By Sola Ogundipe
In a new discovery that could reshape global cancer diagnosis and treatment, scientists at the University of California – San Diego have identified a key biological marker linked to the early development of pancreatic cancer, one of the world’s most lethal malignancies.
The new study, published in Cell Reports, reveals that cellular stress and inflammation—often triggered by environmental factors or chemotherapy—activate a protein called STAT3. This activation, in turn, boosts another protein, Integrin β3 (ITGB3), which accelerates the growth and spread of pancreatic ductal adenocarcinoma (PDAC) – the most common and aggressive form of pancreatic cancer, responsible for the majority of deaths tied to the disease.
When researchers used drugs to block STAT3 in genetically engineered mice, the tumors grew more slowly, were less aggressive, and showed reduced potential to spread. Scientists dubbed the interaction between STAT3 and ITGB3 the “STRESS UP” gene signature, noting it could become a crucial tool for spotting precancerous activity and predicting tumour behavior—long before symptoms appear.
Globally, pancreatic cancer remains a stubborn medical challenge. The World Health Organization estimates that over 460,000 people die from pancreatic cancer every year and in many countries, the disease is diagnosed in its advanced stages due to vague symptoms like abdominal or back pain, weight loss, jaundice, and digestive changes.
By the time patients seek help, the cancer has often progressed to stage three or four, when treatment is far less effective. The five-year global survival rate is around 10 percent, and for late-stage diagnoses, it drops to 3 percent.
Pancreatic cancer also presents treatment difficulties due to its resistance to chemotherapy and the location of the pancreas deep within the abdomen, which limits surgical options. While surgery, radiation, and chemotherapy remain standard approaches, these are often palliative rather than curative, especially in late-stage cases. Increasingly, targeted therapies and immunotherapy are showing promise, but early detection remains the ultimate key to improving survival rates.
“If we can identify the STRESS UP signal early in patients, we might be able to prevent tumors from forming altogether—especially with drugs already on the market that are known to block STAT3,” said Dr. David Cheresh, Lead Researcher and Pathologist on the UC San Diego team.
The discovery may also have implications beyond pancreatic cancer. The STAT3-ITGB3 pathway and STRESS UP gene group are believed to play similar roles in cancers affecting the lungs, breast, and skin—all areas where inflammation can drive malignant growth. Researchers now aim to develop molecules that could stop this chain reaction across multiple types of cancer.
Breakthroughs like this offer a glimmer of hope against the burden of pancreatic cancer, By harnessing the power of molecular signatures and understanding the drivers of tumor aggression, scientists may be poised to rewrite the future of cancer care—turning what was once an incurable diagnosis into a manageable condition.
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