Pancreatic cancer’s deadliest trait may be its ability to stay invisible — and researchers in Rochester say they are beginning to understand why.
Scientists at the University of Rochester Medical Center have identified a key mechanism that allows pancreatic tumor cells to evade the body’s immune defenses, a discovery that could open the door to more effective treatments for one of the most lethal forms of cancer.
The findings, published this week in the journal Developmental Cell, focus on how certain cancer cells avoid detection even after surgery, often leading to recurrence months or years later.
Pancreatic cancer remains one of the most difficult cancers to treat, with a five-year survival rate of just 13%. Even when tumors are successfully removed, hidden cancer cells can persist in the body, eventually resurfacing and spreading.
Researchers led by surgeon-scientist Dr. Darren Carpizo found that a gene known as Dec2 plays a central role in helping those cells stay concealed. The gene regulates a molecule on the surface of tumor cells, effectively disguising them from the immune system’s T cells, which are responsible for identifying and destroying threats.
When scientists disabled the Dec2 gene in laboratory models, immune cells were able to detect and attack pancreatic cancer cells more effectively. The finding suggests Dec2 could become a potential target for future therapies designed to make tumors more visible to the immune system.
The research also uncovered a second, unexpected factor: timing.
The Dec2 gene follows a circadian rhythm — a biological “clock” that causes its activity to rise and fall throughout the day. That fluctuation appears to influence how effectively immune cells can attack cancer, offering a possible explanation for why some immunotherapy treatments perform better at certain times.
Clinicians have observed that immunotherapy administered in the morning may yield better results than treatments given later in the day. The new findings provide a biological basis for that pattern, suggesting that treatment timing could play a more critical role than previously understood.
The discovery arrives as interest grows in emerging treatments such as mRNA vaccines for pancreatic cancer. Early clinical trials have shown promising results, with some patients experiencing extended survival after generating an immune response against the disease.
But those treatments have not worked for everyone. In one recent trial, only half of participants responded to the vaccine.
Researchers say their findings may help explain why. If Dec2 prevents immune cells from recognizing tumor cells, it could limit the effectiveness of therapies that rely on that immune response. Targeting the gene may improve outcomes for patients who do not currently benefit from these treatments.
The study builds on ongoing research at Rochester’s Wilmot Cancer Institute, where scientists are exploring how the tumor microenvironment — the surrounding network of cells and tissues — enables cancer to grow and resist treatment.
While the findings are still in the laboratory stage, researchers say they represent a meaningful step toward understanding a disease that has long resisted conventional therapies.
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