Category Archives: Gene Medicine

WALTHAM, Mass.--(BUSINESS WIRE)--

Interleukin Genetics, Inc. (OTCQB: ILIU.PK - News) announced today the publication of a peer-reviewed study which found that Interleukin-1 (IL-1) gene variations are associated with increased risk of periodontal disease. The study, which appears on the Journal of Periodontologys website, in advance of appearing in the print edition, was led by Nadeem Y. Karimbux, D.M.D., Associate Professor of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine.

The study assessed the potential value of IL-1 genetic variations in the risk for developing severe periodontal disease. The IL-1 genetic variations in the published study are included in Interleukin Genetics PST Genetic Test, the first genetic test to analyze genes for variations that identify an individuals predisposition for over-expression of inflammation and risk for periodontal disease. Researchers reviewed 27 published studies on IL-1 genetics and periodontal disease from 1997 through June 2011 which examined Caucasian adults, 35 years or older with adult periodontal disease, to determine whether there was a significant association between the presence of the IL-1 gene variations and the severity and progression of periodontal disease. Thirteen studies qualified for the quantitative meta-analysis, which found significant effects for the two individual gene variations (IL1A OR=1.48; and IL1B OR= 1.54) and for a composite genotype that combines minor alleles at each locus (OR= 1.51). Some heterogeneity was evident, but there was no indication of publication bias.

This review and meta-analysis show that IL1A and IL1B genetic variations are significant contributors to chronic periodontitis in Caucasians, said Dr. Karimbux. Having this actionable information can assist dentists in establishing more aggressive treatment protocols for patients at increased risk.

Periodontal disease is caused by a chronic bacterial infection that activates inflammation which destroys the gums and bone supporting the teeth. If left untreated, periodontitis leads to tooth loss. Studies have shown that people with chronic and prolonged inflammatory periodontal disease are at an increased risk of several systemic conditions, such as heart disease, strokes, rheumatoid arthritis and certain chronic pulmonary diseases.

Periodontal disease is one of the most common chronic diseases worldwide, but fortunately most individuals develop only a mild form of periodontitis that when caught early, can be easily treated. We now know that approximately 8 to 13 percent of the adult population will develop more destructive forms of periodontitis, and most of those at risk can be identified early based on smoking, IL-1 genetics and diabetes, said Kenneth Kornman D.D.S., PhD., study author and Chief Scientific Officer of Interleukin Genetics. While additional studies should be undertaken to look at specific periodontal conditions and additional ethnicities, this study reaffirms the role genetics plays in adult oral and overall health.

About Interleukin Genetics, Inc. Interleukin Genetics, Inc. (OTCQB: ILIU.PK - News) develops and markets a line of genetic tests under the Inherent Health and PST brands.The products empower individuals to prevent certain chronic conditions and manage their existing health and wellness through genetic-based insights with actionable guidance. Interleukin Genetics leverages its research, intellectual property and genetic panel development expertise in metabolism and inflammation to facilitate the emerging personalized healthcare market. The Company markets its tests through partnerships with health and wellness companies, healthcare professionals and other distribution channels. Interleukin Genetics flagship products include its proprietary PST genetic risk panel for periodontal disease and tooth loss susceptibility sold through dentists and the Inherent Health Weight Management Genetic Test that identifies the most effective diet and exercise program for an individual based on genetics. Interleukin Genetics is headquartered in Waltham, Mass. and operates an on-site, state-of-the-art DNA testing laboratory certified under the Clinical Laboratory Improvement Amendments (CLIA). For more information, please visit http://www.ilgenetics.com.

About PST The PST Genetic Test identifies individuals with increased risk for severe and progressive periodontal disease and significant tooth loss based on a proprietary panel of genetic variations that predispose an individual to over-express inflammation. In August 2010, Interleukin Genetics announced the initiation of a landmark clinical study on risk factors predictive of periodontal disease progression to tooth loss using a new version of the PST Genetic Test. This clinical studybeing conducted at the University of Michigan School of Dentistry and led by Dr. William Giannobile, Director of the Michigan Center for Oral Health Researchis designed to test whether risk factors, including genetic information, can guide more successful intervention and thus reduce the adverse outcomes of periodontal disease, such as tooth loss.

