Archive for the ‘Gene Therapy Research’ Category

Editor's Choice Academic Journal Main Category: Lymphoma / Leukemia / Myeloma Also Included In: Cancer / Oncology;Genetics Article Date: 16 Mar 2012 - 9:00 PDT

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Ross Levine, M.D., lead author of the study, member of Memorial Sloan-Kettering's Human Oncology Pathogenesis Program, and a medical oncologist on the Leukemia Service at Memorial Sloan-Kettering, said:

We also want to use existing therapies more intelligently. It helps a great deal to know which subset of patients will actually benefit from intensive therapies, such as a higher dose of chemotherapy or a bone marrow transplant."

Currently, there are just a few known genetic biomarkers that clinicians rely on in order to predict outcome in individuals suffering with leukemia. Although these biomarkers provide helpful information for some patients with AML, for the majority it is hard to predict the chance for a cure.

The researchers used a method that incorporated information from a set of genes. This allowed them to categorize almost two-thirds of patients into clearly defined prognostic groups.

Dr. Levine, explained:

"Our goal was not to ask whether a certain gene or two raised or lowered risk, but to determine whether a combination of characteristics from a set of genes made it possible to precisely stratify patients according to risk."

The team examined blood or bone marrow samples from 502 individuals with AML who took part in a clinical trial conducted by Martin S. Tallman, M.D., Chief of Memorial Sloan-Kettering's Leukemia Service. The aim of the trial was to determine whether increasing the standard dose of chemotherapy would improve survival for individuals with AML under the age of 60.

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Leukemia Patients' Outcomes Predicted With Genetic Profiling

ScienceDaily (Mar. 15, 2012) A collaborative discovery involving Kansas State University researchers may improve animal health and save the U.S. pork industry millions of dollars each year.

Raymond "Bob" Rowland, a virologist and professor of diagnostic medicine and pathobiology, was part of the collaborative effort that discovered a genetic marker that identifies pigs with reduced susceptibility to porcine reproductive and respiratory syndrome, or PRRS. This virus costs the U.S. pork industry more than $600 million each year.

"This discovery is what you call a first-first," Rowland said. "This discovery is the first of its kind for PRRS but also for any large food animal infectious disease. I have worked in the field for 20 years and this is one of the biggest advances I have seen."

Rowland and researchers Jack Dekkers from Iowa State University and Joan Lunney from the Agricultural Research Service discovered a genetic marker called a quantitative trait locus, or QTL, which is associated with porcine reproductive and respiratory syndrome virus susceptibility. This discovery is a first step in controlling and eliminating the virus.

The research recently appeared in the Journal of Animal Science. The project's beginning and future center around Kansas State University, Rowland said.

It begins at the university because Rowland is involved with an organization called the PRRS Host Genetics Consortium, or PHGC, which initiated and provided more than $5 million for the research. Rowland is co-director of the consortium, which is a collaboration among the United States Department of Agriculture, the National Pork Board and Genome Canada as well as universities and industry members. Rowland is also director of the USDA-funded PRRS Coordinated Agriculture Project, known as PRRS CAP.

"The PRRS Host Genetics Consortium takes fundamental science and turns it into utility," Rowland said.

Kansas State University's new Large Animal Research Center is the site of much of the project's experimental work. The researchers obtain multiple measurements -- including growth, weight gain, performance and virus measurements -- over time. They have collected samples from more than 2,000 pigs since they began the study in 2007, for a total of more than 100,000 samples that are stored or distributed to the consortium's collaborators.

The university shipped samples to the Agricultural Research Service for genomic DNA preparations to identify differences among more than 60,000 genes. The data was transferred to Iowa State University for genetic analysis that led to the discovery of the QTL.

The collaborators at Iowa State University created a common database so that all the data collected during the project can be accessed at multiple locations by researchers and the breeding industry for the next several decades.

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Animal health breakthrough: Research uncovers genetic marker that could help control, eliminate PRRS virus

PHILADELPHIA A growing body of evidence underscores the importance of human gut bacteria in modulating human health, metabolism, and disease. Yet bacteria are only part of the story. Viruses that infect those bacteria also shape who we are. Frederic D. Bushman, PhD, professor of Microbiology at the Perelman School of Medicine at the University of Pennsylvania, led a study published this month in the Proceedings of the National Academy of Sciences that sequenced the DNA of viruses -- the virome -- present in the gut of healthy people.

Nearly 48 billion bases of DNA, the genetic building blocks, were collected in the stools of 12 individuals. The researchers then assembled the blocks like puzzle pieces to recreate whole virus genomes. Hundreds to thousands of likely distinct viruses were assembled per individual, of which all but one type were bacteriophages viruses that infect bacteria -- which the team expected. The other was a human pathogen, a human papillomavirus found in a single individual. Bacteriophages are responsible for the toxic effects of many bacteria, but their role in the human microbiome has only recently started to be studied.

To assess variability in the viral populations among the 12 individuals studied, Bushman's team, led by graduate student Samuel Minot, looked for stretches of bases that varied the most.

Their survey identified 51 hypervariable regions among the 12 people studied, which, to the team's surprise, were associated with reverse transcriptase genes. Reverse transcriptase enzymes, more commonly associated with replication of retroviruses such as HIV, copy RNA into DNA. Of the 51 regions, 29 bore sequence and structural similarity to one well-studied reverse transcriptase, a hypervariable region in the Bordetella bacteriophage BPP-1. Bordetella is the microbe that causes kennel cough in dogs.

BPP-1 uses reverse transcriptase and an error-prone copying mechanism to modify a protein to aid in entering and reproducing in a wide array of viral targets. Bushman and colleagues speculate that the newly discovered hypervariable regions could serve a similar function in the human virome, and microbiome, by extension.

"It appears there's natural selective pressure for rapid variation for these classes of bacteriophages, which implies there's a corresponding rapidly changing environmental factor that the phage must be able to quickly adapt to," says Minot. Possible reasons for change, say the authors, include evading the immune system and keeping abreast of ever-evolving bacterial hosts a kind of mutation-based host-pathogen arms race. Whatever the case, Minot says, such variability may be helping to drive evolution of the gut microbiome: "The substrate of evolution is mutation."

Evolutionary analysis of the 185 reverse transcriptases discovered in this study population suggests that a large fraction of these enzymes are primarily involved in generating diversity. Now, Minot says, the challenge is to determine the function of the newly discovered hypervariable regions, and understand how their variability changes over time and in relationship to disease.

"This method opens a whole new world of 'diversity-generating' biology to discover what these clearly important systems are actually doing," he says.

In addition to Bushman and Minot, co-authors are Stephanie Grunberg (Department of Microbiology); Gary Wu (Division of Gastroenterology); and James Lewis (Department of Biostatistics and Epidemiology), all from Penn.

