A research team led by investigators from Mayo Clinic’s campus in Jacksonville, Florida, and the University of Oslo, Norway, has identified a molecule that pushes normal pancreatic cells to transform their shape, laying the groundwork for the development of pancreatic cancer, one of the most difficult tumors to treat. The team’s findings, reported online on February 20, 2015 in Nature Communications, suggest that inhibiting the gene, protein kinase D1 (PKD1), and its protein could halt progression and spread of this form of pancreatic cancer, and possibly even reverse the transformation. “As soon as pancreatic cancer develops, it begins to spread, and PKD1 is key to both processes. Given this finding, we are busy developing a PKD1 inhibitor that we can test further,” says the study’s co-lead investigator, Peter Storz, Ph.D., a cancer researcher at the Mayo Clinic. “We need a new strategy to treat, and possibly prevent, pancreatic cancer. While these are early days, understanding one of the key drivers in this aggressive cancer is a major step in the right direction,” he says. In the U.S., pancreatic cancer is the fourth most common cause of deaths due to cancer, according to the American Cancer Society. A quarter of patients do not live longer than a year after diagnosis. The title of the Nature Communications article is “Protein Kinase D1 Drives Pancreatic Acinar Cell Reprogramming and Progression to Intraepithelial Neoplasia.” Pancreatic cancer can occur when acinar cells--pancreatic cells that secrete digestive enzymes--morph into duct-like structures. This usually occurs after injury or inflammation of the pancreas, and is a reversible process. However, the presence of oncogenic signaling (Kras mutations, EGF-R) can push these duct cells to develop lesions that are at risk for tumor development.
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