Promising breakthrough could provide new avenues of research into fourth deadliest cancer.

Teri Brentnall, M.D., of the University of Washington, reported the discovery of a gene, which, when mutated, causes pancreatic cancer in families. This discovery may allow for earlier detection of the disease as well as for intervention in patients who are at a high-risk because two or more members of their family have the disease. It also has promising implications for better understanding the sporadic instances of pancreatic cancer that occur in the general population. 

“One of the most devastating aspects of pancreatic cancer is that far too often it is detected after it has spread. Dr. Brentnall’s discovery of this gene opens up promising new avenues of research regarding two of the most important objectives in the fight against pancreatic cancer—early detection and treatment,” says Robert Vizza, president of The Lustgarten Foundation for Pancreatic Cancer Research, which provided funded in the early stages of research.

Dr. Brentnall’s team suspected that a certain gene was responsible but they did not know which one. Dr. Brentnall and the team first identified a family (Family X) with extremely high occurrences of pancreatic cancer and, therefore, a seemingly genetic disposition toward the disease.  They then developed new methods for detecting the disease at its earliest stages. 

This not only allowed them to detect precancer—something previously impossible through old screening methods—it also allowed them to determine which family members carried the lethal gene. By comparing the DNA profiles of the individuals in the family who had precancer to those who were disease-free, Dr. Brentnall discovered that a certain gene, called Palladin, when mutated, is responsible for causing pancreatic cancer.

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