Seattle, WA and New York, NY (Dec. 12, 2006) - An international group of researchers has discovered that the mutated form of a gene called Palladin causes familial pancreatic cancer. The findings, published online today (Dec. 12) in the peer-reviewed journal PLoS-Medicine, may help explain why the disease is so deadly. The research project was led by Dr. Teri Brentnall, University of Washington associate professor of medicine, and supported by The Lustgarten Foundation, Canary Foundation, and other private sources.
Pancreatic cancer is usually a fatal diagnosis. One of the deadliest types of cancer, it is the fourth leading cause of cancer deaths overall, and third-leading cause of cancer deaths for people aged 40 to 60 in the United States. Most people with the disease die within a year of diagnosis; about 95 percent of patients die within five years. Researchers estimate that at least ten percent of all pancreatic cancer cases are inherited.
The discovery also reveals that the Palladin gene behaves abnormally in both the hereditary and non-hereditary, or sporadic, forms of pancreatic cancer. Previous studies by co-author Dr. Carol Otey, associate professor of physiology at the University of North Carolina, have revealed that when the Palladin gene is functioning properly, it gives a cell its shape and enables the cell to move. In the case of pancreatic cancer, a mutation in Palladin allows the cell to move much more quickly than normal, essentially invading the surrounding, healthy tissue.
Palladin, identified six years ago by Otey, is involved in the cytoskeleton,
the structural backbone of all human cells. Brentnall discovered that
Palladin played a role in pancreatic cancer and began to collaborate with
Otey. The team believes that the mutated Palladin causes cancer by causing
the cytoskeleton to malfunction, which allowed the cells to move much more
quickly than normal c
Contact: Clare Hagerty
University of Washington