Pancreatic cancer is one of the deadliest forms of cancer, known for growing fast and being very difficult to treat.
Most people diagnosed with this disease don’t survive long because the cancer often resists treatment.
Even when new drugs are used, the cancer cells usually find a way to fight back by switching to other survival methods.
But a team of scientists from several German universities may have found a new way to treat this aggressive cancer. The study was done by researchers from the University Medical Center Göttingen, the Technical University of Munich, Georg-Speyer-Haus in Frankfurt, and Charité Hospital in Berlin.
Their research focused on stopping two different pathways that cancer cells use to survive. The results, published in the journal Gastroenterology, are promising and could open the door to better treatments for patients.
The researchers discovered that blocking two specific processes in cancer cells at the same time could kill them more effectively. These processes are called the PI3Kα/δ signaling pathway and the SUMO signaling pathway.
On their own, stopping just one of these doesn’t do much—because cancer cells quickly switch to using the other one. But when both are shut down together, the cancer cells can’t adapt, and they die.
The research team, led by Dr. Matthias Wirth and Dr. Günter Schneider, tested this combination treatment in animal models. Not only did the tumors shrink, but the body’s immune system was also activated to attack the cancer.
This means the treatment works in two ways: it kills the cancer cells directly and also helps the immune system fight them more effectively.
Pancreatic cancer is hard to treat because it is so good at defending itself. Traditional treatments like chemotherapy often fail. Even newer drugs that aim at specific cancer-related genes lose their power quickly.
One of the key reasons is the PI3K signaling pathway, which plays a big role in helping cancer grow and spread. But earlier efforts to block this pathway didn’t work well, because the cancer used a backup plan—SUMOylation.
SUMOylation is a process where small proteins attach to other proteins in the cell, changing how they work. This helps cancer cells survive under stress, especially when treatments are trying to destroy them.
The researchers found that if you stop PI3K, the cancer quickly activates SUMOylation to stay alive. That’s why hitting both at the same time works better.
Dr. Ulrich Keller, one of the study’s senior authors, said that this is the first time anyone has shown how these two pathways depend on each other. If one is blocked, the other steps in to protect the cancer. But when both are stopped, the cancer has no way to escape.
Another important finding was that the combination therapy didn’t just affect the cancer cells—it also helped the immune system. Immune cells were able to enter the tumor and destroy it more easily. Dr. Wirth, another lead author, said this dual effect makes the new treatment strategy very promising.
While this research was done in animals and not yet in humans, the scientists believe it has real potential. More studies will be needed before doctors can use it in clinics, but the early results are strong. According to Dr. Wirth, this new approach uncovers a weakness in pancreatic cancer that has never been used before.
In conclusion, the study shows that blocking both PI3K and SUMO signaling pathways at the same time can stop pancreatic cancer more effectively than past methods.
It works by cutting off the cancer’s ability to adapt and by helping the immune system fight back. This could become an important step forward in treating a disease that has so far been extremely difficult to control.
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The study is published in Gastroenterology.
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