Here’s a rewritten version of the article, focusing on clarity and conciseness while retaining the key details:
New Gene Signature Could Predict aggressive Pancreatic Cancer
San Diego, CA – Researchers at the University of California San Diego School of Medicine have identified a crucial link between cellular stress, inflammation, and the progression of pancreatic ductal adenocarcinoma (PDAC), one of the deadliest forms of cancer. This revelation could lead to an early warning system for the disease, potentially allowing for detection before it becomes life-threatening.
Previous research indicated that inflammation and cellular stress activate a protein called STAT3 in pancreatic cells, contributing to tumor growth and treatment resistance. The new study sheds light on how STAT3 achieves this.
The UC San Diego team found that in the face of inflammatory signals and low oxygen levels (a common stressor), STAT3 activates specific genes essential for cell adaptation. Notably, they discovered that STAT3 turns on the gene integrin β3 (ITGB3) in both mouse and human pancreatic cells.
Key findings from the study include:
ITGB3’s Role: Increased expression of ITGB3 was found to promote the initial advancement and accelerate the progression of PDAC tumors.
Chemotherapy’s Impact: Inflammation and stress caused by chemotherapy also activated STAT3, leading to higher ITGB3 levels in PDAC cells.
Blocking the Pathway: Inhibiting the STAT3 pathway that controls ITGB3 expression slowed down tumor initiation.
The “STRESS” Signature: STAT3 activates a group of 10 genes, including ITGB3, which the researchers have named the “STRESS” gene signature. This signature proved to be a more accurate predictor of pancreatic cancer development and tumor aggressiveness compared to existing gene signatures.
These findings hold significant promise for precision medicine. The “STRESS” signature could be used to develop early screening tools for precancerous cells. Furthermore,it may help clinicians identify patients at higher risk of aggressive disease and predict their response to traditional treatments as the cancer progresses.
The researchers are now investigating molecules that can block the inflammation-driven activation of ITGB3. This approach could potentially be applied to other cancers that affect tissue surfaces,such as lung,breast,and skin cancers,to prevent tumor progression,spread,and drug resistance.
Source: University of California – San Diego
Journal Reference: Campos,A. D., et al. (2025). A STAT3/integrin axis accelerates pancreatic cancer initiation and progression. Cell Reports. doi.org/10.1016/j.celrep.2025.116010
