Pancreatic cancer is one of the deadliest forms of cancer. It’s hard to detect in the early stages and even harder to treat once it’s been found. Because symptoms often appear late, most patients are diagnosed when the cancer is already advanced. As a result, the five-year survival rate is just 12%, making it one of the leading causes of cancer-related deaths.
But a recent study has brought some hope. Researchers from the Sloan Kettering Institute in New York and IRB Barcelona in Spain have discovered new details about how pancreatic cancer starts and spreads. Their findings, published in the journal Science, could help improve early diagnosis and treatment in the future.
All cancers begin with changes in DNA, called mutations. These changes can cause cells to grow and divide uncontrollably. In pancreatic cancer, one mutation is particularly common: a change in a gene called KRAS.
Normally, this gene helps control cell growth. But when it mutates, it’s like a car with a stuck gas pedal—it keeps pushing cells to grow even when they shouldn’t. This mutation is also seen in other types of cancer, like lung and colon cancer, making it a key player in cancer development.
However, the study shows that mutations alone don’t explain everything. Inflammation in the pancreas also plays an important role. Inflammation can be caused by infections, injuries, or other diseases.
When pancreatic tissue becomes inflamed, it creates a favorable environment for cancer to develop and spread. In fact, researchers found that just one or two days after tissue damage, cells already start to behave differently—they become more active and begin to interact more with nearby cells.
The team focused on the most common type of pancreatic cancer, called pancreatic ductal adenocarcinoma, or PDAC. They studied genetically modified mice that develop this type of cancer in a way that closely mimics how it happens in humans.
By following the changes in individual cells over time, they were able to see how healthy cells slowly turn into cancerous ones.
One of their most important findings was the discovery of “cell plasticity.” This means that certain cells are able to change their identity and function. For example, a normal cell might change into a different type of cell that is more aggressive or better at spreading. Inflammation increases this ability to change, making it easier for the cancer to grow and spread.
They also found that the process of these changes follows a fairly consistent pattern. This is important because if scientists can predict how and when these changes happen, they might be able to stop or slow them down in the future.
To better understand these early changes, the researchers used a technique called single-cell analysis. This allowed them to study one cell at a time instead of looking at groups of cells all at once. Through this method, they identified special cells that acted like communication centers in the early stages of cancer.
These “hub” cells had high levels of genes that help cells talk to each other and to the immune system. This communication may be what drives cancer growth and helps it spread.
What does all this mean for patients? If scientists can find ways to spot these early changes or block the communication between cells, it might be possible to catch pancreatic cancer sooner—before it becomes deadly. This research could also lead to new treatments that target the earliest steps of cancer, rather than trying to fight it once it’s already advanced.
While there’s still a lot of work to do, this study is a big step forward. It gives scientists a clearer view of how pancreatic cancer begins and spreads. More importantly, it gives patients and families new reasons to hope. With continued research, we may one day find ways to detect this deadly cancer earlier—and even prevent it entirely.
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