A new study reveals why pancreatic cancer is so resistant to treatment and points to a promising way to overcome it. Researchers found that a specific group of immune cells, called tumor-associated macrophages, help tumors build an “immunosuppressive fortress” that protects them from chemotherapy and immunotherapy.
The study identified a key pathway involving a lipid signal (LysoPS) and a receptor called GPR34 on these macrophages. When cancer cells are damaged by treatment, they release LysoPS, which activates GPR34. This causes the macrophages to suppress the immune system by exhausting T cells and hiding cancer signals, allowing tumors to survive and grow.
Importantly, the researchers discovered that high levels of GPR34 are linked to poorer survival and faster recurrence in patients. They also found that blocking GPR34 in lab models made treatments like chemotherapy and Surufatinib more effective, while restoring immune activity.
These findings suggest that targeting GPR34 could help break treatment resistance and improve outcomes in pancreatic cancer, though further clinical studies are needed.