What's Next In Health

A study to appear in the June 2007 issue of The FASEB Journal describes a new agent, called "Zorro-LNA," which has the potential to stop genetic disorders in their tracks. In the study, researchers from the Karolinska Institute in Stockholm, Sweden, describe how they developed Zorro-LNA to bind with both strands of a gene’s DNA simultaneously, effectively disabling that gene. This development has clinical implications for virtually every human condition caused by or worsened by dominant defective genes. Examples include: Huntington’s disease, familial high cholesterol, polycystic kidney disease, some instances of glaucoma and colorectal cancer, and neurofibromatosis, among others.

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In the most comprehensive look at genetic risk factors for type 2 diabetes to date, a U.S.-Finnish team, working in close collaboration with two other groups, has identified at least four new genetic variants associated with increased risk of diabetes and confirmed existence of another six. The findings of the three groups, published simultaneously today in the online edition of the journal Science, boost to at least 10 the number of genetic variants confidently associated with increased susceptibility to type 2 diabetes – a disease that affects more than 200 million people worldwide.

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A new hereditary breast cancer gene has been discovered by scientists at the Lundberg Laboratory for Cancer Research and the Plastic Surgery Clinic at the Sahlgrenska Academy in Sweden. The researchers found that women with a certain hereditary deformity syndrome run a nearly twenty times higher risk of contracting breast cancer than expected.

Several research teams around the world have long been searching for new hereditary breast cancer genes, but thus far few have been found.

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University of Virginia researchers have discovered that microRNAs, a form of genetic material, can function as tumor suppressors in laboratory studies.

In the May 1 issue of Genes & Development, UVa researchers Drs. Yong Sun Lee and Anindya Dutta have shown that microRNAs can suppress the overexpression of a gene called HMGA2. This gene is related to creation of fatty tissue and certain tumors, as well as diet-induced obesity.

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Large swaths of garbled human DNA once dismissed as junk appear to contain some valuable sections, according to a new study by researchers at the Stanford University School of Medicine and the University of California-Santa Cruz. The scientists propose that this redeemed DNA plays a role in controlling when genes turn on and off.

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Oregon Health & Science University neuroscientists are eyeing a protein as a potential therapeutic target for multiple sclerosis because de-activating it protects nerve fibers from damage.

OHSU researchers, working with colleagues at the Portland Veterans Affairs Medical Center and the University of Padova in Italy, have shown that genetically inactivating a protein called cyclophilin D can protect nerve fibers in a mouse model of multiple sclerosis. Cyclophin D is a key regulator of molecular processes in the nerve cell's powerhouse, the mitochondrion, and can participate in nerve fiber death. Inactivating cyclophilin D strengthens the mitochondrion, helping to protect nerve fibers from injury. The findings are published today in Proceedings of the National Academy of Sciences.

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Researchers at the Moores Cancer Center at the University of California, San Diego report that they have developed a new method for detecting cancer very early in its development, when it consists of just a few cells. The best existing detection methods are not able to detect a tumor until it consists of about one million cells.

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Using a new type of drug that targets a specific genetic defect, researchers at the University of Pennsylvania School of Medicine, along with colleagues at PTC Therapeutics Inc. and the University of Massachusetts Medical School, have for the first time demonstrated restoration of muscle function in a mouse model of Duchenne's muscular dystrophy (DMD). The research appears ahead of print in an advanced online publication of Nature.

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Mayo Clinic researchers, along with collaborators from the National Institutes of Health (NIH) and University of Oslo, Norway, have discovered that a miscue of the body’s genetic repair system may cause Huntington’s disease, a fatal condition that affects 30,000 Americans annually by destroying their nervous system. Until now, no one knew how Huntington’s begins, only that it is incurable. The findings appear in the online issue of the journal Nature.

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Genetic and epigenetic variations ensure that no two people are exactly alike, and the same holds true for any two cancers. Now, researchers have the tools and the knowledge to help predict how individuals will respond to cancer therapies, enabling them to create more effective therapies for individual cancers – personalized medicine. At the 2007 Annual Meeting of the American Association for Cancer Research, researchers present new biomarkers – and techniques for determining biomarkers – that could determine how an individual might respond to drug or radiation therapy.

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Cancer is a natural consequence of human evolution. Our genes have not developed to give us long and happy lives. They are optimized to copy themselves into the next generation - irrespective of our personal desires. According to Jarle Breivik, an associate professor at the University of Oslo, Norway, we are therefore unlikely to find a final solution to cancer.

Doing research at the Institute of Basic Medical Sciences, Breivik explores the connection between cancer development and Darwinian evolution. In a recent interview with Scientific American, and the research magazine Apollon, published by the University of Oslo, he concludes that “Cancer is a fundamental consequence of the way we are made. We are temporary colonies made by our genes to propagate themselves to the next generation. The ultimate solution to cancer is that we would have to start reproducing ourselves in a different way.”

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A cancer-suppressing gene has been successfully delivered into the tumors of stage 4 lung cancer patients via an intravenously administered lipid nanoparticle in a phase I clinical trial at The University of Texas M. D. Anderson Cancer Center. The gene, FUS1, also was found to be active in the metastatic non-small cell lung cancer tumors.

"We've treated 13 patients in this first-in-human study and we've seen an exciting proof of concept with no significant drug-related toxicity," says principal investigator Charles Lu, M.D., associate professor in M. D. Anderson's Department of Thoracic, Head and Neck Medical Oncology.

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Scientists have identified the most clear genetic link yet to obesity in the general population as part of a major study of diseases funded by the Wellcome Trust, the UK's largest medical research charity. People with two copies of a particular gene variant have a 70% higher risk of being obese than those with no copies.

Obesity is a major cause of disease, associated with an increased risk of type 2 diabetes, heart disease and cancer. It is typically measured using body mass index (BMI). As a result of reduced physical activity and increased food consumption, the prevalence of obesity is increasing worldwide. According to the 2001 Health Survey for England, over a fifth of males and a similar proportion of females aged 16 and over in England were classified as obese. Half of men and a third of women were classified as overweight.

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An international research team – including investigators from Massachusetts General Hospital (MGH) and the Broad Institute of Harvard University and Massachusetts Institute of Technology – has identified several novel genetic variations associated with the risk of Crohn's disease. One of the identified genes establishes a role for autophagy, a previously unsuspected biological pathway, in Crohn's disease pathology; and the report documents functional studies which establish that this gene is integral to immune responses to intestinal bacteria. The report will appear in the journal Nature Genetics and is receiving early online release.

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Scientists have known for more than a decade that individuals with a certain gene are at higher risk for developing Alzheimer’s disease. Now a new study helps explain why this is so.

The research, led by scientists at the Oklahoma Medical Research Foundation (OMRF), has uncovered a molecular mechanism that links the susceptibility gene to the process of Alzheimer’s disease onset. The findings appear in the April 11 issue of The Journal of Neuroscience and may lead to new pathways for development of Alzheimer’s therapeutics.

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