Researchers at Oregon State University (OSU) and Oregon Health & Science University have discovered a genetic function that helps one of the most important “tumor suppressor” genes (p53) to do its job and prevent cancer. Finding ways to maintain or increase the effectiveness of this gene function – attributable to a gene is called Grp1-associated scaffold protein, or Grasp – could offer an important new avenue for human cancer therapies, scientists said. The findings were published online on January 6, 2014 in Photochemical and Photobiological Sciences, a journal of the Royal Society of Chemistry. The Grasp gene was studied in the skin of mice in this research, but is actually expressed at the highest levels in the brain, heart, and lung, studies have shown. It appears to play a fundamental role in the operation of the p53 tumor suppressor gene, which is a focus of much modern cancer research. The p53 gene is involved in repair of DNA damage and, if the damage is too great, causing a mutated cell to die before it can cause further problems, up to and including cancer. Dysfunction of p53 genetic pathways have been linked to more than half of all known cancers - particularly skin, esophageal, colon, pancreatic, lung, ovarian, and head and neck cancers. “DNA mutations occur constantly in our bodies just by ordinary stresses, something as simple as exposure to sunlight for a few seconds,” said Dr. Mark Leid, professor of pharmacology and associate dean for research in the OSU College of Pharmacy, and one of the lead authors on this study. “Just as constantly, the p53 gene and other tumor suppressors are activated to repair that damage,” Dr. Leid said. “And in cases where the damage is too severe to be repaired, p53 will cause the apoptosis, or death of the mutated cell.
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