Researchers at Fox Chase Cancer Center have identified how pancreatic tumors feed themselves through scar tissue — and a protein that could be blocked to starve them.
Pancreatic ductal adenocarcinoma, the most common form of the disease, surrounds itself with cancer-associated fibroblasts: cells that build connective tissue. The resulting collagen compresses blood vessels, cutting the tumor’s blood supply. Somehow the cancer cells kept growing anyway. The study, published in Nature Cancer, explains one mechanism.
The fibroblasts acquire cholesterol from the bloodstream and hand it directly to cancer cells through a process called trogocytosis — one cell taking small pieces of another’s membrane during contact. The transfer depends on a protein called anoctamin 6, or ANO6, which prepares the fibroblast membrane for the exchange.
“Cancer-associated fibroblasts are not passive bystanders,” said co-senior author Igor Astsaturov. “They actively support tumor growth by transferring lipids to cancer cells.”
When researchers reduced or eliminated ANO6 in fibroblasts, the cells became far less effective at supporting cancer cell survival, and tumors in mouse models grew substantially more slowly. The same process also appeared to blunt the immune response: cytotoxic T lymphocytes, the immune cells that kill cancer cells, were hindered by the lipid transfer.
The finding is early — mouse and laboratory models, not patients — but it identifies a target that acts on both the tumor’s supply line and the immune system’s ability to reach it.
Source: ScienceDaily/SciTechDaily report of the Nature Cancer study; Fox Chase Cancer Center, Oct. 30, 2026. Photo: Shixart1985, CC BY 2.0, via Wikimedia Commons. Illustrative.
