
Pancreatic cancer is one of the deadliest cancers because it’s very hard to detect early and often spreads before treatment can begin.
Many people don’t know they have it until it’s already advanced. Sadly, only about 12 out of every 100 people diagnosed with pancreatic cancer live longer than five years.
But now, a new study gives hope. Scientists have learned more about how this cancer begins and spreads. The research was done by teams from the Sloan Kettering Institute at Memorial Sloan Kettering Cancer Center and IRB Barcelona.
Their work was published in the journal Science and could lead to better ways to find and treat pancreatic cancer in the future.
Most cancers start when DNA in cells becomes damaged, causing the cells to grow in the wrong way. In pancreatic cancer, one damaged gene called KRAS is very common. This gene normally controls how cells grow.
But when it mutates, it makes cells grow too fast—like a car that can’t stop accelerating. This mutation is not only seen in pancreatic cancer, but also in lung and colon cancers.
However, gene mutations alone don’t cause cancer. The new study shows that inflammation plays a big role too. Inflammation is the body’s response to injury or disease, and it can create an environment that helps cancer grow.
The scientists found that even just a day or two after the pancreas is injured, inflammation can make cells behave differently. They become more active and more likely to start forming cancer.
The researchers focused on a type of cancer called pancreatic ductal adenocarcinoma (PDAC). It’s the most common and most aggressive form of pancreatic cancer. They used specially bred mice that had the same genetic changes as human patients. This helped them watch how healthy cells slowly turned into cancer cells, one step at a time.
One of their most important discoveries was something called “cell plasticity.” This means cells can change their identity and function. These changing cells can adapt and talk to other cells more easily. Inflammation helps this process, making it easier for cancer to grow and spread.
The scientists also found that this transformation doesn’t happen randomly. It follows a pattern. If this pattern can be understood and controlled, it might be possible to stop cancer before it starts.
To get a closer look at these early changes, the team used a tool called single-cell analysis. This lets them study each individual cell. They found certain cells that were like “communication hubs.”
These cells were very active and talked a lot with the immune system and nearby cells. The researchers used computer models to find that these shapeshifting cells had lots of genes linked to communication, which may help cancer spread faster.
This research is important because it helps us understand how pancreatic cancer begins. If doctors can catch these changes early, they may be able to treat the disease before it becomes too serious. New treatments might focus on stopping the first changes in cells or blocking the harmful communication between cells.
Even though more research is needed, this study is a big step toward better tests, treatments, and maybe even a cure one day. For now, it offers new hope to people who face this difficult cancer.
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