Pancreatic cancer is one of the most dangerous forms of cancer in the world. It is known for being very difficult to detect and very hard to treat. I
n many cases, the disease grows quietly inside the body without causing clear symptoms. By the time doctors find it, the cancer has often already spread to other parts of the body. Because of this, treatment options can be limited and survival rates remain low.
Today, only about 12 out of every 100 people diagnosed with pancreatic cancer live for more than five years after diagnosis. This makes pancreatic cancer one of the deadliest cancers.
For many years, scientists have been trying to understand how the disease begins and why it grows so aggressively. Learning how pancreatic cancer starts could help doctors detect it earlier and develop better treatments.
A new study by researchers from the Sloan Kettering Institute in New York and the Institute for Research in Biomedicine (IRB Barcelona) in Spain is offering important new insights.
The scientists focused on the earliest stages of pancreatic cancer, long before the disease becomes aggressive. Their goal was to understand what changes happen inside cells when cancer first begins. The findings were published in the scientific journal Science.
Most cancers begin with mutations. These are small changes in the DNA inside our cells. DNA acts like an instruction manual that tells cells how to grow, divide, and function. When certain parts of the DNA are damaged, cells may start behaving in abnormal ways. Instead of growing and dividing in a controlled manner, they may begin to multiply uncontrollably.
In pancreatic cancer, one of the most common mutations occurs in a gene called KRAS. This gene normally plays an important role in controlling cell growth. It helps tell cells when to grow and when to stop.
However, when the KRAS gene becomes mutated, it can act like a gas pedal that is stuck down. The cell keeps receiving signals to grow and divide, even when it should stop.
KRAS mutations are extremely common in pancreatic cancer. In fact, they are found in the vast majority of cases. The same gene mutation also appears in several other cancers, including lung and colorectal cancer. Because of this, scientists consider KRAS one of the most important genes involved in cancer development.
But the researchers discovered that a mutation alone may not be enough to trigger aggressive cancer. Another important factor appears to be inflammation. Inflammation is the body’s natural response to injury or infection. It causes tissues to become swollen, irritated, or red as the immune system tries to repair damage.
However, inflammation in the pancreas may create an environment that helps cancer grow. The study found that even short periods of inflammation—lasting just a day or two—can change how cells behave.
During inflammation, cells begin communicating more actively with each other. They may also change their shape and become more mobile. These changes can make it easier for cancer cells to develop and spread.
To study these early changes, the scientists focused on the most common and aggressive form of pancreatic cancer, called pancreatic ductal adenocarcinoma, or PDAC. This type of cancer accounts for most pancreatic cancer cases.
The research team used specially engineered mice that carried the KRAS mutation. This allowed them to observe how healthy pancreatic cells gradually transform into cancer cells.
One of the most surprising discoveries was how flexible these cells can be. Scientists call this ability “cellular plasticity.” Plasticity means that a cell can change its identity and behavior depending on the situation.
In the case of pancreatic cancer, early cancer cells can shift their role and adapt to their environment. This flexibility helps them survive, grow, and interact with other cells.
The researchers also discovered that some cells become important communication centers. These cells act like hubs that send and receive signals between different cells in the tumor environment. Using advanced techniques that study cells one by one, known as single-cell analysis, the scientists identified these hub cells as key drivers of cancer development.
These hub cells contained many genes that help them communicate with nearby cells, including immune cells. This communication network appears to help cancer cells grow faster and organize themselves more effectively. Inflammation seems to strengthen this network, making the disease progress even more quickly.
Importantly, the scientists observed that these early changes in pancreatic cells follow a predictable pattern. This discovery is exciting because predictable patterns can sometimes be interrupted. If researchers can identify the steps that happen before cancer fully develops, they may be able to design treatments that stop the process early.
For example, future therapies might aim to reduce harmful inflammation in the pancreas or block the communication signals used by these hub cells. Another possibility is developing screening tools that detect the earliest cellular changes before a tumor forms.
Although this research does not provide an immediate cure, it represents an important step forward. By understanding the early biology of pancreatic cancer, scientists are getting closer to detecting the disease earlier and developing more effective treatments.
Pancreatic cancer remains a major global health challenge, but studies like this give researchers valuable clues about how the disease begins. Each new discovery helps open the door to better prevention, earlier diagnosis, and improved therapies 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.
The findings were published in the journal Science.
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