The research was supported by grants from the National Institutes of Health, Pennsylvania Department of Health, and the Crohn's and Colitis Foundation of America.

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Genetic Variation in Human Gut Viruses Could be Raw Material for Inner Evolution, Perelman School of Medicine Study ...

Public release date: 15-Mar-2012 [ | E-mail | Share ]

Contact: Phyllis Edelman pedelman@genetics-gsa.org 301-351-0896 Genetics Society of America

Bethesda, MD March 15, 2012 -- A new research report appearing in the March 2012 issue of the journal Genetics shows why the development of a cure and new treatments for HIV has been so difficult. In the report, an Australian scientist explains how he used computer simulations to discover that a population starting from a single human immunodeficiency virus can evolve fast enough to escape immune defenses. These results are novel because the discovery runs counter to the commonly held belief that evolution under these circumstances is very slow.

"I believe the search for a cure for AIDS has failed so far because we do not fully understand how HIV evolves," said Jack da Silva, Ph.D., author of the study from the School of Molecular and Biomedical Science at the University of Adelaide in Adelaide, Australia. "Further insight into the precise genetic mechanisms by which the virus manages to so readily adapt to all the challenges we throw at it will, hopefully, lead to novel strategies for vaccines and other control measures."

To make this discovery, da Silva used computer simulation to determine whether, under realistic conditions, the virus could evolve as rapidly as had been reported if the virus population started from a single individual virus. This was done by constructing a model of the virus population and then simulating the killing of virus-infected cells by the immune system, along with mutation, recombination and random genetic changes, due to a small population size, affecting viral genes. Results showed that for realistic rates of cell killing, mutation and recombination, and a realistic population size, that the virus could evolve very rapidly even if the initial population size is one.

"A cure for HIV/AIDS has been elusive, and this report sheds light on the reason," said Mark Johnston, Ph.D., Editor-in-Chief of the journal Genetics. "Now that we know HIV rapidly evolves, even when its population size is small, we may be able to interfere with its ability to evolve so we can get the most out of the treatments that are developed."

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ABOUT GENETICS: Since 1916, Genetics has covered high quality, original research on a range of topics bearing on inheritance, including population and evolutionary genetics, complex traits, developmental and behavioral genetics, cellular genetics, gene expression, genome integrity and transmission, and genome and systems biology. Genetics, the peer-reviewed, peer-edited journal of the Genetics Society of America is one of the world's most cited journals in genetics and heredity.

ABOUT GSA: Founded in 1931, the Genetics Society of America (GSA) is the professional membership organization for scientific researchers, educators, bioengineers, bioinformaticians and others interested in the field of genetics. Its nearly 5,000 members work to advance knowledge in the basic mechanisms of inheritance, from the molecular to the population level. The GSA is dedicated to promoting research in genetics and to facilitating communication among geneticists worldwide through its conferences, including the biennial conference on Model Organisms to Human Biology, an interdisciplinary meeting on current and cutting edge topics in genetics research, as well as annual and biennial meetings that focus on the genetics of particular organisms, including C. elegans, Drosophila, fungi, mice, yeast, and zebrafish. GSA publishes Genetics, a leading journal in the field and a new online, open-access publication, G3: Genes|Genomes|Genetics. For more information about GSA, please visit http://www.genetics-gsa.org. Also follow GSA on Facebook at facebook.com/GeneticsGSA and on Twitter @GeneticsGSA.

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Computer simulations help explain why HIV cure remains elusive

By a GenomeWeb staff reporter

NEW YORK (GenomeWeb News) Dealing with incidental findings uncovered in whole-genome and whole-exome sequencing studies has been a contentious issue in the move to bring next-generation sequencing into the clinic.

A paper published today in Genetics in Medicine finds that physicians generally agree that those findings should be returned to adult patients, especially when medical intervention is possible. They differ, however, in their opinions on whether the findings should be returned to pediatric patients.

"This is the first study to ask specialists in genetics and laboratory medicine about the conditions they would like to see returned to clinicians who order genome sequencing," Robert Green, a geneticist at Brigham and Women's Hospital and Harvard Medical School and co-leader of the study, said in a statement. "It was heartening that the majority of specialists agreed that many incidental findings should be returned."

Co-led by Green and Howard Jacob, director of the human and molecular genetics center at the Medical College of Wisconsin, the researchers surveyed 16 genetics specialists on their recommendations for returning genetic information.

The specialists were questioned about whether they would return known pathogenic mutations, mutations that were likely to be pathogenic, and variants to known disease genes but with unknown consequences, from 99 genetic conditions and disease predisposition genes.

Around 80 percent of the specialists agreed on the return of known pathogenic mutations for 64 different diseases, and all of them agreed on the return of results for 21 different conditions for things like cancer risk and other diseases where there is the potential for medical intervention.

Opinions differed however, on returning results to children. For instance, while all the participants agreed that known variants conferring risk for hereditary breast and ovarian cancer should be returned to adults, only 75 percent thought that information should be shared with children.

Additionally, there was less agreement about what to do with findings that predicted risk for diseases for which there are no treatments, such as Huntington's disease or Alzheimer's.

Around 60 percent of the specialists said that known mutations in the genes for Huntington's disease should be returned to adults, but only 31 percent thought those findings should be returned to children. Half thought that mutations to APOE, which suggests a predisposition to Alzheimer's, should be returned to adults, while 25 percent said that the finding should be returned to children.

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Incidental Findings from Sequencing Studies Should be Returned, Say Genetics Specialists

AMES, Iowa, March 15, 2012 (GLOBE NEWSWIRE) -- NewLink Genetics Corporation (Nasdaq:NLNK - News), today announced that financial results for the company's fourth quarter and year ended December 31, 2011 will be released after the market closes on Thursday, March 29, 2012. The NewLink management team will host a conference call discussing the company's financial results and recent developments on Thursday, March 29, 2012 at 5:00 p.m. (EDT). The call can be accessed by dialing (877) 303-6919 (domestic) or (253) 237-1194 (international) five minutes prior to the start of the call and providing the passcode 62462759. A replay of the call will be available approximately two hours after the completion of the call and can be accessed by dialing (855) 859-2056 (domestic) or (404) 537-3406 (international), providing the passcode 62462759. The replay will be available for two weeks from the date of the live call.

The live, listen-only webcast of the conference call can be accessed by visiting the investors section of the NewLink website at http://investors.linkp.com/. A replay of the webcast will be archived on the company's website for two weeks following the call.

