Pancreatic cancer is one of the deadliest cancers in the world. Each year, about half a million people are diagnosed with it, and nearly as many die.
One of the main reasons it is so deadly is that the cancer becomes resistant to treatment. When this happens, the drugs stop working, and the cancer spreads to other parts of the body.
Now, scientists at the University of Virginia have uncovered a hidden process that explains how pancreatic cancer cells resist treatment. Their findings, published in the journal Science Signaling, could lead to better ways to treat this aggressive disease.
The researchers focused on a specific type of pancreatic cancer called pancreatic ductal adenocarcinoma. This is the most common form of the disease and is very hard to treat, often being diagnosed at a late stage.
At the heart of their discovery is a process called epithelial-mesenchymal transition, or EMT for short. Normally, cancer cells start out in an “epithelial” state, where they are stationary and grow in clusters. But during EMT, the cells change shape and behavior.
They become “mesenchymal” cells—spindle-shaped and able to move around the body. This allows the cancer to spread and become resistant to treatment.
The scientists used a powerful mathematical approach called information theory to trace the signals that lead to EMT. They found that a molecule called ERK (a type of enzyme called a kinase) plays a central role in triggering EMT.
But what’s even more interesting is that when they blocked ERK, another molecule called JNK stepped in to keep EMT going. This shows how clever and adaptable cancer cells can be.
In their experiments, the researchers were able to analyze these signals at the level of individual cells. They discovered that not all cancer cells go through EMT in the same way.
Some fully transform, while others are in a “hybrid” state between the two forms. These hybrid and mesenchymal cells are the ones most likely to resist chemotherapy and spread to other parts of the body.
The study also found that cells exposed to certain growth factors were more likely to start EMT. The greater the mix of different cell types in a tumor—the more “heterogeneous” it was—the worse the outcome for the patient.
This breakthrough is important because it could help doctors figure out which drugs to use based on the signals happening inside the tumor. Blocking ERK or JNK, or both, might prevent EMT and make treatments more effective.
Even though this research is still in the early stages, it gives hope. It shows how deep knowledge of cell behavior and signaling can lead to smarter cancer treatments. With pancreatic cancer having such a low survival rate—only about 10 to 13% over five years—new treatment strategies are urgently needed.
The scientists believe that combining ERK inhibitors with current cancer drugs could help stop EMT and improve the odds for patients. Their work brings us one step closer to better therapies for one of the world’s deadliest cancers.
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