New clue could help detect one of the deadliest cancers sooner, doctors say
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Pancreatic cancer has long been recognized for its stealthy progression and devastating consequences, often slipping under the radar until it reaches an advanced and dangerous stage.
A recent wave of scientific findings may be poised to challenge that grim pattern in a significant way. Researchers at the University of California–San Diego have uncovered a promising biological indicator
that might allow doctors to detect the disease well before it becomes life-threatening or untreatable. If the discovery proves reliable over time, it could open the door to much earlier intervention—and for patients, that shift could represent a rare and valuable opportunity for hope.
In the study, researchers engineered mice with a mutation in the KRAS gene, which mimics how pancreatic cancer develops in humans.
They noticed that when cells are under stress or inflamed, they activate a protein called STAT3, a known player in helping tumors survive.
STAT3 then turns on another protein, Integrin β3 (ITGB3), which fuels the most common and aggressive type of pancreatic cancer:
pancreatic ductal adenocarcinoma. This interaction not only helped tumors form but made them more likely to spread and resist treatment.
Even more concerning, STAT3 and ITGB3 didn’t just respond to the disease—they were triggered by chemotherapy, too.
The very treatments used to kill the cancer appeared to reinforce the same mechanism that makes it stronger.
Researchers believe this harmful feedback loop helps explain why pancreatic cancer becomes so aggressive and difficult to stop once it starts.
As co-author David Cheresh told Newsweek, “Given the fact that STAT3 plays such an important role in many cancers… prompted us to drill down on which genes in particular are associated with cancer development, progression and drug resistance.”
Also read: Stop confusing this with anxiety! Here's how to spot a deadly condition before it's too late
This led researchers to define a 10-gene signature called “STRESS UP” that helps identify cells at risk of becoming full-blown cancer.
Detecting this gene signature early could indicate whether abnormal cells are likely to turn malignant—and how invasive they might become.
The team believes that existing drugs used to treat other diseases could be repurposed to block STAT3, interrupting the process before cancer develops or spreads. Blocking STAT3 early in mice slowed tumor growth and reduced the risk of it reaching other organs.
Pancreatic cancer kills around 52,000 Americans each year, and survival rates remain devastatingly low. Often diagnosed at stage three or four, the five-year survival rate plummets to just 3 percent by the time it’s considered advanced.
Early symptoms—such as back pain, abdominal discomfort, jaundice, and pale or floating stools—are vague and easily misread as more common digestive issues. Many patients mistake them for irritable bowel syndrome or chronic stress, delaying a potentially life-saving diagnosis.
Scientists believe inflammation caused by smoking, obesity, or diabetes may drive the mutation process by making cells more likely to divide and mutate.
In the mouse models, researchers showed that stressful environments like low oxygen levels only made the cancer cells more invasive. STAT3 responded by ramping up ITGB3, fueling cancer’s spread and reinforcing the STRESS UP gene pattern. The cycle, left unchecked, made pancreatic tumors more aggressive and harder to fight.
Also read: Game-changing cancer breakthrough—is this the cure we've been waiting for?
But there’s now cautious optimism. “Having knowledge of this gene signature in patients could be valuable since there are known drugs… that block STAT3 activation,” said Cheresh.
That means early screening tools may finally be possible for a disease that, until now, has offered little in the way of warning. The researchers now plan to study how to shut down ITGB3 in other cancers linked to inflammation, such as breast, lung, and skin cancer.
Read next: Warning: Emerging research uncovers a critical link between everyday behaviors and serious health threats
Are we finally close to diagnosing pancreatic cancer before it becomes a death sentence? Should more energy be focused on blocking inflammation in high-risk patients? Tell us what you think in the comments—especially if this is a disease that’s touched your life.
A recent wave of scientific findings may be poised to challenge that grim pattern in a significant way. Researchers at the University of California–San Diego have uncovered a promising biological indicator
that might allow doctors to detect the disease well before it becomes life-threatening or untreatable. If the discovery proves reliable over time, it could open the door to much earlier intervention—and for patients, that shift could represent a rare and valuable opportunity for hope.
In the study, researchers engineered mice with a mutation in the KRAS gene, which mimics how pancreatic cancer develops in humans.
They noticed that when cells are under stress or inflamed, they activate a protein called STAT3, a known player in helping tumors survive.
STAT3 then turns on another protein, Integrin β3 (ITGB3), which fuels the most common and aggressive type of pancreatic cancer:
pancreatic ductal adenocarcinoma. This interaction not only helped tumors form but made them more likely to spread and resist treatment.
New clue could help detect one of the deadliest cancers sooner, doctors say. Image source: National Cancer Institute / Unsplash
Even more concerning, STAT3 and ITGB3 didn’t just respond to the disease—they were triggered by chemotherapy, too.
The very treatments used to kill the cancer appeared to reinforce the same mechanism that makes it stronger.
Researchers believe this harmful feedback loop helps explain why pancreatic cancer becomes so aggressive and difficult to stop once it starts.
As co-author David Cheresh told Newsweek, “Given the fact that STAT3 plays such an important role in many cancers… prompted us to drill down on which genes in particular are associated with cancer development, progression and drug resistance.”
Also read: Stop confusing this with anxiety! Here's how to spot a deadly condition before it's too late
This led researchers to define a 10-gene signature called “STRESS UP” that helps identify cells at risk of becoming full-blown cancer.
Detecting this gene signature early could indicate whether abnormal cells are likely to turn malignant—and how invasive they might become.
The team believes that existing drugs used to treat other diseases could be repurposed to block STAT3, interrupting the process before cancer develops or spreads. Blocking STAT3 early in mice slowed tumor growth and reduced the risk of it reaching other organs.
Pancreatic cancer kills around 52,000 Americans each year, and survival rates remain devastatingly low. Often diagnosed at stage three or four, the five-year survival rate plummets to just 3 percent by the time it’s considered advanced.
Early symptoms—such as back pain, abdominal discomfort, jaundice, and pale or floating stools—are vague and easily misread as more common digestive issues. Many patients mistake them for irritable bowel syndrome or chronic stress, delaying a potentially life-saving diagnosis.
Scientists believe inflammation caused by smoking, obesity, or diabetes may drive the mutation process by making cells more likely to divide and mutate.
In the mouse models, researchers showed that stressful environments like low oxygen levels only made the cancer cells more invasive. STAT3 responded by ramping up ITGB3, fueling cancer’s spread and reinforcing the STRESS UP gene pattern. The cycle, left unchecked, made pancreatic tumors more aggressive and harder to fight.
Also read: Game-changing cancer breakthrough—is this the cure we've been waiting for?
But there’s now cautious optimism. “Having knowledge of this gene signature in patients could be valuable since there are known drugs… that block STAT3 activation,” said Cheresh.
That means early screening tools may finally be possible for a disease that, until now, has offered little in the way of warning. The researchers now plan to study how to shut down ITGB3 in other cancers linked to inflammation, such as breast, lung, and skin cancer.
Read next: Warning: Emerging research uncovers a critical link between everyday behaviors and serious health threats