About NewLink Genetics Corporation

NewLink Genetics Corporation is a biopharmaceutical company focused on discovering, developing and commercializing novel immunotherapeutic products to improve cancer treatment options for patients and physicians. NewLink's portfolio includes biologic and small-molecule immunotherapy product candidates intended to treat a wide range of oncology indications. NewLink's product candidates are designed with an objective to harness multiple components of the innate immune system to combat cancer, either as a monotherapy or in combination with current treatment regimens, without incremental toxicity. NewLink's lead product candidate, HyperAcute Pancreas cancer immunotherapy is being studied in a Phase 3 clinical trial in surgically-resected pancreatic cancer patients (patient information is available at http://www.pancreaticcancer-clinicaltrials.com). This clinical trial is being performed under a Special Protocol Assessment with the U.S. Food and Drug Administration. NewLink and its collaborators have completed patient enrollment for a Phase 1/2 clinical trial evaluating its HyperAcute Lung cancer immunotherapy product candidate for non-small cell lung cancer and a Phase 2 clinical trial for its HyperAcute Melanoma cancer immunotherapy product candidate. NewLink also is developing d-1-methyltryptophan, or D-1MT, a small-molecule, orally bioavailable product candidate from NewLink's proprietary indoleamine-(2, 3)-dioxygenase, or IDO, pathway inhibitor technology. Through NewLink's collaboration with the National Cancer Institute, NewLink is studying D-1MT in various chemotherapy and immunotherapy combinations in two Phase 1B/2 safety and efficacy clinical trials. For more information please visit http://www.linkp.com.

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NewLink Genetics Announces 2011 Fourth Quarter and Year-End Conference Call and Webcast

Newswise Infants with Batten disease, a rare but fatal neurological disorder, appear healthy at birth. But within a few short years, the illness takes a heavy toll, leaving children blind, speechless and paralyzed. Most die by age 5.

There are no effective treatments for the disease, which can also strike older children. And several therapeutic approaches, evaluated in mouse models and in young children, have produced disappointing results.

But now, working in mice with the infantile form of Batten disease, scientists at Washington University School of Medicine in St. Louis and Kings College London have discovered dramatic improvements in life span and motor function by treating the animals with gene therapy and bone marrow transplants.

The results are surprising, the researchers say, because the combination therapy is far more effective than either treatment alone. Gene therapy was moderately effective in the mice, and bone marrow transplants provided no benefit, but together the two treatments created a striking synergy.

The research is reported online in the Annals of Neurology.

Until now, this disease has been refractory to every therapy that has been thrown at it, says senior author Mark Sands, PhD, professor of medicine and of genetics at the School of Medicine. The results are the most hopeful to date, and they open up a new avenue of research to find effective therapies to fight this devastating disease.

The combination therapy did not cure the disease, the scientists caution, but mice that received both treatments experienced significant, lasting benefits.

Mice that got gene therapy and a bone marrow transplant lived nearly 18.5 months, more than double the lifespan of untreated mice with the disease. (Healthy laboratory mice live about 24 months.) And for a significant portion of their lives, motor skills in mice that got both therapies were indistinguishable from those in normal, healthy mice.

While bone marrow transplants carry significant risks, especially in children, the researchers say they may be able to combine gene therapy with another treatment to achieve the same results. This same approach potentially could be used to treat other forms of Batten disease.

Batten disease is an inherited genetic disorder that strikes fewer than five of every 100,000 U.S. children but is slightly more common in northern Europe. There are several forms of the disease, diagnosed at different ages, and all are related to the inability of cells to break down and recycle proteins.

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Combination Treatment in Mice Shows Promise for Fatal Neurological Disorder in Kids

The professor leading a trial in cystic fibrosis treatment said that there is "huge excitement" about a new type of gene therapy.

Professor Eric Alton, UK Cystic Fibrosis Gene Therapy Consortium Coordinator from Imperial College, told the Today programme's Justin Webb that his team is "excited and enthused" but insisted that it was important not to hype the potential breakthrough.

The trial is being funded by the National Institute for Health Research and the Medical Research Council and it is hoped that it will ultimately lead to a cure for the inherited disorder which affects around 9,500 people in the UK and 90,000 around the world.

Professor Alton told the Today programme's Justin Webb that the "biggest snag is the evolution of the lungs" which, as well as preventing germs and infections from getting in, also stop gene therapy from being effective, so his team has spent the last decade trying to find "tricks to slip the gene in."

"This is difficult science that needs to be built up gradually," he said. But if it is successful the scientists involved could "book their tickets to Stockholm to pick up their Nobel Prize".

Get in touch with Today via email , Twitter or Facebook or text us on 84844.

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AUDIO: 'Exciting' new cystic fibrosis therapy

LEUVEN, BELGIUM--(Marketwire -03/15/12)- TiGenix NV (EURONEXT: TIG) today gave a business update and announced financial results for the full year 2011.

Business highlights

Financial highlights

"TiGenix has created a new and strong basis in 2011 on which we can build going forward and we have strengthened our position as the European leader in cell therapy," says Eduardo Bravo, CEO of TiGenix. "We have delivered on our promises: we have obtained national reimbursement for ChondroCelect in Belgium and made progress in other European markets. We advanced all clinical stem cell programs on plan, and raised substantial funds from specialized healthcare investors and through non-dilutive financing. Today, TiGenix is well-positioned to reach the next value-enhancing inflection points."

Business Update

Successful integration of Cellerix reinforces leadership position in cell therapyIn May 2011, TiGenix closed the business combination with the stem cell therapy company Cellerix, creating the European leader in cell therapy. During 2011 the Company succeeded in rapidly integrating both entities. The Company now combines top line revenues with an advanced pipeline of clinical stage regenerative and immuno-modulatory products. TiGenix's operations are supported by a strong commercial and manufacturing infrastructure for advanced cell therapies, an experienced international management team and a solid cash position.

As a result of the merger, the Company's development focus has shifted from early stage preclinical programs towards a number of highly promising clinical stage products for inflammatory and autoimmune disorders of high unmet medical need, each addressing markets in excess of EUR 1 billion. TiGenix product pipeline is based on a proprietary stem cell platform that exploits expanded allogeneic (donor-derived) adult stem cells derived from human adipose (fat) tissue ('eASCs'). The platform has been extensively characterized in line with requirements of the European Medicines Agency (EMA) and is supported by exhaustive preclinical and CMC packages.

Given its focus on cell therapy, TiGenix is in the process of divesting its ChondroMimetic franchise, which is based on a biomaterial platform. To be able to concentrate on its core business and move forward with a clean slate, TiGenix has decided to write-off the intellectual property related to the OrthoMimetics acquisition.

ChondroCelect commercial roll-out progressing with first national reimbursementChondroCelect obtained reimbursement in Belgium in May 2011, and is today available in 22 specialized treatment centers.

