A new discovery from the University of Virginia Health System shows how pancreatic cancer fuels its growth and may help explain how promising cancer drugs work. This type of cancer is among those with the lowest survival rate, therefore any new theory about how to treat it could be useful for mankind.
“Pancreatic cancer is a very difficult problem. It has been a very difficult problem for a long time. The survival for pancreatic cancer patients is very low compared to other tumors,” said researcher David F. Kashatus, PhD, of the University of Virginia School of Medicine and the UVA Cancer Center. “We’re really trying to understand the biology so that scientists and drug developers can be more informed as they try to tackle this disease. Any progress we can make, no matter how small, is going to be an improvement over the current state of affairs.”
How the horrible disease works
David F. Kashatus spent many years to try to figure it all out and now he thinks he finally got it. He first proposed the research project 6 years ago, while interviewing at UVA. Kashatus tried to understand how it affected pancreatic cancer’s growth the strange changes in the shape of mitochondria, the powerhouses of cells, in cancers driven by mutations in the RAS gene.
Kashatus concluded that when the mutated RAS gene gets activated, it causes the mitochondria to fragment. This process supports the earliest shifts toward cancer’s new fueling phase. The mitochondria were playing a very unusual role. Their division was actually helping cancer come back with “new powers”.
How can it be treated?
The new study proposes a new way of fighting pancreatic cancer, with basically the tumor’s own “weapons”. Ironically, you might consider it that way, since Kashatus found out that blocking mitochondrial division in tumor samples largely prevented the tumors from growing. And when they did grow, the cancer cells lost mitochondrial function, which means game over for the disease.
“This mitochondrial fragmentation is really playing two distinct roles: On the one hand, it’s promoting this shift in metabolism. But it’s also promoting mitochondrial health,” Kashatus said. “These two things are combining to drive the pancreatic tumor growth process. So I think this is something that could be therapeutically valuable. But it also really teaches us about pancreatic tumor growth in general.”
The new study from University of Virginia Health System helps to answer a great mystery that has been around for decades: why and how do cancers rewire cells to fuel themselves using a much more inefficient process? Let’s hope the discovery will help doctors find some efficient cancer drugs, considering the fact that David F. Kashatus tells us that drugs targeting the inhibiting of mitochondrial division from tumor samples are already under development.