Certain statements contained herein are forward-looking statements, including statements that the clinical studies have the potential to expand the use of the PST Genetic Test. Because such statements include risks and uncertainties, actual results may differ materially from those expressed or implied by such forward-looking statements. Factors that could cause actual results to differ materially from those expressed or implied by such forward-looking statements include, but are not limited to, those risks and uncertainties described in the Interleukin Genetics annual report on Form 10-K for the year ended December 31, 2010 and other filings with the Securities and Exchange Commission. Interleukin Genetics disclaims any obligation or intention to update these forward-looking statements.

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Newly Published Meta-Analysis Study Finds that IL-1 Gene Variations Contained in Interleukin Genetics’ PST Test are ...

23-02-2012 10:18 Because we want to understand what genes are required for blood vessel development, Courtney Griffin studies certain enzymes that help turn genes on and off. These enzymes are specifically involved in relaxing DNA that is normally tightly coiled up in our cells. Dr. Griffin is now an Assistant Member in the Cardiovascular Biology Research Program at the Oklahoma Medical Research Foundation after receiving her BA from Harvard University and her Ph. D. from the University of California San Francisco School of Medicine

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TEDxOU - Courtney Griffin - Epigenetics and the Influence of Our Genes - Video

Public release date: 6-Mar-2012 [ | E-mail | Share ]

Contact: Dr. Hilary Glover hilary.glover@biomedcentral.com 44-203-192-2370 BioMed Central

Spinal muscular atrophy (SMA) is an incurable, and progressive, disease caused by an inheritable defect in the gene SMN1. Depending on the severity of the mutation it can result in the loss of spinal cord motor neurons, muscle wasting (atrophy) and even death of an affected child. A new study published in Biomed Central's open access journal BMC Medicine shows that Fasudil, a ROCK inhibitor, can improve both the size of muscle fibers and their connection to motor neurons. Fasudil also increased the lifespan and improved the movement of SMA mice.

SMA affects 1 in 6,000 births and is the leading cause of death in young children. In its less severe form the muscle wasting of SMA traps bright young children within their bodies. Researchers from the Ottawa Hospital Research Institute and the University of Ottawa realized that SMA caused problems in regulation of the ROCK intracellular signaling pathway and that inhibiting this pathway could increase the lifespan of SMA mice.

By targeting the ROCK pathway in spinal cord and muscles, Fasudil bypasses the genetic defect SMN1. Dr Kothary, who led the team, explained, "Fasudil increased the lifespan of SMA mice from 30 to 300 days, allowing them to survive well into adulthood. Although it had no apparent effect on the damaged neurons themselves, Fasudil increased muscle size and the endplate junction between muscles and their motor neurons. Consequently, the mice were also better coordinated, better groomed, and could move about more freely than untreated SMA mice."

Melissa Bowerman from the Ottawa Hospital Research Institute continued, "Finding a cure for SMA is still a long way off, however we hope that treatment with drugs like Fasudil, which goes some way towards restoring normal developmental, or HDAC inhibitors, which alter how genes are regulated, along with nutrition and physiotherapy will provide a package of therapy to improve the quality and length of life of SMA children."

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Notes to Editors

1. Fasudil improves survival and promotes skeletal muscle development in a mouse model of spinal muscular atrophy Melissa Bowerman, Lyndsay M Murray, Justin G Boyer, Carrie L Anderson and Rashmi Kothary BMC Medicine (in press)

Please name the journal in any story you write. If you are writing for the web, please link to the article. All articles are available free of charge, according to BioMed Central's open access policy.

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Fasudil bypasses genetic cause of spinal birth defect

Public release date: 6-Mar-2012 [ | E-mail | Share ]

Contact: Kim Irwin kirwin@mednet.ucla.edu 310-206-2805 University of California - Los Angeles Health Sciences

Cancer is tough to kill and has many ways of evading the drugs used by oncologists to try and eliminate it.

Now, researchers at UCLA's Jonsson Comprehensive Cancer Center have uncovered how an advanced form of melanoma gets around an inhibitor, Zelboraf, which targets the mutated BRAF gene.