TiGenix is selling ChondroCelect in the UK, the Netherlands, Germany, and Spain under managed access and private insurance schemes, while pursuing national reimbursement in these countries and France.

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TiGenix Reports Full Year 2011 Financial Results

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By a GenomeWeb staff reporter

NEW YORK (GenomeWeb News) Marker Gene Technologies today announced a three-year, $1.6 million grant from the National Institutes of Health to further the company's screening technology directed at drugs for lysosomal storage disease.

The Eugene, Ore.-based company will use the Phase II Small Business Innovation Research grant from the National Institute of Neurological Disorders and Stroke to develop live cell and tissue assays to screen drug candidates using fluorogenic, targeted substrate reporters of lysosomal enzyme activity.

According to the grant abstract, in Phase I work, MGT established the feasibility of its technology "by preparing new fluorogenic glycosidase, esterase, phosphatase, lipase and sulfatase substrates for lysosomal enzymes and demonstrated differential staining in living cells that were from normal or were of disease origin or upon induction of inhibition of lysosomal enzyme activities."

In the next phase of research funded by the Phase II grant, the new substrates will be assayed in vitro "for their ability to measure specific and localized inhibition or induction of lysosomal enzymes in living cells as well as differentiate individual enzyme activities in a cell- or tissue-specific manner."

MGT will also validate the new systems for use in high-throughput screening for drug discovery and for use in clinical diagnostics for evaluating the occurrence and progression of disease and monitoring the effectiveness of therapeutic treatments.

Lysosomal storage diseases are metabolic disorders of the nervous systems and include Tay-Sachs, Gaucher's, and Niemann-Pick disease. About one in every 100,000 people has a lysosomal storage disease, MGT said.

"The new substrates and the resulting detection systems will provide innovative methods to quantitate lysosomal enzyme function and to screen for the influence of secondary drug or protein administration, making them useful medical research tools for a variety of significant biochemical and medical applications," MGT President and CEO John Naleway said in a statement.

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Marker Gene Gets $1.6M SBIR Grant to Build Out Screening Tech for Lysosomal Storage Disease

Public release date: 14-Mar-2012 [ | E-mail | Share ]

Contact: Alicia Reale alicia.reale@uhhospitals.org 216-844-5158 University Hospitals Case Medical Center

CLEVELAND -- New research published in the March 15 issue of the New England Journal of Medicine (embargoed 5 pm ET March 14) identifies gene mutations associated with improved overall survival with higher doses of chemotherapy for patients with acute myeloid leukemia (AML).

According to one of the authors, Hillard M. Lazarus, MD, Director of Novel Cell Therapy at Seidman Cancer Center at University Hospitals Case Medical Center and Professor of Medicine at Case Western Reserve University School of Medicine, the findings explain why some AML patients are more likely to benefit from higher does of the chemotherapy drug daunorubicin.

"This is yet another advance in the era of 'individualizing' a patient's care," said Dr. Lazarus. "These significant findings will provide an important new tool to predict patients' response to cancer-fighting therapies and will help physicians avoid over-treating some patients and under-treating others."

The new study performed an analysis of mutations in 18 genes in 398 patients younger than 60 years of age with AML who were randomly assigned to receive therapy with high-dose or standard dose daunorubicin. Researchers validated their prognostic findings in an independent set of 104 patients.

The researchers found that mutations in two genes (DNMT3A and NPM1) and translocations (movement of part of one gene to another gene, the MLL gene) were associated with improved patient outcomes with the higher doses of daunorubicin chemotherapy in AML patients.

"Information of this type could be used by a clinician for treatment planning at diagnosis and the start of therapy," said Dr. Lazarus. "That is, if the patient has the mutation in question, the clinician can go ahead and give the higher chemotherapy dose. If the patient does not have the mutation, a higher dose may not be of benefit."

The multi-site study is an analysis of genetic factors from patients who participated in a landmark 2009 study which changed the routine treatment practice for AML. That study, also published in the New England Journal of Medicine, demonstrated for the first time that a more intense initial regimen using higher doses of daunorubicin significantly improved remission rate (70.6% vs. 57.3% with a standard dose) and improved overall survival (median, 23.7 vs. 15.7 months). More patients achieved remission with only one cycle of therapy, rather than two cycles, more patients proceeded to transplant, and overall outcome was significantly improved.

Dr. Lazarus said, "These findings show how genetic information can be used to 'tailor' therapy for patients. Now the challenge before us is to find a way to provide this genetic information in a timely and affordable way to influence treatment decisions for patients. Hopefully we can answer additional important questions such as these by continuing to enroll patients onto clinical trials"

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Study finds genes improving survival with higher chemo doses in leukemia

Newswise NEW YORK, MARCH 14, 2012 Researchers have identified a set of genetic abnormalities in patients with acute myelogenous leukemia (AML) that doctors can use to more accurately predict patients prognoses and select treatments that are most likely to benefit them. The study, led by investigators at Memorial Sloan-Kettering Cancer Center, will be published in the March 22 issue of the New England Journal of Medicine.

Our study shows that genetic profiling makes it possible to more precisely categorize which patients are most likely to have their leukemia return after treatment, says the studys lead author Ross Levine, MD, a member of Memorial Sloan-Ketterings Human Oncology Pathogenesis Program. We also want to use existing therapies more intelligently. It helps a great deal to know which subset of patients will actually benefit from intensive therapies, such as a higher dose of chemotherapy or a bone marrow transplant, adds Dr. Levine, who is also a medical oncologist on the Leukemia Service at Memorial Sloan-Kettering.

At present, clinicians rely on only a handful of known genetic biomarkers (early markers of disease) to predict outcome in leukemia patients, and these biomarkers provide useful information for only a subset of patients. For most people diagnosed with AML, it is difficult to predict the chance for a cure.

The method used in the study incorporates information from an array of genes and allows nearly two-thirds of patients to be categorized into clearly defined prognostic groups. Our goal was not to ask whether a certain gene or two raised or lowered risk, but to determine whether a combination of characteristics from a set of genes made it possible to precisely stratify patients according to risk, Dr. Levine says.

The researchers analyzed blood or bone marrow samples from 502 patients with AML who were participating in a clinical trial. Such samples are routinely taken for research purposes during trials with patient consent. The trial, led by Martin S. Tallman, MD, Chief of Memorial Sloan-Ketterings Leukemia Service, explored whether increasing the standard dose of chemotherapy in AML patients under age 60 would improve survival.

The team that performed the genetic analysis, which included investigators from Memorial Sloan-Kettering, Weill Cornell Medical College, and other institutions, analyzed the samples for abnormalities, or mutations, within 18 genes known to have alterations in people with AML. The researchers noted the relationship between the mutations present in each patient and how that patient ultimately fared with the disease receiving either the standard or increased chemotherapy dose.

