Hospital, founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of more than $750 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, transplantation biology and photomedicine.

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The above story is reprinted from materials provided by Massachusetts General Hospital.

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Journal Reference:

K. Bergethon, A. T. Shaw, S.-H. Ignatius Ou, R. Katayama, C. M. Lovly, N. T. McDonald, P. P. Massion, C. Siwak-Tapp, A. Gonzalez, R. Fang, E. J. Mark, J. M. Batten, H. Chen, K. D. Wilner, E. L. Kwak, J. W. Clark, D. P. Carbone, H. Ji, J. A. Engelman, M. Mino-Kenudson, W. Pao, A. J. Iafrate. ROS1 Rearrangements Define a Unique Molecular Class of Lung Cancers. Journal of Clinical Oncology, 2012; DOI: 10.1200/JCO.2011.35.6345

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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

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New genetic subtype of lung cancer defined

SALT LAKE CITY, Jan. 31, 2012 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc. (Nasdaq:MYGN - News) today announced results for its second fiscal quarter and six months ending December 31, 2011. Revenue for the second fiscal quarter was $122.8 million, an increase of 22 percent over the $100.4 million reported in the second fiscal quarter of 2011. Earnings per diluted share were $0.33, an increase of 27 percent over the same period of the prior year.

"These results represent the second quarter in a row of 20 percent or greater year-over-year revenue growth," said Peter D. Meldrum, President and Chief Executive Officer of Myriad Genetics, Inc. "As a result, I'm pleased to announce increased guidance for fiscal 2012. We remain focused on delivering strong top-line growth and implementing our broader strategic plan to diversify revenue across multiple disease indications and geographies."

Analysis of Second Fiscal Quarter 2012

Molecular diagnostic testing revenue in the second fiscal quarter equaled $117.6 million, an increase of 17 percent compared to the prior year period. This increase was driven by strong growth across all segments and products. Oncology revenue equaled $79.8 million, an increase of 15 percent over the second quarter of 2011. Women's Health revenue totaled $37.9 million, an increase of 22 percent over the same period in the prior year. Revenue from the BRACAnalysis(R) test, which represented 82.6 percent of total revenue in the second quarter, was $101.4 million, a 14 percent increase over the same period of the prior year. Revenue from the COLARIS(R) and COLARIS AP(R) tests, which represented 8.9 percent of total revenue during the quarter, was $10.9 million, an increase of 56 percent compared to the same fiscal quarter of the prior year. Myriad's remaining molecular diagnostic tests contributed $5.3 million to second quarter revenue, an increase of 24 percent over the same period in the prior year, and accounted for 4.3 percent of total revenue. Companion diagnostic service revenue in the second fiscal quarter equaled $5.2 million and represented 4.2 percent of total company revenue. There is no prior year revenue, as the Company acquired this business in May 2011. Operating income was $45.5 million, an increase of 18 percent from the prior year period. This record level of operating income included the impact of a 68 percent increase in R&D investment to support the Company's existing molecular diagnostic tests and future product opportunities. Net income for the second fiscal quarter was $28.3 million, an increase of 17 percent over the $24.2 million reported in same period of the prior year. The Company repurchased 927,709 shares of its common stock during the quarter under its previously announced stock repurchase program. Diluted weighted average shares outstanding were 86.2 million in the second fiscal quarter as compared to 93.6 million in the same period of the prior year. The Company ended the quarter with $428.3 million in cash, cash equivalents and marketable investment securities. Days sales outstanding for Myriad's accounts receivable improved to 32 days, compared with 37 days in the same period of the prior year. Bad debt expense in the second fiscal quarter equaled 5.2 percent of revenue, compared with 4.2 percent in the same period of the prior year.

Year-to-Date Performance

Total revenue for the first half of fiscal 2012 was $233.3 million, an increase of 21 percent over $192.3 million reported for the half of fiscal 2011. Operating income for the first half of fiscal 2012 was $86.9 million, an increase of 17 percent year-over-year. Net income for the first half of fiscal 2012 equaled $53.4 million, compared to $46.7 million for the first half of the prior year, an increase of 14 percent. In the first half of fiscal 2012, diluted earnings per share increased 24 percent to $0.62 from $0.50 for the same period of the prior year.

Fiscal Year 2012 Outlook

The Company has increased its expectations for fiscal year 2012 financial performance. Total revenue is now expected to be $465 million to $475 million, an increase from the $445 million to $465 million previously announced. This level of revenue is expected to result in fully diluted earnings per share of $1.24 to $1.28, up from the original guidance of $1.20 to $1.25. Molecular diagnostic revenue is now expected to range between $440 million and $450 million and companion diagnostic service revenue continues to be expected to range between $24 million and $26 million. These projections are forward looking statements and are subject to the risks summarized in the safe harbor statement at the end of this press release. The Company will provide further detail on its business outlook during the conference call it is holding today to discuss its fiscal results for the second fiscal quarter and first half of fiscal 2012.

Conference Call and Webcast

A conference call will be held on Tuesday, January 31, 2012, at 4:30 p.m. Eastern time to discuss Myriad's second fiscal quarter and first half 2012 financial results and fiscal year 2012 outlook. The dial-in number for domestic callers is (888) 225-2734. International callers may dial (303) 223-2685. All callers will be asked to reference reservation number 21566441. An archived replay of the call will be available for seven days by dialing (800) 633-8284 and entering the reservation number above. The conference call will also be available through a live Webcast at http://www.myriad.com.

