Scientists have found a way to break through the protective barrier that makes pancreatic cancer particularly resistant to treatment. Blocking a single receptor protein disrupts the inflammatory network surrounding the tumor, reduces the number of immune-suppressing cells and enhances the attack by immune T cells. The study was published in the journal JCI Insight.
The study was conducted by specialists at the Sylvester Comprehensive Cancer Center at the University of Miami. The target was IL1RAP, a common “helper” receptor through which many inflammatory molecules transmit their signals. Pancreatic tumors surround themselves with dense inflammatory and scar tissue that prevents drugs and immune cells from reaching cancer cells.
By blocking IL1RAP, the scientists disrupted this “chain reaction” of signaling in laboratory experiments: the number of immunosuppressive cells decreased, fibrosis was reduced, while T-cell activity increased. In effect, the tumor was stripped of part of its defenses, making it more vulnerable to the immune system.
Pancreatic cancer is one of the deadliest forms of cancer: it is often diagnosed at an advanced stage and responds poorly to treatment. The results have so far been obtained at the preclinical stage, but the researchers are already planning a clinical trial in which IL1RAP-targeted therapy will be combined with chemoimmunotherapy in patients with resectable tumors before surgery. This will allow researchers to observe how the biology of the tumor changes in response to treatment.
Most patients with pancreatic cancer die within five years of diagnosis, and the prognosis has improved little over the past several decades. One reason is the dense barrier of connective tissue and inflammatory cells that effectively shields the tumor from the immune system and prevents chemotherapy drugs from reaching their target. Therefore, approaches aimed at disrupting this protective barrier are considered one of the most promising areas of cancer research.
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