Our findings have important clinical implications for patients with AML, demonstrating that genetic profiling can improve current prognostic models and help guide therapeutic decisions so patients have an optimal result, says Dr. Tallman, who is a co-author of the new study. Moving forward, the challenge will be to provide this genetic information in a timely and affordable way to influence treatment decisions prospectively, he adds.

The analysis allowed the researchers to determine specific risk levels for a variety of gene-mutation combinations. They also were able to establish that the higher chemotherapy dose used in the trial benefited only some of the patients. The investigators took into account variables such as patient age and gender and validated the results in a separate group of patients to ensure that the profiling approach will be generally applicable beyond the current trial.

Dr. Levine and his Memorial Sloan-Kettering colleagues are working to translate the results from the study into clinical use. Weve already developed genetic tests, which can be used to test for this set of mutations in patients, and were in the process of making sure they work well in practice, he says. We have preliminary evidence that they perform well, and were hoping to have a pilot study soon as a step toward getting it into the clinic. We want to show this approach can be used not just at Memorial Sloan-Kettering but throughout the leukemia community.

The American Cancer Society estimates that 13,780 people in the United States will be diagnosed with AML in 2012 and that more than 10,000 people will die from the disease.

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Genetic Profiling Can Help Doctors More Accurately Predict Prognosis and Guide Treatment Decisions for Leukemia Patients

Newswise The diagnosis of myelodysplastic syndrome, a blood cancer, often causes confusion. While some patients can be treated with repeated blood transfusions, others require chemotherapy, leaving some uncertainty about whether the syndromes actually are cancer.

Now, using the latest DNA sequencing technology, scientists at the Washington University School of Medicine in St. Louis have shown that the blood disease is an early form of cancer with characteristics that are very similar to the fatal leukemia to which it often progresses. And by mapping the genetic evolution of cancer cells in seven patients with myelodysplastic syndromes who later died of leukemia, they have found clues to suggest that targeted cancer drugs should be aimed at mutations that develop early in the disease.

The research, by a large team of Washington University researchers at the Siteman Cancer Center, appears online March 14 in the New England Journal of Medicine.

The scientists sequenced all the DNA the genome of tumor cells from the patients over time. While some cancer cells in each patient acquired new mutations as they evolved, they always retained the original cluster of mutations that made the cells cancerous in the first place.

This discovery, which must be confirmed in larger studies, suggests that drugs targeted to cancer mutations might be more effective if they are directed toward genetic changes in the original cluster of cancer cells called the founding clone. Drugs that target mutations found exclusively in later-evolving cancer cells may kill those cells but likely wouldnt damage founding clones that do not carry the later mutations.

Its probably not enough to know that a particular mutation exists in cancer cells, says senior author Timothy Graubert, MD, associate professor of medicine at the School of Medicine who also treats patients at Barnes-Jewish Hospital. We likely will need to dig deeper to find out whether a mutation is in the founding clone that initiated the cancer or in a later-evolving clone.

In other words, think of this cancer as a tree, Graubert says.

To kill a tree, you have to pull out the roots, he says. If you only cut off a limb, it will just grow back. Were saying that to be effective, targeted cancer drugs probably need to attack mutations at the root of this disease.

About 28,000 Americans are diagnosed with myelodysplastic syndromes each year, most over age 60. They occur when blood cells produced in the bone marrow dont fully develop and immature cells crowd out healthy ones. In about one-third of patients, the disease progresses to a fatal form of leukemia.

As part of the new research, Graubert and his colleagues teamed with researchers at Washington Universitys Genome Institute who sequenced the genomes of cancer cells after the patients developed acute myeloid leukemia. Then, they determined whether the mutations they found were present when the same patients were first diagnosed with myelodysplastic syndromes.

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Scientists Map Genetic Evolution of Leukemia

EDMONDS, Wash., March 14, 2012 /PRNewswire/ --Washington Center for Pain Management is participating in a nationwide FDA-cleared adult stem cell study testing novel treatment for chronic low back pain and has enrolled its first patient. The study will test the use of Mesenchymal Precursor Cells (MPCs) adult stem cells derived from bone marrow that will be directly injected into the lumbar disc. The minimally invasive procedure may offer an alternative to back surgery for eligible patients with chronic pain from degenerative discs.

An estimated 30 million people in the United States suffer from back pain. Degenerative disc disease is the most common cause of low-back pain, which develops with the gradual loss of a material called proteoglycan, which cushions the bones of the spine and enables normal motion.

Most patients with low-back pain respond to physical therapy and medications, but in advanced cases, artificial disc replacement or spinal fusion -- removal of the degenerated discs and the fusion of the bones of the spine -- is necessary. However, these surgeries often are not entirely effective.

"Millions of Americans are debilitated by chronic low back pain," says Dr Hyun Joong Hong MD, the lead investigator at The Washington Center for Pain Management. "This promising therapy is at the cutting edge of medical science and has the potential to create a paradigm shift in our approach to minimally invasive solutions to this disease."

Researchers will enroll approximately 100 study participants. About fifteen participants will be enrolled at The Washington Center for Pain Management and the rest at 11 other medical centers throughout the United States. The trial is scheduled to last for three years.

Washington Center for Pain Management is enrolling study participants suffering from moderate low-back pain for a minimum of six months and whose condition has not responded to other, conventional treatments.

Once enrolled, patients are randomly assigned to one of four treatment groups:

Patients will receive a single injection of their assigned test agent directly into the center of the target discs within their spine and will be monitored for safety. Patients will also be monitored using imaging to identify any changes in their disease condition or disease progression. Use of pain medications, self-reports of pain, subsequent surgical interventions and assessments of disability, quality of life, productivity and activity will be evaluated. Repair of the disc and reduction of chronic back pain will be assessed in each patient.

Promising results have been observed in prior research using animal models when stem cells were investigated for the repair of damaged spine discs. The cells were well tolerated in these study animals.

This study is sponsored by Mesoblast Limited, a world leader in the development of biologic products for the broad field of regenerative medicine. Mesoblast has the worldwide exclusive rights to a series of patents and technologies developed over more than 10 years relating to the identification, extraction, culture and uses of adult Mesenchymal Precursor Cells (MPCs). The MPCs are derived from young adult donors' bone marrow and are immune tolerant.

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Washington Center for Pain Management Begins Enrollment in United States Stem Cell Therapy Study in Subjects With ...

The U.S. Food and Drug Administration has received a complaint alleging the Houston company involved in Gov. Rick Perry's unregulated adult stem-cell operation is a potential danger to patients and not in compliance with federal law.

