Pancreatic cancer is one of the deadliest forms of cancer. It’s very hard to detect in the early stages, and by the time it’s found, it often has already spread.
Because of this, treatment is difficult, and survival rates are low. Right now, only about 12 out of every 100 people diagnosed with pancreatic cancer live more than five years.
But new research gives hope. Scientists have recently learned more about how pancreatic cancer begins and spreads. These new findings could help doctors catch the disease earlier and find better ways to treat it.
The study was a joint effort between researchers at Memorial Sloan Kettering Cancer Center in the United States and IRB Barcelona in Spain. Their work was published in the journal *Science*, one of the world’s leading science publications.
So, how does pancreatic cancer start? Like many cancers, it begins with changes in a person’s DNA, called mutations. These mutations cause cells to grow out of control. One key gene involved in pancreatic cancer is called KRAS.
This gene usually helps control how cells grow. But when it mutates, it becomes like a stuck gas pedal—making cells grow too fast. This mutated KRAS gene is also seen in other cancers, like lung and colon cancer.
But a mutation alone is not enough to cause pancreatic cancer. The study found that inflammation—swelling caused by injury or illness—plays a major role.
When the pancreas becomes inflamed, it creates an environment that helps cancer start and grow. Just one or two days of inflammation can start to change healthy cells, making them more likely to turn into cancer.
The researchers studied the most common type of pancreatic cancer, called pancreatic ductal adenocarcinoma (PDAC). They used mice that had been genetically changed to develop this kind of cancer in the same way humans do. This let the scientists watch the disease develop in real time, from healthy cells to cancerous ones.
One of the most interesting discoveries was about how flexible some cells in the pancreas are. These cells can change their identity, like shapeshifters.
This makes it easier for cancer to grow and spread. The study found that inflammation makes these cells even more adaptable. These shapeshifting cells can send and receive signals that help the cancer grow faster.
To study these changes closely, the scientists used a special technique called single-cell analysis. Instead of looking at a large group of cells, this method looks at one cell at a time.
They found that some cells in the tumors acted as “communication hubs.” These cells had many genes that let them send messages to other cells, including immune cells. This communication helped the cancer grow and spread more quickly.
What does this mean for the future? Now that scientists understand more about how pancreatic cancer starts, doctors may be able to catch it earlier—before it spreads too far. If we can block the early changes in cells, we may be able to slow down or even stop the disease.
There’s still a lot of work to do before this leads to a cure. But this study is a big step forward. It gives researchers a better picture of how pancreatic cancer begins and spreads. And with that knowledge, they can start working on new ways to diagnose and treat it.
For patients and families affected by pancreatic cancer, this discovery offers hope. Learning more about how the disease works may one day lead to better treatments—and better chances of survival.
If you care about cancer, please read studies about Scientists find important cause of pancreatic cancer and findings of Scientists find a big cause of liver cancer.
For more information about cancer, please read studies about Research shows a surprising cause of cancer and findings of The surprising impact of anxiety drugs on pancreatic cancer survival.
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