About Myriad Genetics

Myriad Genetics, Inc. (Nasdaq:MYGN - News) is a leading molecular diagnostic company dedicated to developing and marketing transformative tests to assess a person's risk of developing disease, guide treatment decisions and assess a patient's risk of disease progression and disease recurrence. Myriad's portfolio of nine molecular diagnostic tests are based on an understanding of the role genes play in human disease and were developed with a focus on improving an individual's decision making process for monitoring and treating disease. With fiscal year 2011 annual revenue of over $400 million and more than 1,000 employees, Myriad is working on strategic directives, including new product introductions, companion diagnostics, and international expansion, to take advantage of significant growth opportunities. For more information on how Myriad is making a difference, please visit the Company's website: http://www.myriad.com.

Myriad, the Myriad logo, BRACAnalysis, Colaris, Colaris AP, Melaris, TheraGuide, Prezeon, OnDose, Panexia and Prolaris are trademarks or registered trademarks of Myriad Genetics, Inc. in the United States and foreign countries. MYGN-F, MYGN-G

Safe Harbor Statement

This press release contains "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995, including statements relating to the Company's focus on delivering strong top-line growth and implementing its broader strategic plan to diversify revenue across multiple disease indications and geographies; the Company's investment in R&D to support its existing molecular diagnostic tests and future product opportunities; the Company's increased guidance for fiscal year 2012 under the caption "Fiscal Year 2012 Outlook;"and the Company's strategic directives under the caption "About Myriad Genetics". These "forward-looking statements" are based on management's current expectations of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by forward-looking statements. These risks and uncertainties include, but are not limited to: the risk that sales and profit margins of our existing molecular diagnostic tests and companion diagnostic services may decline or will not continue to increase at historical rates; the risk that we may be unable to expand into new markets outside of the United States; the risk that we may be unable to develop or achieve commercial success for additional molecular diagnostic tests and companion diagnostic services in a timely manner, or at all; the risk that we may not successfully develop new markets for our molecular diagnostic tests and companion diagnostic services, including our ability to successfully generate revenue outside the United States; the risk that licenses to the technology underlying our molecular diagnostic tests and companion diagnostic services and any future products are terminated or cannot be maintained on satisfactory terms; risks related to delays or other problems with manufacturing our products or operating our laboratory testing facilities; risks related to public concern over genetic testing in general or our tests in particular; risks related to regulatory requirements or enforcement in the United States and foreign countries and changes in the structure of healthcare payment systems; risks related to our ability to obtain new corporate collaborations and acquire new technologies or businesses on satisfactory terms, if at all; risks related to our ability to successfully integrate and derive benefits from any technologies or businesses that we acquire; the development of competing tests and services; the risk that we or our licensors may be unable to protect the proprietary technologies underlying our tests; the risk of patent-infringement and invalidity claims or challenges of our patents; risks of new, changing and competitive technologies and regulations in the United States and internationally; and other factors discussed under the heading "Risk Factors" contained in Item 1A in our most recent Annual Report on Form 10-K filed with the Securities and Exchange Commission, as well as any updates to those risk factors filed from time to time in our Quarterly Reports on Form 10-Q or Current Reports on Form 8-K. All information in this press release is as of the date of the release, and Myriad undertakes no duty to update this information unless required by law.

MYRIAD GENETICS, INC. AND SUBSIDIARIES CONDENSED CONSOLIDATED INCOME STATEMENTS (Unaudited)

(in thousands, except per share amounts) Three Months Ended Six Months Ended
Dec. 31, 2011 Dec. 31, 2010 Dec. 31, 2011 Dec. 31, 2010

Molecular diagnostic testing $117,610 $100,440 $221,579 $192,298 Companion diagnostic services 5,201 -- 11,684 -- Total revenue 122,811 100,440 233,263 192,298

Costs and expenses:

Cost of molecular diagnostic testing 12,815 12,046 24,115 23,058 Cost of companion diagnostic services 3,302 -- 6,364 -- Research and development expense 10,243 6,092 18,748 11,853 Selling, general, and administrative expense 50,986 43,716 97,100 83,210 Total costs and expenses 77,346 61,854 146,327 118,121

Operating income 45,465 38,586 86,936 74,177

Other income (expense):

Interest income 1,382 548 1,856 1,269 Other (64) (80) (205) (214) Total other income 1,318 468 1,651 1,055

Income before income taxes 46,783 39,054 88,587 75,232

Income tax provision (benefit) 18,487 14,863 35,193 28,503

Net income $28,296 $24,191 $53,394 $46,729

Earnings per share:

Basic $0.33 $0.26 $0.63 $0.51 Diluted $0.33 $0.26 $0.62 $0.50

Weighted average shares outstanding

Basic 84,498 91,528 84,870 92,395 Diluted 86,231 93,647 86,602 94,178

Condensed Consolidated Balance Sheets
Dec. 31, 2011 Jun. 30, 2011

(In thousands)

Cash, cash equivalents, and marketable investment securities $428,259 $417,314

Trade receivables, net 42,988 50,272

Other receivables 1,083 575

Prepaid taxes 16,569 --

Inventory, net 10,294 8,218

Prepaid expenses 3,087 2,949

Equipment and leasehold improvements, net 24,329 23,080

Note receivable 17,667 --

Other assets 8,000 --

Intangibles, net 16,265 16,715

Goodwill 56,850 56,051

Deferred tax assets 35,867 35,653

Total assets $661,258 $610,827

Accounts payable and accrued liabilities $32,612 $33,040

Deferred revenue 2,434 1,347

Uncertain tax benefits 9,448 9,648

Stockholders' equity 616,764 566,792

Total liabilities and stockholders' equity $661,258 $610,827

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Myriad Genetics Reports Second Quarter Fiscal Year 2012 Results

Arthur Chovnick, a professor at the University of Connecticut, was a pioneer in the field of genetics whose influence was felt across the field of molecular genetics and biology.