In an eight-page letter sent last month, University of Minnesota bioethicist Leigh Turner called on the FDA to investigate Celltex Therapeutics Corp., which banks people's stem cells for future reinjection in the event of disease or injury. Perry was the company's first customer last year.

"It appears their business plan involves injecting or infusing on a for-profit, commercial basis non-FDA-approved adult stem cells into paying customers," Turner wrote in the Feb. 21 letter. "This plan conflicts with FDA regulations governing human stem cells."

An FDA spokeswoman declined comment, but Turner said an agency official told him the matter has been assigned to an investigator and is being taken seriously.

Celltex co-founder David Eller said Tuesday night he is confident the company will "meet all FDA specifications." He emphasized that Celltex doesn't administer stem cells, but stores and processes them at the behest of doctors who later reinject them into patients.

Dr. Stanley Jones, a Houston orthopedic surgeon, injected Perry's stem cells during his back surgery in July.

The plan by Celltex and Perry to make Texas a leader in the therapy have been controversial since details about the governor's procedure became known last summer. The therapy, drawing on the ability of adult stem cells to replenish dying cells, is promising but thought by most medical researchers to need much more clinical study before it is commercialized.

Stem cells are a kind of medicine known as biologics, therapy involving living cells rather than chemicals. Most medical experts say that adult stem-cell therapy involves more than the "minimal manipulation" the agency allows without its oversight because the cells are isolated, cultured in a laboratory and stored for some period of time before being reinjected.

The FDA has recently stepped up enforcement of unregulated adult stem cell activity, though legal experts interviewed last fall by the Chronicle said it was unclear whether the agency would look into Perry's procedure because he seemed fully informed and unharmed by it.

The Texas Medical Board is currently considering a policy that would require providers of stem cells and other experimental drugs to use them only with the permission of independent review committees that assess trials for patient safety. The policy comes up for final approval in April.

Link:
Perry's stem-cell firm draws FDA scrutiny

To: MEDICAL, NATIONAL AND SCIENCE EDITORS

--Anti-Inflammatory Drugs May Offer Novel Treatment for Heart Disease, Say Gene Researchers in Large Study--

PHILADELPHIA, March 14, 2012 /PRNewswire-USNewswire/ -- A large international study indicates that anti-inflammatory drugs may become a new tool for preventing and treating coronary heart disease (CHD), the leading global cause of death. In investigating a specific gene variant linked to inflammation and heart disease, the researchers used the Cardiochip, a gene analysis tool designed by Brendan J. Keating, Ph.D., a researcher in the Center for Applied Genomics at The Children's Hospital of Philadelphia, and co-author of the study.

Scientists already knew that inflammation is associated with atherosclerosis, the buildup of fatty deposits on artery walls that causes CHD, but until now, no one had identified an inflammatory agent causing the disease. Likewise, it was unknown whether a drug targeted at reducing inflammation might treat CHD.

The current study focused on the interleukin-6 receptor (IL6R), a signaling protein found in the blood that increases inflammatory responses. "This study provides robust evidence that IL6R is implicated in coronary heart disease," said Keating. "Furthermore, our analysis showed that an existing anti-inflammatory drug, acting on this receptor, may offer a new potential approach for preventing CHD."

The study, which appeared online today in The Lancet, was performed by the IL6R Mendelian Randomisation Analysis Consortium, an international research team led by Dr. Juan Pablo Casas, Professor Aroon D. Hingorani, and Dr. Daniel I. Swerdlow, all of University College London in the U.K. The study was a meta-analysis of data from 40 existing studies that included nearly 133,500 participants from the U.S. and Europe. Mendelian randomization is a research method that uses knowledge of genes and biological mechanisms to predict likely effects of a new drug before conducting a clinical trial, with its high cost and potential risk of side effects.

A companion study in the same issue of The Lancet, by the IL6R Genetics Consortium and Emerging Risk Factors Collaboration, found that a genetic variant in the IL6R gene, which carries the code for the IL6R protein, dials down inflammation and thus lowers the risk of heart disease.

The study in which Keating participated focused on SNPs (single nucleotide polymorphisms) single-base changes in the IL6R gene that codes for the IL6R protein.

Among the research team's tools was a DNA array, the IBC Human CVD BeadChip, also called the Cardiochip, created by Keating in 2006 and since used in many large gene studies. That chip contains DNA markers for 2000 gene variants implicated in cardiovascular disease. When brought into contact with test samples of DNA from research participants, the chip detects specific SNPs in the sample --gene variants that may affect biological functions and risks of heart disease among the participants.

They found that one SNP, the gene variant rs8192284, altered several biological markers associated with inflammation. Those results were similar to those found in trials of tocilizumab, an anti-inflammatory drug currently used to treat rheumatoid arthritis. By inhibiting the action of IL6R, this drug reduces the painful inflammation common in rheumatoid arthritis.

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Gene Chip, Invented by Children's Hospital of Philadelphia Scientist, Pinpoints New Target to Prevent Heart Disease

--Anti-Inflammatory Drugs May Offer Novel Treatment for Heart Disease, Say Gene Researchers in Large Study--

Newswise Philadelphia, March 14, 2012 A large international study indicates that anti-inflammatory drugs may become a new tool for preventing and treating coronary heart disease (CHD), the leading global cause of death. In investigating a specific gene variant linked to inflammation and heart disease, the researchers used the Cardiochip, a gene analysis tool designed by Brendan J. Keating, Ph.D., a researcher in the Center for Applied Genomics at The Childrens Hospital of Philadelphia, and co-author of the study.

Scientists already knew that inflammation is associated with atherosclerosis, the buildup of fatty deposits on artery walls that causes CHD, but until now, no one had identified an inflammatory agent causing the disease. Likewise, it was unknown whether a drug targeted at reducing inflammation might treat CHD.

The current study focused on the interleukin-6 receptor (IL6R), a signaling protein found in the blood that increases inflammatory responses. This study provides robust evidence that IL6R is implicated in coronary heart disease, said Keating. Furthermore, our analysis showed that an existing anti-inflammatory drug, acting on this receptor, may offer a new potential approach for preventing CHD.

The study, which appeared online today in The Lancet, was performed by the IL6R Mendelian Randomisation Analysis Consortium, an international research team led by Dr. Juan Pablo Casas, Professor Aroon D. Hingorani, and Dr. Daniel I. Swerdlow, all of University College London in the U.K. The study was a meta-analysis of data from 40 existing studies that included nearly 133, 500 participants from the U.S. and Europe. Mendelian randomization is a research method that uses knowledge of genes and biological mechanisms to predict likely effects of a new drug before conducting a clinical trial, with its high cost and potential risk of side effects.

