Two researchers at the Geisel School of Medicine at Dartmouth have helped to identify switches that can turn on or off genes associated with colorectal cancer. The finding offers clues about the development of colorectal cancer and could—potentially—provide targets for new therapies. Dr. Jason Moore, Third Century Professor of genetics and the director of the Institute for Quantitative Biomedical Sciences, and Richard Cowper-Sal.lari, a graduate student in Dr. Moore's lab, were part of a team that included researchers from Case Western Reserve University and the Cleveland Clinic. The team published its findings in Science Express, the online prepublication site for the journal Science, on April 12, 2012. Many studies of cancer and other diseases have looked for genetic variations that lead to disease. But for this study, Dr. Moore, Cowper-Sal.lari, and their colleagues examined sections of DNA that do not code for proteins—sections that have sometimes been referred to as "junk DNA." Long overlooked, junk DNA has gained more attention of late as it has become clear that it can regulate the expression of genes. "We're now starting to assign function to what historically has been known as the junk DNA—stuff in between genes that we weren't really sure what it did, if it did anything at all," Dr. Moore says. Proteins that bind to noncoding sections far away from a gene, Dr. Moore explains, can help turn that gene on or off. The researchers looked at specific sections of noncoding DNA in nine colorectal cancer samples and three samples of healthy colon tissue. They found patterns in the sections of noncoding DNA that differed depending on whether the tissue was cancerous or healthy. They refer to these sections as variant enhancer loci (VELs).
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