"Arthur did something that has effectively jump-started enormous strides in the genetics of higher organisms," said Hal Krider, a former professor of genetics at UConn. "He was probably the most recognized, under-honored geneticist, but people with Nobel prizes would call and ask him for advice."

Chovnick, 84, of Chaplin, died Sept. 5.

One anecdote from his life reflected Chovnick's stature in the world of genetics. When his daughter Lisa was taking a biology course, she learned about Watson and Crick, who discovered the structure of DNA, but when the home phone rang one day and a caller identified himself as Francis Crick, Lisa hung up on him. "Quit joking," she told the Nobel Prize winner the next time he called.

Later that night, Arthur Chovnick picked up the phone himself. "Hello, Francis," he said.

"People of that stature were available to Arthur all the time," said Krider. "Everybody knew him. He was very, very well known and inordinately highly regarded."

Chovnick conducted experiments on drosophila melanogaster, a relative of the humble fruit fly that, rather than being a laboratory pest, is a valuable scientific specimen used for years in genetics research. First used to study heredity, the fly is now used in the study of disease as scientists search for the genes responsible for Alzheimer's or Parkinson's or Huntington's.

Drosophila genes are nearly identical to human genes. They also reproduce very quickly, meaning mutations may be studied in weeks rather than months or years. They have only four chromosomes. Even better, no groups picket against drosophila experimentation as they do against higher-order species.

"It is easy to grow and manipulate, and they have genes like us," said Christine Rushlow, a Chovnick-trained geneticist who is a professor at New York University. "We use them as a model system to see how genes work. We share so many genes."

Chovnick, known for pioneering work in gene organization and in demonstrating the way traits cross over within a gene, could look at events that were rare and re-create them.

Chovnick, born in Brooklyn, N.Y., on Aug. 2, 1927, grew up in Queens, where he graduated from Jackson High School in 1944. He was the oldest of four children born to Fannie and Herman Chovnick, who had both emigrated from Russia. He attended Indiana University for a year before joining the U.S. Navy, where he served on a hospital ship. After he was discharged, he returned to Indiana and obtained his undergraduate degree in 1949 and his master's in 1951. He got a doctorate in genetics from Ohio State University two years later, and obtained a grant from the National Institutes of Health that continued until 1995, one of the longest continuous NIH grants.

He spent two years at the University of Connecticut doing research and teaching before going to the Cold Spring Harbor Laboratory in Long Island, first as assistant director, then as director. In 1962, he returned to UConn as a professor, where he remained until he retired in 1994. He was a fellow of the American Association for the Advancement of Science and a founding member of the Connecticut Academy of Science and Engineering.

Chovnick was revered as a mentor as well as a teacher, his colleagues said.

"He left you alone, except he would always teach or help you," Rushlow said. "He was a great analytical thinker, which he could do in his head because he was so experienced."

He helped his students design experiments that would create a certain type of drosophila — with pink eyes for example, or missing a wing — to help them create their own mutations. "You see the consequences to the fly, and what it is doing to the fly," Rushlow said.

Chovnick also did early work on cloning, providing a fly with unusual chromosomes for other scientists to study. He studied how to regulate the activity of genes.

"When things go wrong because genes are out of control, you get disease," Rowlson said. "He was at the forefront, a leader in the genetics field, and famous for the work he had done." He also understood how genes recombine and how a new DNA sequence is created with potentially new effects.

Today, as scientists intensify their search for the genetic cause of disease, Chovnick's work is significant.

"He was a seminal character in the transition from classical genetics to modern genetic cloning and gene manipulation," said Krider, his former colleague.

"He was a very careful and highly creative thinker with a keenly analytical mind," said Arthur Hilliker, a professor at York University in Toronto, who studied under and later collaborated with Chovnick.

Originally posted here:
Genetics Pioneer Was UConn Professor, Mentor

SALT LAKE CITY, Jan. 31, 2012 /PRNewswire/ -- RemedyMD, the leading provider of Translational Research Informatics, will launch Investigate™ Cell Therapy at the American Society for Blood and Marrow Transplantation BMT Tandem Meetings Feb. 1 – Feb. 5 in San Diego, Calif. (Booth #604).

(Logo: http://photos.prnewswire.com/prnh/20120127/SF43320LOGO)

"Investigate Cell Therapy is designed to improve research efficiencies, facilitate pattern recognition and accelerate discoveries in BMT centers," said Hank Wu, Investigate product manager for RemedyMD.

Fully integrated with ComprehensiveBMT™, Investigate Cell Therapy is the world's only blood and marrow research management system capable of integrating next-generation sequencing, cross-disease registries, and long-term complications and outcomes to advance cell therapy research. Researchers benefit from:

Aggregation of disparate data types from bench to bedside data sources with an intelligent ontology that harmonizes biospecimen, registry and outcomes data 360-degree perspective of phenotypic and genotypic data for subjects, patients, diseases Configurability that keeps up with the pace of research, without waiting for software coding or database administration Multisite, real-time research collaboration without the cost and complexity of infrastructure building and maintenance A suite of reporting, analysis, and data visualization tools that enable drag-and-drop reporting by researchers, scientists, and clinicians without writing SQL

Investigate Cell Therapy leverages the same research platform implemented at the Blood Research Institute of the Blood Center of Wisconsin to integrate lab information management systems (LIMS), study design and tracking, patient registries, and data mining and visualization.

"Research is fundamentally an exercise in pattern recognition," said Gary Kennedy, Founder and CEO of RemedyMD. "Bringing the power of Investigate™ to bear on cell therapy research will provide blood and marrow researchers with the technology they need to recognize new patterns and increase the speed of discovery."