A companion study in the same issue of The Lancet, by the IL6R Genetics Consortium and Emerging Risk Factors Collaboration, found that a genetic variant in the IL6R gene, which carries the code for the IL6R protein, dials down inflammation and thus lowers the risk of heart disease.

The study in which Keating participated focused on SNPs (single nucleotide polymorphisms) single-base changes in the IL6R gene that codes for the IL6R protein.

Among the research teams tools was a DNA array, the IBC Human CVD BeadChip, also called the Cardiochip, created by Keating in 2006 and since used in many large gene studies. That chip contains DNA markers for 2000 gene variants implicated in cardiovascular disease. When brought into contact with test samples of DNA from research participants, the chip detects specific SNPs in the sample gene variants that may affect biological functions and risks of heart disease among the participants.

They found that one SNP, the gene variant rs8192284, altered several biological markers associated with inflammation. Those results were similar to those found in trials of tocilizumab, an anti-inflammatory drug currently used to treat rheumatoid arthritis. By inhibiting the action of IL6R, this drug reduces the painful inflammation common in rheumatoid arthritis.

Further analysis of data from CHD patients and controls showed that subjects carrying the gene variant had a lower risk of CHD. What this tells us is that IL6R blockers such as tocilizumab mimic the benefits of having this gene variant, said Keating. A next step will be for cardiology researchers to design and carry out clinical trials to determine whether tocilizumab or similar anti-inflammatory drugs will prevent heart disease.

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Gene Chip Invented by CHOP Scientist Pinpoints New Target to Prevent Heart Disease

WEDNESDAY, March 14 (HealthDay News) -- By analyzing gene mutations in patients with acute myeloid leukemia, researchers were able to more accurately predict which ones had the best chances of going into remission, and which ones would respond well to standard treatments or needed more aggressive treatment.

Doctors from Memorial Sloan-Kettering Cancer Center in New York City analyzed 18 genes from about 500 patients with acute myeloid leukemia (AML). AML is a cancer of the bone marrow, or the soft tissue that forms blood cells.

The patients had previously taken part in a clinical trial for a chemotherapy drug, daunorubicin, and researchers knew how everyone had fared in that study.

In the new analysis, the scientists used the latest gene-sequencing technology to determine what mutations were present in the cancer cells of the patients, and whether the presence of those mutations predicted how well people did.

They found that certain combinations of mutations were associated with both better or worse chances of survival, and that those genetic predictors could be used to determine whether patients would respond to the standard dose of daunorubicin or whether they should receive a higher, more aggressive dose of the drug.

Currently, some cancer hospitals already do a limited genetic analysis in leukemia patients to look for three mutations that are associated with a low or high risk of relapse, experts explained.

But about 60 percent of people fall into the intermediate category, said senior study author Dr. Ross Levine, an associate member in the Human Oncology and Pathogenesis Program at Sloan-Kettering. That leaves oncologists with a lot of uncertainty about how aggressively to treat those patients and what to tell them about their prognosis.

"If you know patients have a high chance of cure, you would pursue a standard therapeutic route," Levine said. "If you have a patient with a low chance of cure, you might consider more aggressive or investigational therapies."

Using the information from the more extensive analysis, about half of the patients who were in the intermediate risk could be put into a low- or high-risk category, Levine said.

"What we found was by studying the DNA of patients with leukemia and classifying all 500 patients, you could identify a set of mutations, which allows us to more accurately separate those at high risk of relapse, at intermediate risk of relapse and at low risk of relapse," Levine said. "Specifically, risk stratification with more extensive mutational profiling better predicts outcome than current classification schema."

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Detailed Gene Scan Might Help Guide Leukemia Treatment

Green revolution:Fast-track breeding is beginning to develop crops that can produce more and healthier food without controversial genetic engineering.

In Zambia during the current planting season, a corn crop will go into the fields that begins the process of rapidly boosting vitamin A content by as much ten-fold helping to address a nutritional deficiency that causes 250,000-500,000 children to go blind annually, most of them in Africa and Asia. In China, Kenya, and Madagascar, also this planting season, farmers will put out a crop of Artemisia annua that yields 20 to 30 percent more of the chemical compound artemisinin, the basis for what is now the worlds standard treatment for malaria.

Both improvements are happening because of fast-track breeding technology that promises to produce a 21st-century green revolution. It is already putting more food on tables though its unclear whether it can add enough food to keep pace as the worlds human population booms to 9 billion people by 2050.

Fast-track breeding is also giving agronomists a remarkable tool for quickly adapting crops to climate change and the increasing challenges of drought, flooding, emerging diseases, and shifting agricultural zones. And it can help save lives: In the absence of prevention, half those victims of vitamin A deficiency now die shortly after going blind, according to the World Health Organization; and in 2010, lack of adequate treatment meaning artemisinin contributed to the deaths of 655,000 children from malaria.

The fast-track technology, called marker-assisted selection (MAS), or molecular breeding, takes advantage of rapid improvements in genetic sequencing, but avoids all the regulatory and political baggage of genetic engineering. Bill Freese, a science policy analyst with the Center for Food Safety, a nonprofit advocacy group, calls it a perfectly acceptable tool. I dont see any food safety issue. It can be a very useful technique if its used by breeders who are working in the public interest.

Molecular breeding isnt genetic engineering, a technology that has long alarmed critics on two counts. Its methods seem outlandish taking genes from spiders and putting them in goats, or borrowing insect resistance from soil bacteria and transferring it into corn and it has also seemed to benefit a handful of agribusiness giants armed with patents, at the expense of public interest.

By contrast, molecular breeding is merely a much faster and more efficient way of doing what nature and farmers have always done, by natural selection and artificial selection respectively: It takes existing genes that happen to be advantageous in a given situation and increases their frequency in a population.

In the past, farmers and breeders did it by walking around their fields and looking at individual plants or animals that seemed to have desirable traits, like greater productivity, or resistance to a particular disease. Then they went to work cross-breeding to see if they could tease out that trait and get it to appear reliably in subsequent generations. It could take decades, and success at breeding in one trait often meant bringing along some deleterious fellow traveler, or inadvertently breeding out some other essential trait.

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Fast-track breeding could bring a second Green Revolution

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

Viral Genetics (Pinksheets: VRAL.PK - News) today published its March 2012 Letter to Shareholders. Providing updates on the companys progress, the letter discusses the recent Pre-IND filing for its Lyme Disease drug candidate, notes other drugs in the pipeline that have developed out of the companys Metabolic Disruption Technology Platform, and talks about progress in proving the efficacy of the yield enhancement in the companys algal biofuels subsidiary, VG Energy.

The letter is available on the companys website at http://www.viralgenetics.com/shareholder-letters/Letter-to-Shareholders-Mar-12.PDF.

