Pancreatic cancer is one of the most dangerous and difficult cancers to treat. It often goes unnoticed until it’s already advanced, and by that time, treatment options are limited.
Sadly, only about 12 out of every 100 people diagnosed with pancreatic cancer survive for more than five years. But now, new research is offering hope by helping scientists understand how this cancer starts and spreads.
Researchers from the Sloan Kettering Institute in New York and IRB Barcelona in Spain have made a big discovery. Their study, recently published in the journal Science, looks closely at the earliest stages of pancreatic cancer, before it becomes aggressive. The goal is to find ways to detect and treat it much earlier, when treatment is more likely to work.
Most cancers begin with mutations—tiny changes in a person’s DNA that cause cells to behave abnormally. In pancreatic cancer, one particular mutation is found over and over again. It happens in a gene called KRAS, which usually helps control how cells grow and divide.
But when KRAS is damaged, it acts like a stuck gas pedal, pushing cells to grow nonstop. This same mutation is also seen in other cancers like lung and bowel cancer, which shows how important it is.
But a damaged gene isn’t the whole story. The study found that inflammation—when body tissues become swollen or irritated—can speed up the cancer process. Inflammation may be caused by an injury, illness, or even long-term irritation of the pancreas.
Just a day or two of inflammation can make cells behave differently. It helps them talk to each other more, change shape, and move around, which makes it easier for cancer to grow and spread.
To explore this, scientists studied the most common and aggressive type of pancreatic cancer, called pancreatic ductal adenocarcinoma (PDAC). They used mice that had been genetically altered to develop this kind of cancer. This allowed them to follow the disease from its very beginning, watching how healthy cells slowly turn into cancer cells.
One of the most interesting things they found was how flexible the cells were. This ability to change and adapt is called “plasticity.” It means that a cell can shift its identity and act differently when needed.
In the case of pancreatic cancer, this flexibility lets early cancer cells adapt to their environment, send and receive signals more easily, and work together to grow faster. Inflammation makes this process even more active.
What’s more, the researchers noticed that these changes in cells happen in a predictable way. That’s exciting, because it means that scientists might eventually find a way to stop or slow down the process before it becomes full-blown cancer.
To better understand how this all works, the team studied individual cells one by one, using a technique called single-cell analysis.
They found that some of these shapeshifting cells act as central “hubs” for communication. These hub cells were rich in genes that help them talk to nearby cells, including immune cells. That communication seems to speed up the growth and spread of cancer.
All of this could help scientists find new ways to catch pancreatic cancer earlier, before it spreads and becomes harder to treat. If we can target these early changes—like stopping inflammation or interfering with the hub cells’ communication—we might be able to slow down or even prevent the cancer from taking hold.
This research is an important step forward. It doesn’t offer an instant cure, but it gives scientists a better understanding of how pancreatic cancer begins and grows. That’s the first step toward better detection tools, new treatments, and perhaps one day, a cure.
For now, the study offers real hope. By looking closely at how pancreatic cancer starts, scientists are opening new doors—and that could make a big difference for patients in the future.
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