RemedyMD will demonstrate Investigate Cell Therapy at BOOTH #604 at the 2012 Tandem Meetings in San Diego, Calif. beginning Feb. 1 – Feb. 5.

This product is for research use only and is not intended for clinical or cell processing purposes.

About RemedyMD, Inc.

RemedyMD is the leading provider of registries and registry-based products for Life Science Research. RemedyMD's disease registry software is cutting-edge research management software which enables researchers, clinicians and scientists to collect, aggregate, harmonize, and analyze data from widely disparate sources and then use Mosaic™ Platform tools and applications to identify patterns that result in accelerated discoveries and better clinical data management. For more information visit: www.RemedyMD.com.

Media Contacts

Kristofer Beldin, RemedyMD, (801) 870-9407 (cell), kris.beldin@remedymd.com

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RemedyMD Announces Investigate Cell Therapy, a Revolutionary Research Management System for Blood and Marrow ...

Inactivating Kras caused tumors to disappear, suggesting possible treatment target

Newswise — ANN ARBOR, Mich. — A mutant protein found in nearly all pancreatic cancers plays a role not only in the cancer’s development but in its continued growth, according to a new study from University of Michigan Comprehensive Cancer Center researchers. The finding suggests a possible target for developing new ways to treat this deadly disease.

Researchers have known that mutations in the Kras gene are what cause pancreatic cancer to develop. These mutations are frequently seen in common precancerous lesions, suggesting it has an early role in pancreatic cancer.

The new study, published in the February Journal of Clinical Investigation, finds that in mice, mutant Kras also keeps the tumor growing and helps precancerous tumors grow into invasive cancer. When the researchers turned off Kras, the tumors disappeared and showed no signs of recurring.

The researchers were able to manipulate Kras in a mouse model that they designed to look at Kras at various points in pancreatic cancer development. In the precancerous lesions, turning off Kras eliminated the tumors in mice and the pancreas tissue returned to normal, with no signs of the cancer returning. With invasive cancer, inactivating Kras killed off the cancer but left the pancreas with fibrous areas similar to scar tissue. Tumors did not recur.

Researchers hope this finding provides the basis for future drug development.

“Right now no drugs specifically target Kras, but there are drugs that target the cellular processes downstream of Kras. We next need to figure out which of these downstream effectors of Kras are important in pancreatic cancer,” says study author Marina Pasca di Magliano, Ph.D., assistant professor of surgery and of cell and developmental biology at the U-M Medical School.

Kras is also known to play a role in lung and colon cancer. But it is likely the biggest player in pancreatic cancer, where more than 90 percent of all tumors have mutated Kras. Pancreatic cancer is one of the most deadly types of cancer: about 4 percent of patients are alive five years after their diagnosis. The disease is often diagnosed when surgery is not an option and it tends to be resistant to available chemotherapies.

“There is a dire need for new therapies for pancreas cancer based on a better understanding of the biology of this disease. My lab is now looking at the downstream inhibitors of Kras to try to find the best target,” Pasca di Magliano says.

Note to patients: This research was based in mice and needs further testing before any possible treatments are available for clinical trials. For information about current pancreatic cancer treatments, call the U-M Cancer AnswerLine at 800-865-1125.

Pancreatic cancer statistics: 43,140 Americans will be diagnosed with pancreatic cancer this year and 36,800 will die from the disease, according to the American Cancer Society

Additional authors: Meredith A. Collins, Filip Bednar, Yaqing Zhang, Jean-christophe Brisset, Stefanie Galban, Craig J. Galban, Sabita Rakshit, and Karen S. Flannagan, all from U-M; and N. Volkan Adsay from Emory University

Funding: U-M Biological Scholar Program; National Cancer Institute; U-M Gastrointestinal Specialized Program of Research Excellence (SPORE); Pancreatic Cancer Action Network; American Association for Cancer Research; Michigan Gastrointestinal Peptide Research Center

Disclosure: None

Reference: Journal of Clinical Investigation, Vol. 122, No. 2, February 2012

Resources:
U-M Cancer AnswerLine, 800-865-1125
U-M Comprehensive Cancer Center, http://www.mcancer.org
Clinical trials at U-M, http://www.UMClinicalStudies.org/cancer

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Gene Linked to Pancreatic Cancer Growth

WASHINGTON, D.C. — Researchers at the U.S. Department of Energy’s (DOE’s) Joint BioEnergy Institute (JBEI) recently announced a major breakthrough in engineering systems of RNA molecules through computer-assisted design.

This could lead to important improvements across a range of industries, including the development of cheaper advanced biofuels. 

Scientists will use these new “RNA machines,” to adjust genetic expression in the cells of microorganisms. 

This will enable scientists to develop new strains of Escherichia coli (E. coli) that are better able to digest switchgrass biomass and convert released sugars to form three types of transportation fuels — gasoline, diesel and jet fuels.

“This is a perfect example of how our investments in basic science innovations can pave the way for future industries and solutions to our nation’s most important challenges,” Energy Secretary Steven Chu said in a news release.

“This breakthrough at the Joint BioEnergy Institute holds enormous potential for the sustainable production of advanced biofuels and countless other valuable goods.”

A breakthrough with E. coli could make it cheaper to produce fuel from switchgrass or other non-food biomass plants to create advanced biofuels with the potential to replace gasoline. 

While the work at the JBEI remains focused on the development of advanced biofuels, its researchers believe their concepts may help other researchers to develop many other desired products, including biodegradable plastics and therapeutic drugs. 

For example, some researchers have started a project to investigate how to use the “RNA machines” to increase the safety and efficacy of medicine therapies to treat diseases, including diabetes and Parkinson’s.

