Other tagging events, however, seem to depend on cellular processes and environmental changes, some of which could be the result, rather than the cause, of disease. In other words, those tagging events are under genetic control,” he says. “The details of what causes a particular sequence to be tagged are unclear, but it seems that some tagging events depend on certain DNA sequences. To complicate matters, Feinberg notes, the attachment of the tags to particular DNA sequences can itself be regulated by genes. One probable factor involves chemical “tags” that attach to DNA sequences, part of a so-called epigenetic system that helps regulate when and how DNA sequences are “read,” how they’re used to create proteins and how they affect the onset or progress of disease. According to Feinberg, several DNA mutations are known to confer risk for RA, but there seem to be additional factors that suppress or enhance that risk. It is thought to be an autoimmune disease, meaning that the body’s immune system attacks its own tissues, an assault led primarily by white blood cells. Rheumatoid arthritis is a debilitating disease that causes inflammation, stiffness, pain and disfigurement in joints, especially the small joints of the hands and feet. “Our study analyzed both and shows how genetics and epigenetics can work together to cause disease,” he says. Most genetic changes associated with disease do not occur in protein-coding regions of DNA, but in their regulatory regions, explains Andrew Feinberg, M.D., M.P.H., a Gilman scholar, professor of molecular medicine and director of the Center for Epigenetics at the Johns Hopkins University School of Medicine’s Institute for Basic Biomedical Sciences. 20, the researchers at Johns Hopkins and the Karolinska Institutet say their study bridges the gap between whole-genome genetic sequencing and diseases that have no single or direct genetic cause. In a report published in Nature Biotechnology Jan. And they suspect their experimental method can be applied to predict similar risk factors for other common, noninfectious diseases, like type II diabetes and heart ailments. By teasing apart the tagging events that result from RA from those that help cause it, the scientists say they were able to spot tagged DNA sequences that may be important for the development of RA. In one of the first genome-wide studies to hunt for both genes and their regulatory “tags” in patients suffering from a common disease, researchers have found a clear role for the tags in mediating genetic risk for rheumatoid arthritis (RA), an immune disorder that afflicts an estimated 1.5 million American adults.
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