Pancreatic cancer is notoriously difficult to detect, and even harder to treat. But new research suggests the disease doesn’t begin with rogue cells—it starts with a conversation. Scientists have discovered the nervous system actively participates in pancreatic cancer development, even *before* a tumor forms, potentially opening new avenues for early intervention.
Nerves and Cancer: A Surprising Connection
Researchers pinpoint a feedback loop between nerves and cancer-promoting cells, offering a potential new target for therapies.
- The nervous system isn’t just a bystander in pancreatic cancer—it’s an active participant from the start.
- Tumor-promoting cells, called myCAFs, attract nerve fibers, creating a microenvironment that fuels cancer growth.
- Disrupting this nerve-myCAF communication could offer a new therapeutic strategy, potentially enhancing the effectiveness of existing treatments.
- Experiments in mice showed a nearly 50% reduction in tumor growth when the sympathetic nervous system was disabled.
Q: Can targeting the nervous system help treat pancreatic cancer? A: Research indicates that disrupting the communication between the nervous system and cancer-promoting cells may slow tumor growth and improve treatment outcomes, offering a promising new approach to fighting this deadly disease.
Jeremy Nigri, a postdoctoral researcher at Cold Spring Harbor Laboratory (CSHL), explains a well-known phenomenon called perineural invasion: “This means cancer cells will migrate within the nerve and use the nerve as a way to metastasize.” But the CSHL team’s recent work, published in Cancer Discovery, reveals the story begins much earlier.
Using advanced 3D imaging techniques, researchers found that myCAFs—fibroblasts that promote tumor growth—actively signal to attract nerve fibers. These aren’t just randomly wandering nerves; the imaging revealed a dense network weaving through and around the myCAFs and early lesions. “When we first saw this picture, I was shocked,” Nigri says. “I couldn’t even imagine the lesion like this. I’d only ever seen it in 2D.”
The team’s experiments uncovered a vicious cycle. MyCAFs attract nerve fibers from the sympathetic nervous system—the body’s “fight-or-flight” response system. These nerves release norepinephrine, a neurotransmitter that binds to the fibroblasts, triggering a calcium spike. This spike doesn’t just encourage pre-cancerous growth; it also draws in *more* nerve fibers, reinforcing the loop.
Because this myCAF-nerve interaction happens so early in the disease process, interrupting it could be a powerful therapeutic strategy. The findings suggest that existing drugs, such as doxazosin, might be effective when combined with standard treatments like chemotherapy or immunotherapy. “The next step will be to study this more in detail and try to find a way to block the crosstalk between fibroblasts and nerves,” Nigri says. “With support from groups like the Lustgarten Foundation and Pancreatic Cancer Action Network, we hope to one day help improve patient outcomes.”
What does this mean for patients? It suggests a future where pancreatic cancer isn’t just treated *after* it’s detected, but potentially prevented from gaining a foothold in the first place.
Related reading
