Pancreatic cancer is one of the most dangerous and difficult cancers to treat. Many patients do not notice any symptoms in the early stages, so the disease is often discovered only after it has already spread to other parts of the body.
Because of this, pancreatic cancer has one of the lowest survival rates among major cancers. Today, only about 12% of people diagnosed with pancreatic cancer survive longer than five years.
Doctors and scientists have spent many years trying to understand why this cancer grows so quickly and why it is so hard to stop.
Now, researchers from the Sloan Kettering Institute at Memorial Sloan Kettering Cancer Center and IRB Barcelona have made an important discovery that could help scientists better understand how pancreatic cancer begins.
Their findings were published in the journal Science and may one day lead to earlier detection, better treatments, and possibly even ways to prevent the disease before it becomes life-threatening.
Cancer usually begins when damage happens inside a cell’s DNA. DNA contains the instructions that tell cells how to grow, divide, and behave. When these instructions become damaged, cells may begin growing out of control.
In pancreatic cancer, one of the most important damaged genes is called KRAS. This gene normally helps control healthy cell growth. But when KRAS mutates, it acts like a gas pedal that gets stuck, forcing cells to keep growing too fast. KRAS mutations are also common in other cancers, including lung cancer and colon cancer.
However, the scientists discovered that the KRAS mutation alone is not enough to fully trigger pancreatic cancer. Another major factor is inflammation.
Inflammation is part of the body’s natural defense system. It happens when the body reacts to injury, infection, or illness. In the short term, inflammation can help healing. But when inflammation continues for a long time, it can damage tissues and create conditions that help cancer grow.
The researchers found that inflammation can begin changing pancreatic cells very quickly. In fact, only one or two days after the pancreas is injured, cells already begin showing signs of abnormal activity. These early changes may push healthy cells toward becoming cancer cells.
The team focused on pancreatic ductal adenocarcinoma, often called PDAC. This is the most common and aggressive form of pancreatic cancer.
To better understand how the disease develops, the scientists used mice with the same KRAS mutations found in human patients. This allowed them to carefully watch the cancer develop step by step.
One of the most important discoveries involved something called “cell plasticity.” This means cells can change their identity and behavior. Instead of staying stable and healthy, some cells begin transforming into more flexible, “shape-shifting” cells that can adapt easily to their environment.
These altered cells appear to communicate strongly with nearby cells, including immune cells. The scientists believe this communication may help cancer spread more quickly throughout the pancreas and beyond.
The researchers also discovered that this transformation process is not random. The cells seem to change in a specific order. This finding is important because it suggests there may be certain stages where doctors could interrupt the process before full cancer develops.
To study these changes in greater detail, the scientists used an advanced technique called single-cell analysis.
This method allowed them to examine individual cells one by one instead of studying large groups of cells together. By doing this, they found certain cells that acted like communication centers, constantly sending signals to nearby cells.
These “hub” cells may play a major role in helping tumors grow and survive. The researchers think these early communication signals could become future targets for new cancer treatments.
The study gives scientists a much clearer picture of how pancreatic cancer may begin in its earliest stages. Instead of appearing suddenly, the disease may slowly develop through a series of small but organized changes inside cells.
Understanding these first steps could completely change how pancreatic cancer is treated in the future. If doctors can detect these dangerous cell changes early enough, they may be able to stop cancer before it spreads.
Future treatments might block inflammation, prevent cell plasticity, or stop harmful communication between cells. Scientists also hope this research could lead to better screening tests for people at high risk of pancreatic cancer.
Although more research is still needed before these discoveries can be turned into treatments for patients, experts say the findings offer real hope. Pancreatic cancer has long been one of the hardest cancers to fight, but this study may open the door to new strategies that could save lives in the future.
If you care about cancer, please read studies that a low-carb diet could increase overall cancer risk, and vitamin D supplements could strongly reduce cancer death.
For more information about health, please see recent studies about how drinking milk affects the risks of heart disease and cancer and results showing higher intake of dairy foods linked to higher prostate cancer risk.
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