Biological systems are incredibly complex, which makes it difficult to engineer systems of microorganisms that will produce desired products in predictable amounts. 

JBEI’s work, featured in the Dec. 23 issue of “Science” magazine, is the first of its kind to set up and adjust a RNA system in a predictable way. 

Specifically, researchers focused their design-driven approach on RNA sequences that can fold into complicated three dimensional shapes, called ribozymes and aptazymes. 

By using JBEI-developed computer-assisted models and simulations, researchers then created complex RNA-based control systems that are able to program a large number of genes. 

In microorganisms, “commands” that are sent into the cell will be processed by the RNA-based control systems, enabling them to help develop desired products.

One of the major goals of synthetic biology is to produce valuable chemical products from simple, inexpensive and renewable starting materials in a sustainable manner. 

Computer-assisted models and simulations like the one JBEI developed are essential for doing so. 

Up to this point, such tools for biology have been limited, and JBEI’s breakthrough in applying computer assisted design marks an important technical and conceptual achievement for this field. 

To view additional details about this research, visit http://newscenter.lbl.gov/news-releases/2011/12/22/cad-for-rna/.

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Genetic breakthroughs help develop cheaper biofuels: DOE

11-12-2011 09:20 A decade ago, scientists announced that they had produced the first draft of the human genome, the 3.6 billion letters of our genetic code. It was seen as one of the greatest scientific achievements of our age, a breakthrough that would usher in a new age of medicine. A decade later, Horizon finds out how close we are to developing the life-changing treatments that were hoped for. Horizon follows three people, each with a genetic disease, as they go behind the scenes at some of Britain's leading research labs to find out what the sequencing of the human genome has done for them - and the hope this remarkable project offers all of us.

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Miracle Cure A Decade of the Human Genome - BBC Horizon (HD). 720p - Video

Public release date: 31-Jan-2012
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Contact: Katie Marquedant
kmarquedant@partners.org
617-726-0337
Massachusetts General Hospital

A report from investigators at the Massachusetts General Hospital (MGH) Cancer Center has defined the role of a recently identified gene abnormality in a deadly form of lung cancer. Tumors driven by rearrangements in the ROS1 gene represent 1 to 2 percent of non-small-cell lung cancers (NSCLC), the leading cause of cancer death in the U.S. The researchers show that ROS1-driven tumors can be treated with crizotinib, which also inhibits the growth of tumors driven by an oncogene called ALK, and describe the remarkable response of one patient to crizotinib treatment.

"ROS1 encodes a protein that is important for cell growth and survival, and deregulation of ROS1 through chromosomal rearrangement drives the growth of tumors," says Alice Shaw, MD, PhD, of the MGH Cancer Center ? co-lead author of the paper which has been published online in the Journal of Clinical Oncology. "This finding is important because we have drugs that inhibit ROS1 and could lead to the sort of dramatic clinical response we describe in this paper."

The current findings add ROS1 to the list of genes known to drive NSCLC growth when altered ? a list that includes KRAS, mutations of which account for about 25 percent of cases; EGFR, accounting for 10 to 15 percent; and ALK, rearranged in about 4 percent. Altogether, known cancer-causing genetic changes have been found in a little more than half of NSCLC tumors. Originally identified in brain tumors, ROS1 rearrangement previously had been identified in one NSCLC patient and one NSCLC cell line. The current study was designed to determine the frequency of ROS1 rearrangement in NSCLC and to define the characteristics of patients with ROS1-rearranged tumors.

The investigators screened tumor samples from more than 1,000 NSCLC patients treated at the MGH, Vanderbilt University, the University of California at Irvine, and Fudan University in Shanghai, China. ROS1 rearrangement was identified in 18 tumor samples, for a prevalence of 1.7 percent; ALK rearrangements were identified in 31 samples, with no samples showing alterations in both genes. Patients with ROS1-positive tumors tended to be younger, never to have smoked and to have a type of lung cancer called adenocarcinoma ? characteristics very similar to those of ALK-positive patients.

An earlier MGH study of an experimental ALK inhibitor had found the drug suppressed the growth of a ROS1-positive cell line in addition to ALK-positive cell lines, suggesting that ROS1-positive tumors might be sensitive to the ALK-inhibitor crizotinib. This observation led corresponding author John Iafrate, MD, PhD, and his team to develop a diagnostic test that could identify ROS1-positive tumors. Around the time that test became clinically available, a lung cancer patient whose tumor had not responded to drugs targeting EGFR mutations was referred to the MGH Cancer Center for genetic testing. His tumor was negative for ALK but later proved to harbor a ROS1 rearrangement, and he was enrolled in an extension of the crizotinib clinical trial first reported in the October 28, 2010, New England Journal of Medicine.

"When he enrolled in the trial last April, this patient was extremely sick ? with significant weight loss and very low oxygen levels ? and was barely able to walk," says Shaw. "Within a few days of starting crizotinib, he felt better; and by the time we scanned his chest at seven weeks, the tumors had essentially disappeared from his lungs." Nine months after starting crizotinib therapy, this patient continues to do well. Additional ROS1-positive patients have been enrolled in this trial at MGH, at UC Irvine and at the University of Colorado.

###

Shaw is an assistant professor of Medicine and Iafrate is an associate professor of Pathology at Harvard Medical School. Co-lead authors are Kristin Bergethon, MGH Pathology, and Sai-Hong Ignatius Ou, MD, PhD, University of California at Irvine. The study was supported by grants from the National Institutes of Health and from Pfizer, which received FDA approval for crizotinib in August 2011.

