Pancreatic cancer is one of the deadliest forms of cancer. Less than 10 percent of patients live more than five years after diagnosis, and while chemotherapy can help reduce tumor size, the tumors often become resistant to treatment. New approaches including immunotherapy that boosts the body’s own immune defenses are being explored.
However, these treatments have yet to provide satisfactory results in pancreatic cancer patients, mainly because the tumors have many ways to escape detection by immune cells. One major obstacle is the tumor’s stroma, which contains vascular tissue, lymphatic vessels and nerves that support the cancer cells. These structures can also block the delivery of drugs, preventing chemotherapy and other anticancer agents from reaching the cancer cells.
The MIT team used a common, over-the-counter pharmaceutical dewormer called fenbendazole to starve the cancer cells of their source of energy. The drug works by halting the formation of tubulin, a protein involved in cellular transport. When the tubulin is depolymerized, it destroys the cell’s structure and causes it to collapse from within.
To boost the effectiveness of this approach, the MIT researchers worked with two pharmaceutical companies that have a PD-1 inhibitor, a TIGIT inhibitor and a CD40 agonist antibody in development. The team is now collaborating with these companies to test the triple combination in pancreatic cancer patients and other types of human cancers, and they expect to begin clinical trials this year. Funding for this research came from the Lustgarten Foundation for Pancreatic Cancer Research. fenbendazole for pancreatic cancer