After being diagnosed with pancreatic cancer, the likely outcome is—in a word—bleak. At a time when cancers can be treated so successfully as to give the patient a good quality of life, pancreatic cancer remains one of the last holdouts. It is the fourth most deadly form of cancer in the United States. One in four patients won’t last a year.

Pancreatic cancer is one of the most deadly forms of cancer.

One of the main hurdles for successfully treating this type of cancer is how quickly it spreads. Oftentimes, pancreatic cancer is not diagnosed until having spread to such an extent that even the most aggressive treatments can only delay the inevitable.

As a result, the goal of researchers has been to peer back in time to the origins of pancreatic cancer—in the hopes that they can find a way to halt the disease before it begins to wreak irreversible damage on the body. And now, an international team of researchers believes they have identified a gene that could be the key culprit.

Reporting in the latest issue of Nature Communications, a joint team of scientists from the Mayo Clinic and the University of Oslo, Norway, have pinpointed a gene—called PKD1—that causes normal, healthy pancreatic cells to literally morph into a new, duct-like cell structure. And it is this change in shape that can sometimes lead to pancreatic cancer.

“As soon as pancreatic cancer develops, it begins to spread, and PKD1 is key to both processes,” said Peter Storz, one of the study’s lead authors, in a news release. “Given this finding, we are busy developing a PKD1 inhibitor that we can test further.”

The purpose of the inhibitor, says Storz, is to neutralize PKD1—stopping the cancer in its tracks.

Using pancreatic cells derived from mouse models, the research team tested the effects of PKD1 by turning it on and off at specific intervals, similar to flipping a light switch. In the presence of PKD1, the team observed the pancreas cells rapidly changing shape into the more dangerous, duct-like cells. And when they shut off PKD1, the percentage of cells that underwent shape shifting dropped.

The team’s success at developing this model cannot be understated. As Storz explained:

“This model tells us that PKD1 is essential for the initial transformation…to duct-like cells, which can then become cancerous. If we can stop that transformation from happening—or perhaps reverse the process once it occurs—we may be able to block or treat cancer development and its spread.”

Currently, the teams are developing potential PDK1 inhibitors for further testing—and bring some hope that the prognosis for pancreatic cancer may not always be so dire.

Said Storz: “While these are early days, understanding one of the key drivers in this aggressive cancer is a major step in the right direction.”