Additional co-authors are Ryohei Katayama, Eugene Mark, Julie Batten, Eunice Kwak, Jeffrey Clark, Jeffrey Engelman, and Mari Mino Kenudson, MGH Cancer Center; Christina Siwak-Tapp, University of California at Irvine; Keith D. Wilner, Pfizer; Christine Lovly, Nerina McDonald, Pierre Massion, Adriana Gonzalez, David Carbone, and William Pao, Vanderbilt University Medical Center; Pierre Massion, Nashville Veterans Affairs Medical Center; Rong Fang and Hongbin Ji, Shanghai Institutes for Biological Sciences; and Haiquan Chen, Shanghai Medical College, Fudan University.

Massachusetts General Hospital (http://www.massgeneral.org), founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of more than $750 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, transplantation biology and photomedicine.

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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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Massachusetts General study defines a new genetic subtype of lung cancer

CAMBRIDGE, Mass.--(BUSINESS WIRE)-- Vertex Pharmaceuticals Incorporated (Nasdaq: VRTX - News) 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.

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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FDA Approves KALYDECO™ (ivacaftor), the First Medicine to Treat the Underlying Cause of Cystic Fibrosis

11-08-2011 09:02 Dr. Jennifer Ashton discusses an experimental gene therapy that used modified T-cells to attack tumor cells.

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Promising gene therapy treats Leukemia - Video

23-09-2011 04:14 Further information, videos, are available in topic addressed play lists and complementary video responses. Thanks to the channel: http://www.youtube.com for the Tip. "Genetically modified organisms (GMOs) in your food may make you sick. Studies link GMOs with toxins, allergies, infertility, infant mortality, immune dysfunction, stunted growth, accelerated aging, and death. Whistleblowers were fired, threatened, and gagged. Warnings by FDA scientists were ignored. Expert Jeffrey M. Smith, author of the #1 GMO bestseller Seeds of Deception, and Genetic Roulette, presents SHOCKING evidence why these gene-spliced crops may lead to health and environmental catastrophes. Learn how to protect yourself and discover the Campaign for Healthier Eating in America—a brilliant plan to quickly end the genetic engineering of our food supply." My other three research platforms: http://www.youtube.com http://www.youtube.com http://www.youtube.com

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Jeffrey Smith Dangerous Genetically modified Foods Genetic Roulette Monsanto - Video

By ALLISON STROUSE
astrouse@MorningJournal.com
@AllisonStrouse

MORNING JOURNAL/JIM BOBEL Lorain County Community College students will travel to Vancouver, Canada, in February to present the two projects relating to HIV. Pictured from left to right in front are Alex Fulton, Aryel Clark, Alexis Shawver, Victoria Soewarna and Elyria Catholic High School Mark A. Jaworski. In back are Austyn Lilly, Eric McCallister, Megan Sheldon, Harry Kestler, Jacqueline Makowski and Connor Anderson.

ELYRIA — A group of nine students sat in a second-floor classroom at Lorain County Community College, discussing a deletion mutation gene that they believe could keep someone from contracting HIV and why HIV wasn’t passed on to a Florida girl at birth from her infected mother.

Those are heady topics for anyone, but when eight of the students are high-school aged, its impressive.

Harry Kestler, professor of microbiology at LCCC, and the eight Early College students and an adult student, are members of a research group at the college. Five of them are preparing to travel to Vancouver, Canada, in February to present the two projects and compete with other college students.

In a little less than a month Megan, along with Kestler; Alex Fulton, 16; Victoria Soewarna, 16; Connor Anderson, 16; and Eric McCallister, 32, will be in Vancouver at the American Association for the Advancement of Science annual meeting.

Other students in the research group are Alexis Shawver, 15; Jacqueline Makowski, 15; Aryel Clarke, 16; and Austyn Lilly, 16.

The second project looks at what kept a young girl from Florida from contracting HIV, when her mother gave it to both her younger and older siblings during birth.

“We figured out that all of the children did get the virus from their mother, so it became puzzling as to why she didn’t get infected,” Aryel Clarke, 16, said.

The group explains their projects with ease, only stopping every once in a while to make sure they are explaining it correctly.

The projects are a part of a “research fellowship” that was created after some of the early college students showed interest, according to Kestler.

“Some of them refused to leave,” Kestler recalled of a day in which they shadowed him. Continued...

The program began with more students and over time the numbers dwindled to the current nine students. Of those nine, only one, McCallister, is a “regular” college student.

“The first time I met any of them (the early college students) ... I was blown away by what they knew, I mean for high school kids,” McCallister said. “I’m really impressed by all of them. They know their stuff.”

He has seen other college students come and go from the group, lasting a day, a week, or maybe a month.

“These core group of high school kids have more determination and dedication than any of the college kids that came through here,” he said.

In February, their dedication will be put to test against students from colleges such as Harvard, Duke, and other renowned colleges, according to Kestler.

“They will be competing at the college level and not competing at the high school level,” Kestler said. “We will see how we do up against the big league players.”

The Early College students chosen for the research group are picked following their freshman year, allowing them to participate in the research group for three years, if they chose.

“At the end of the freshman years, we selected students to be in the program,” he said.

“We have some students drop out because they realize it is just not their thing,” Kestler said. “That’s OK. This is something extra.”

The ones with the program now, he expects to be back next year. Continued...

“These are students that are dedicated and they are here for the long haul,” Kestler said.

By being there, they have the chance to partake in university level research, which is one of the reasons for the program, according to Kestler.

“We have a lab here,” he said pointing out that it is not specifically set up for them, but the whole college.

“It’s really like a once in a lifetime opportunity,” Megan said. “I think I can speak for all of us and say that we are really grateful to get to do this.”

This program has helped her realize what she wants to do once she graduates.

“I know I want to do some type of research,” she said. “I can’t picture myself not being in a bio-tech lab at least once a week.”