By examining the part of the melanoma genome that encodes proteins, called the exome, Jonsson Cancer Center scientists discovered that in some patients with BRAF-mutated metastatic melanoma, the mutated BRAF gene driving the cancer becomes amplified as the cancer develops resistance to a BRAF inhibitor. Quite simply, by increasing the copies of the mutated BRAF gene, the melanoma is trying to over produce the drug target protein and outnumber the inhibitor. The findings may lead to alternative ways of preventing or treating resistant melanomas.

"Understanding and solving the problem of how cancer gets around targeted drugs is arguably one of the highest priorities in modern day cancer medicine. In this study, we found that in some patients, the cancer simply makes more of the target, the mutated BRAF gene, so that the drug dose becomes too weak to fight the cancer," said study senior author Dr. Roger Lo, an assistant professor of dermatology and molecular and medical pharmacology and a Jonsson Cancer Center scientist. "If you think of the mutation as a right hand and the BRAF inhibitor as a left hand and the two clasp to be effective, there's clearly an optimal radio to ensure the mutated gene is fully inhibited. Here, we get more of the drug target, which has the same effect as dropping the drug level."

The one-year study is published March 6, 2012, in the peer-reviewed journal Nature Communications.

About 50 percent of patients with metastatic melanoma, or 4,000 people a year, have the BRAF mutation and can be treated with Zelboraf, two pills taken twice a day. Zelboraf was approved by the U.S. Food and Drug Administration for use in metastatic melanoma in August of 2011. Many other common human cancers, including colon, thyroid and lung, also harbor BRAF-mutated subsets, Lo said.

Oncologists cannot give more Zelboraf to these patients to combat the increased number of mutated BRAF genes because the dose approved by the FDA is the maximum tolerated dose, Lo said. However, Zelboraf could perhaps be given with inhibitors of other cell signaling pathways in metastatic melanoma to try and stop patients from becoming resistant.

Lo and his team examined samples of 20 patients for this study, taking their normal tissue, their tumor tissue before treatment with Zelboraf and a sample when the cancer had responded earlier but subsequently became resistant. Using high-throughput DNA sequencing technology, the scientists examined the entire cancer exome to see what changes were occurring that may point to resistant mechanisms. Lo found that five of the 20 patients showed increased copies of the mutated BRAF gene. Cell lines developed from melanoma patients also showed pathways downstream of the amplified gene that could be blocked with inhibitors to fight resistance.

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UCLA scientists uncover mechanism for melanoma drug resistance

Public release date: 6-Mar-2012 [ | E-mail | Share ]

Contact: Cody Mooneyhan cmooneyhan@faseb.org 301-634-7104 Federation of American Societies for Experimental Biology

Bethesda, MDA new research discovery by a team of Stanford and European scientists offers hope that people with atherosclerotic disease may one day be able to avoid limb amputation related to ischemia. A new research report appearing online in the FASEB Journal suggests that the delivery of genes for two molecules naturally produced by the body, called "PDGF-BB" and "VEGF" may successfully cause the body to grow new blood vessels that can save ischemic limbs.

"We hope that our findings will ultimately develop into a safe and effective therapy for the many patients, suffering from blocked arteries in the limbs, who are currently not adequately treated by surgery or drugs," said Helen M. Blau, Ph.D., a senior researcher involved in the work and Associate Editor of the FASEB Journal from the Baxter Laboratory for Stem Cell Biology at the Institute for Regenerative Medicine and Stem Cell Biology at Stanford. "This could help avoid the devastating consequences of limb amputations for both patients and their families."

To make this discovery, Blau and colleagues, including Andrea Banfi (now at Basel University), introduced the genes for PDGF-BB and VEGF into the muscles of mice, either independently or together. When high doses of VEGF alone were produced, they caused the growth of vascular tumors. When the two factors were produced in unbalanced amounts, tumor growth also occurred. When VEGF and PDGF were delivered in a fixed ratio relative to one another, however, no tumors occurred, and blood flow was restored to ischemic muscle tissue and damage repaired without any toxic effects. To achieve a "balanced" delivery of PDGF-BB and VEGF, scientists placed both genes in a single gene therapy delivery mechanism, called a "vector."