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 are 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 Publishes March 2012 Monthly Letter to Shareholders

(Reuters) - Advances in genetic profiling are paving the way for more precise, and effective, treatment of the aggressive bone marrow cancer known as acute mylogenous leukemia, or AML, according to new research.

Two studies, published in the latest edition of the New England Journal of Medicine, show that genetic testing can guide doctors in how best to use current therapies as well as identify new drug targets.

"As lots of studies identify new alterations in genes in leukemia and other cancers, we need to begin to understand how these alterations in DNA can predict outcomes and determine differences in treatment," said Dr. Ross Levine of Memorial Sloan-Kettering Cancer Center in New York, the lead author of one of the studies.

Such personalized therapy is considered the new frontier for medical practice, and hopes for its success underpin a $5.7 billion hostile bid by drugmaker Roche Holding for gene sequencing company Illumina.

The second study, from Washington University in St. Louis, found that 85 percent of bone marrow cells in patients with myelodysplastic syndrome, a blood-related disorder that can precede AML, were linked to mutations in progressive cancer.

The Sloan-Kettering study analyzed bone marrow samples from 502 AML patients for mutations in 18 genes associated with the disease. The researchers were able to categorize two-thirds of the patients into groups clearly defined by their survival chances.

The study found that high-dose chemotherapy improved the rate of survival for patients with three specific genetic mutations, compared with standard-dose chemo.

It also showed that genetic profiling makes it possible to more precisely determine which patients are most likely to have their leukemia return after treatment.

AML is typically cured in about 40 percent of adults between the ages of 18 and 60, according to Levine.

"We were able to identify a very large subset of patients who need new therapies," he said. "Another set was found to do incredibly well with existing therapies, and that is very informative."

Link:
Leukemia gene mutations linked to survival odds

London, March 13 (ANI): Scientists hope to genetically tweak ordinary oranges into 'healthier' blood oranges, which could combat obesity and heart disease.

They have identified the 'ruby' gene that makes the blood orange red.

The distinctive red pigment is believed to have health benefits, which include combating obesity and heart disease.

They also discovered how the gene is activated, raising the possibility of switching it on in ordinary 'blond' orange varieties, the Daily Mail reported.

One recent study found that drinking blood orange juice with a full English breakfast reduced the harmful effects of a fat-laden fry-up.

Blood oranges need a period of cold as they ripen and currently the only place where they can be reliably grown on a commercial scale is in the foothills of Mount Etna in Sicily in the Mediterranean.

As a result, blood orange juice is hard to come by and a carton costs about 1pounds more than ordinary orange juice.

"Blood oranges contain naturally occurring pigments associated with improved cardiovascular health, controlling diabetes and reducing obesity," said Professor Cathie Martin, who led the research team from the John Innes Centre in Norwich.

"Our improved understanding of this trait could offer relatively straightforward solutions to growing blood oranges reliably in warmer climates through genetic engineering," she stated.

The pigments are anthocyanins, chemicals that colour red, purple and blue fruits.

Continued here:
Gene that could turn 'normal' fruit into 'healthier' blood oranges identified

Washington, March 14 (ANI): A gene that can simultaneously protect against cancer and favour its growth has been identified.

Researchers at the Spanish National Cancer Research Centre who made the discovery suspect there may be many more genes that share this double-edged property.

In the words of Oscar Fernandez Capetillo, head of the group responsible for the study, this gene "can be both Dr. Jekyll and Mr. Hyde, in that it can either protect us against the appearance of tumours or promote tumour growth".

The study co-authored by Andre's J. Lopez-Contreras and Paula Gutierrez Martinez, focuses on the activity of Chk1, a gene known for its tumour suppressing effect.

It is what Fernandez-Capetillo calls "a genome guardian, a gene that keeps our genome free of mutations and, therefore, protects against the development of tumours".

The team wished to ascertain whether the tumour-protective effect of Chk1 was magnified in organisms with a larger quantity of the protein it codes for, so they created a mouse with three copies of the gene instead of the normal two.

They then extracted and cultured the animal's cells and turned them cancerous with the aid of other genes. What they observed confounded all expectations: the cells became malignant more easily when carrying an extra copy of Chk1.

The reason for this paradox is that Chk1 has a beneficial effect on healthy cells, but also benefits tumour cells once they have established themselves in the body.

"Initially, Chk1 prevents the appearance of tumours, by limiting the spontaneous mutations that take place in our cells," explained Fernandez Capetillo.

"This is the Dr. Jekyll side. However, advanced tumours exhibit extensive damage to their DNA and it is here that Chk1 comes to the tumour's aid by reducing the damage built up in its genome," he said.

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Gene known to protect against cancer can also promote tumour growth

Genetically engineered microbes that might one day churn out biofuels, clean up toxic waste or generate new medicines need to be proved safe before they are released into the environment, a coalition of 111 environmental and social justice groups said Tuesday.

Led by the environmental advocacy group Friends of the Earth, the coalition also called for stronger government regulations over extreme genetic engineering and a moratorium on the commercial use and release of lab-created organisms.

Without proper safeguards, we risk letting synthetic organisms and their products out of the laboratory with unknown potential to disrupt ecosystems, threaten human health and undermine social, economic and cultural rights, the coalition said in a new report.

The technology to manipulate the genes of bacteria, yeast and other organisms has existed since the 1970s, leading to pest-resistant crops, bacteria that produce human insulin and other breakthroughs.

But in 2010, biologist J. Craig Venter announced that his institute had invented synthetic biology by transplanting the entire genome of one bacterium into a different species, which then reproduced. While not qualifying as an entirely new organism, the lab-built microbe did fuel concerns that this technology presented new and hard-to-quantify risks.

The White House jumped in, with the Presidential Commission for the Study of Bioethical Issues recommending in 2010 that federal agencies adopt a middle course that encouraged enhanced oversight and careful consideration of possible risks but no new laws or regulations.

Environmental groups say those measures dont go far enough.

The field is evolving incredibly rapidly in the face of almost no regulation, said Eric Hoffman of Friends of the Earth. A moratorium puts the brakes on to allow society time to decide which applications are okay and which arent.

Representatives of the biotechnology industry say that genetically modified organisms are already adequately regulated by the Environmental Protection Agency, the U.S. Agriculture Department, the Food and Drug Administration and other agencies.

I think the reports kind of silly, frankly. It makes no sense to call for a moratorium, said Brett Erickson, executive vice president of the Biotechnology Industry Organization, a trade group. Weve been doing genetic engineering for 30years, and weve been doing it safely. People are hyping this as something new.

Read more from the original source:
Environmental groups call for tighter regulation of ‘extreme genetic engineering’