“This is a dedication you have to have,” Megan said. “You have to be able to want this.”

Link:
LCCC students studying gene mutation in HIV fight

MONDAY, Jan. 30 (HealthDay News) -- Researchers studying the link between diabetes and a hormone that affects your so-called "body clock" have identified a genetic mutation in the receptor for the hormone, melatonin, that may to boost the risk of the disease.

The finding could help improve assessment of a person's diabetes risk and could also lead to the development of personalized treatments, according to the study published in the Jan. 29 online edition of the journal Nature Genetics.

The research team from Imperial College London found that people who have rare genetic mutations in the receptor for melatonin have a greatly increased risk for type 2 diabetes.

Melatonin controls the body's sleep-wake cycle. A previous study found that people with common variations in the gene for the melatonin receptor MT2 have a slightly increased risk for type 2 diabetes.

This new study discovered that having any of four rare mutations of the MT2 is associated with a six times increased risk of developing type 2 diabetes.

Melatonin controls the release of insulin, which regulates blood sugar levels. Mutations in the MT2 gene may disrupt the connection between the body clock and insulin release, resulting in abnormal control of blood sugar, the researchers explained.

For their study, the investigators examined the MT2 gene in more than 7,000 people. They identified 40 variants associated with type 2 diabetes, four of which are very rare and make the receptor incapable of responding to melatonin. The effect of these four variants was then confirmed in an additional group of nearly 12,000 people.

"Blood sugar control is one of the many processes regulated by the body's biological clock. This study adds to our understanding of how the gene that carries the blueprint for a key component in the clock can influence people's risk of diabetes," study leader Philippe Froguel, from the School of Public Health, said in an Imperial College London news release.

"We found very rare variants of the MT2 gene that have a much larger effect than more common variants discovered before. Although each mutation is rare, they are common in the sense that everyone has a lot of very rare mutations in their DNA. Cataloging these mutations will enable us to much more accurately assess a person's risk of disease based on their genetics," Froguel added.

While the study found a link between the mutation and diabetes risk, it did not find a cause-and-effect relationship.

More information

The American Diabetes Association offers an overview of diabetes prevention.

Read this article:
Gene Study Sheds Light on Body Clock's Link to Diabetes

Public release date: 30-Jan-2012
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Contact: Emily Benson
SRC@faseb.org
301-634-7010
Federation of American Societies for Experimental Biology

Bethesda, MD ? The Federation of American Societies for Experimental Biology (FASEB) announces the opening of registration for the Science Research Conference (SRC): Post-transcriptional Control of Gene Expression: Mechanisms of mRNA Decay.

This conference will take place June 24-29, 2012 in Steamboat Springs, Colorado. The goal of the conference is to improve our current understanding of the fundamental mechanisms by which post-transcriptional control of RNA stability and translation regulates gene expression in normal and disease states. The program will consist of sessions that will broadly address cutting-edge issues including 5' and 3' end control of mRNA decay, subcellular localization of mRNA translation and decay, and RNA-binding proteins and mRNA fate. Small poster sessions will also enable all participants to contribute to, and learn about, these topics. There is also free time in the program for informal discussions among established and junior principal investigators, post-doctoral trainees and graduate students from the U.S. and abroad. This meeting will bring together sets of researchers who, despite having converging interests, have infrequent opportunities to meet as a group. A particular attraction is to bring together researchers focused on prokaryotic and eukaryotic features of post-transcriptional control to exchange information and stimulate new ideas. The resulting discussions and cross-fertilization will help define critical areas to propel this field forward.

###

Since 1982, FASEB SRC has offered a continuing series of inter-disciplinary exchanges that are recognized as a valuable complement to the highly successful society meetings. Divided into small groups, scientists from around the world meet intimately and without distractions to explore new approaches to those research areas undergoing rapid scientific changes.

In recent years, the SRC series has expanded into non-summer months. To better enhance the SRC series and allow for future expansion of conferences, FASEB's Office of Scientific Meetings and Conferences recently changed the SRC name from Summer Research Conferences to Science Research Conferences.

FASEB SRC has announced a total of 36 SRCs in 2012, spanning from June through October. To register for an SRC, view preliminary programs, or find a listing of all our 2012 SRCs, please visit http://www.faseb.org/SRC.

Additionally, in efforts to continue expanding the SRC series, potential organizers are encouraged to contact SRC staff at SRC@faseb.org. Proposal guidelines can be found by clicking "Submit a Proposal" on our website at http://www.faseb.org/SRC.

FASEB is composed of 26 societies with more than 100,000 members, making it the largest coalition of biomedical research associations in the United States. Celebrating 100 Years of Advancing the Life Sciences in 2012, FASEB is rededicating its efforts to advance health and well-being by promoting progress and education in biological and biomedical sciences through service to our member societies and collaborative advocacy.

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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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FASEB SRC announces conference registration open for: Post-transcriptional Control of Gene Expression: Mechanisms of ...

Bill Gates has a terse response to criticism that the high-tech solutions he advocates for world hunger are too expensive or bad for the environment:  Countries can embrace modern seed technology and genetic modification or their citizens will starve.

When he was in high school in the 1960s, people worried there wouldn’t be enough food to feed the world, Gates recalled in his fourth annual letter, which was published online on January 24 and reported on by the AP in the Huffington Post. But the “green revolution,” which transformed agriculture with high-yield crop varieties and other innovations, warded off famine.

Gates is among those who believe another, similar revolution is needed now. The Bill & Melinda Gates Foundation has spent about $2 billion in the past five years to fight poverty and hunger in Africa and Asia, and much of that money has gone toward improving agricultural productivity.

