Pancreatic cancer is one of the most difficult cancers to detect and treat. By the time it is diagnosed, it is often in its late stages, making it one of the deadliest types of cancer. Right now, only 12% of people diagnosed survive more than five years.
But new research brings hope. Scientists from the Sloan Kettering Institute and IRB Barcelona have made an important discovery about how pancreatic cancer starts and spreads. Their findings, published in Science, could help doctors detect the disease earlier and develop better treatments in the future.
How Pancreatic Cancer Begins
Like most cancers, pancreatic cancer starts with mutations—changes in DNA that disrupt how cells function. A key player in this process is the KRAS gene.
Normally, KRAS helps regulate cell growth, but when it mutates, it forces cells to grow uncontrollably, like a car with a stuck accelerator. This mutation is not unique to pancreatic cancer—it’s also found in lung and colorectal cancers, making it a major focus in cancer research.
Inflammation Fuels Cancer Growth
The study found that mutations alone aren’t enough to trigger cancer. Inflammation—caused by injury, disease, or chronic irritation—creates an environment that helps cancer cells grow and spread.
Even within one or two days of pancreatic tissue damage, inflammation makes cells more active and capable of interacting with their surroundings. This speeds up the cancer process, making early intervention crucial.
How Scientists Studied Early Cancer Changes
To better understand pancreatic cancer, researchers studied pancreatic ductal adenocarcinoma (PDAC)—the most common and aggressive type of pancreatic cancer.
Using genetically modified mice that mimic human pancreatic cancer, they tracked how normal cells transform into cancerous ones. This allowed them to see how cancer develops at the earliest stages, long before a tumor forms.
The Role of Shapeshifting Cells
One of the study’s biggest discoveries was cell plasticity—a cell’s ability to change its identity and take on new roles.
This shapeshifting helps precancerous cells adapt and survive, making them more dangerous. Inflammation increases this ability, helping cancer cells communicate better, spread faster, and escape the immune system.
Interestingly, these changes happen in a predictable pattern. If scientists can understand and control this process, they may one day stop cancer before it even starts.
A Closer Look with Advanced Analysis
The researchers used single-cell analysis, a technology that studies individual cells, to understand how early cancer cells behave.
They discovered certain cells acted as “communication hubs”, interacting with the immune system and other nearby cells. These highly active cells were rich in genes related to signaling and spreading, making them central to cancer growth.
What This Means for the Future
By uncovering how pancreatic cancer begins, scientists hope to develop better ways to detect it earlier, when it might still be treatable.
This research could lead to new screening tools and targeted therapies that slow or stop the disease’s progression.
While there is still much work to be done, these findings represent a major step forward in understanding pancreatic cancer. By studying its earliest changes, scientists are opening new doors for earlier diagnosis, better treatment, and, ultimately, a way to fight this deadly disease.
Copyright © 2025 Knowridge Science Report. All rights reserved.