Although the report shows the feasibility of growing robust and safe new blood vessels that restore blood flow to diseased tissues, Blau points out that "there are multiple challenges to correcting peripheral vasculature disease by using proangiogenic gene therapy strategies. Two important challenges are what to deliver and how to get it to where it can have beneficial effects. Clinical success will require both delivering a gene therapy construct that encodes for effective angiogenic factors and ensuring that the sites of delivery are where the construct can have the greatest clinical benefit."

"This ingenious work, based on the latest techniques of molecular biology, tells us that it is possible to reinvigorate parts of our body that can't get enough blood to keep them going," said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal. "The next question is whether this approach will work in humans and exactly how to deliver the new treatment to places that need it the most."

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Receive monthly highlights from the FASEB Journal by e-mail. Sign up at http://www.faseb.org/fjupdate.aspx. The FASEB Journal is published by the Federation of the American Societies for Experimental Biology (FASEB) and is the most cited biology journal worldwide according to the Institute for Scientific Information. In 2010, the journal was recognized by the Special Libraries Association as one of the top 100 most influential biomedical journals of the past century. 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.

Details: Andrea Banfi, Georges von Degenfeld, Roberto Gianni-Barrera, Silvia Reginato, Milton J. Merchant, Donald M. McDonald, and Helen M. Blau. Therapeutic angiogenesis due to balanced single-vector delivery of VEGF and PDGF-BB. FASEB J. doi:10.1096/fj.11-197400 ; http://www.fasebj.org/content/early/2012/03/05/fj.11-197400.abstract

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Stanford scientists develop gene therapy approach to grow blood vessels in ischemic limbs

ScienceDaily (Mar. 6, 2012) A new research discovery by a team of Stanford and European scientists offers hope that people with atherosclerotic disease may one day be able to avoid limb amputation related to ischemia. A new research report appearing online in the FASEB Journal suggests that the delivery of genes for two molecules naturally produced by the body, called "PDGF-BB" and "VEGF" may successfully cause the body to grow new blood vessels that can save ischemic limbs.

"We hope that our findings will ultimately develop into a safe and effective therapy for the many patients, suffering from blocked arteries in the limbs, who are currently not adequately treated by surgery or drugs," said Helen M. Blau, Ph.D., a senior researcher involved in the work and Associate Editor of the FASEB Journal from the Baxter Laboratory for Stem Cell Biology at the Institute for Regenerative Medicine and Stem Cell Biology at Stanford. "This could help avoid the devastating consequences of limb amputations for both patients and their families."

To make this discovery, Blau and colleagues, including Andrea Banfi (now at Basel University), introduced the genes for PDGF-BB and VEGF into the muscles of mice, either independently or together. When high doses of VEGF alone were produced, they caused the growth of vascular tumors. When the two factors were produced in unbalanced amounts, tumor growth also occurred. When VEGF and PDGF were delivered in a fixed ratio relative to one another, however, no tumors occurred, and blood flow was restored to ischemic muscle tissue and damage repaired without any toxic effects. To achieve a "balanced" delivery of PDGF-BB and VEGF, scientists placed both genes in a single gene therapy delivery mechanism, called a "vector."

Although the report shows the feasibility of growing robust and safe new blood vessels that restore blood flow to diseased tissues, Blau points out that "there are multiple challenges to correcting peripheral vasculature disease by using proangiogenic gene therapy strategies. Two important challenges are what to deliver and how to get it to where it can have beneficial effects. Clinical success will require both delivering a gene therapy construct that encodes for effective angiogenic factors and ensuring that the sites of delivery are where the construct can have the greatest clinical benefit."

"This ingenious work, based on the latest techniques of molecular biology, tells us that it is possible to reinvigorate parts of our body that can't get enough blood to keep them going," said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal. "The next question is whether this approach will work in humans and exactly how to deliver the new treatment to places that need it the most."

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The above story is reprinted from materials provided by Federation of American Societies for Experimental Biology, via EurekAlert!, a service of AAAS.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

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Gene therapy approach to grow blood vessels in ischemic limbs