Gates doesn’t apologize for his endorsement of modern agriculture or sidestep criticism of genetic modification. He told the Associated Press that he finds it ironic that most people who oppose genetic engineering in plant breeding live in rich nations that he believes are responsible for global climate change that will lead to more starvation and malnutrition for the poor.

In his 24-page letter, the Microsoft Corp. chairman lamented that more money isn’t spent on agriculture research and noted that of the $3 billion spent each year on work on the seven most important crops, only 10 percent focuses on problems in poor countries.

“Given the central role that food plays in human welfare and national stability, it is shocking – not to mention short-sighted and potentially dangerous – how little money is spent on agricultural research,” he wrote in his letter, calling for wealthier nations to step up.

Go here to read the rest:
Bill Gates: Embrace Genetic Modification or Starve

22-01-2012 23:39 Jan. 23 (Bloomberg) -- Dana Nieder, mother of three-year-old Maya Nieder, talks with Bloomberg's John Lauerman about her daughter's undiagnosed genetic disorder and her struggles with medical and insurance bureaucracies for advanced testing. (Source: Bloomberg)

Original post:
Mother Seeks Answers to Daughter's Genetic Illness - Video

In this June 6, 2011 file photo, former Pennsylvania Sen. Rick Santorum holds his daughter Bella before announcing he is entering the Republican presidential race, on the steps of the Somerset County Courthouse in Somerset, Pa. Bella has the genetic disorder Trisomy 18, and was hospitalized over the weekend with pneumonia.

(Credit: AP) (CBS) Bella Santorum, the 3-year-old daughter of Republican presidential candidate Rick Santorum, was hospitalized over the weekend with pneumonia and complications from the genetic disorder, Trisomy 18.

Also known as Edwards syndrome, Trisomy 18 occurs when a person is born with three copies of the 18th chromosome, as opposed to two. That extra chromosome interferes with typical childhood development, causing children to be born with clenched hands, crossed legs, feet with rounded bottoms, a small head and jaw, and intellectual disabilities. The disorder can also cause serious heart and kidney problems. Trisomy 18 occurs in about one out of every 3,000 births. It is three times more common in girls than boys, according to the National Institutes of Health.

Unlike Down syndrome, which is caused by an extra chromosome 21, the issues caused by Trisomy 18 are associated with more life-threatening medical complications and 50 percent of babies with Trisomy 18 who are carried to term are stillborn, according to the Trisomy 18 Foundation.

"When a child is born in this situation, they very rarely make it past the first week, because one or two problems can be overwhelming and it just kind of piles up," Dr. Brian McDonough, clinical professor of family medicine at Temple University who is not involved in Bella's care, told CBS Philly.

McDonough said that even a common cold can be deadly for a child with the disorder. He said that since the Bella is over 3 years old, she's probably undergone a great deal of medical care up until now.

"Going to the hospital certainly is not something that would be unexpected," McDonough said, "but every time a child goes to the hospital with Trisomy-18, you worry a great deal."

CBS News reported that on Sunday Rick Santorum said Bella had a "miraculous turnaround" and remains in the hospital.

The Trisomy 18 Foundation has more on the genetic disorder.

Visit link:
Santorum's baby puts spotlight on genetic disorder

CHARLEROI, Belgium--(BUSINESS WIRE)-- The Belgian Biotech Company Delphi Genetics SA is proud to announce the launch of a newly-funded project. Together with academic and Biotech key-players, the company will participate in the development of DNA vaccines using the Staby® technology (antibiotic-free) during the next 3 years. The objective of the project funded by the Walloon region (BioWin project, 2.3 M €) is to develop and produce antibiotic-free DNA vaccines targeting some veterinary diseases.

The project also involves Eurogentec SA, another Belgian Biotech company (part of Kaneka) in charge of large scale DNA production and purification, and two universities: the Catholic University of Louvain in charge of the pharmaceutical and toxicity aspects of the project and the University of Liège in charge of the vaccinology and veterinary issues. “All partners complement one another perfectly” said Cédric Szpirer, CEO and Head of R&D of Delphi Genetics SA and explained:

“Today vaccination is an uncontested way of fighting disease. DNA vaccination seems to be a particularly promising method at this time, especially in the case of veterinary diseases. However, antibiotic-resistance genes are conventionally used during the construction of DNA vaccines but the resistance is increasingly less tolerated by regulatory agencies (FDA, USDA and EMA). In the context of this project, we propose to replace the antibiotic-resistance gene by the Staby® technology developed by Delphi Genetics and already used for production of recombinant proteins (higher yields and no antibiotics). In order to show the efficiency of our technology, we will develop new veterinary vaccines, we will validate that the method is usable for high scale DNA production and we will show its innocuousness.”

About Delphi Genetics

Founded at the end of 2001, Delphi Genetics SA develops technologies for genetic engineering and protein expression by using unique expertise in the domain of plasmid stabilisation systems.

Since 2004, Delphi Genetics has been marketing innovative kits for researchers. Some of these kits contain technologies that have since been licensed for industrial applications; in 2009 Delphi Genetics announced a non-exclusive licence agreement with Sanofi-Pasteur, the human vaccine division of Sanofi and a non-exclusive agreement with GSK in 2010. These agreements allow Sanofi-Pasteur and GSK to apply the StabyExpress® technology in the production of recombinant proteins, thus enabling them to produce a high yield without using antibiotics.

For more information, visit our website: http://www.delphigenetics.com

More:
Delphi Genetics: The New DNAVAC Research Project Targets the Removal of Antibiotics in Veterinary DNA-Vaccine ...

23-01-2012 19:59 For Bio Honors

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Gene Therapy: Dr. Zehhr - Video