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Researchers at The University of Texas MD Anderson Cancer Center have identified a previously unknown pathway that prostate tumors leverage to suppress the immune system by reshaping the tumor microenvironment to resist treatment. A combined targeted therapy approach improved antitumor responses and prolonged survival in preclinical models of castration-resistant prostate cancer.

The study, published in Cancer Discovery, was led by Di Zhao, Ph.D., associate professor of Experimental Radiation Oncology, and Nicholas Navin, Ph.D., chair of Systems Biology.

The findings suggest that tumors use this pathway as a backup physical defense and may explain why therapies targeting the B7-H3 immune checkpoint may show limited efficacy when used alone.

"Our study shows that the immune checkpoint B7-H3 does more than put the brakes on the immune system; it also reshapes the cells surrounding a tumor to help cancer grow and resist treatment," Zhao said.

"By uncovering how this process works, we identified a promising strategy that combines B7-H3-targeted therapy with MEK inhibition. These findings could help guide more effective, personalized treatments for patients whose tumors are unlikely to respond to B7-H3 therapy alone."

Advanced prostate cancer, particularly castration-resistant prostate cancer, often becomes resistant to standard hormone therapies and has shown limited response to many immunotherapies. Researchers believe the problem might involve the surrounding tumor microenvironment, which includes myeloid-derived suppressor cells (MDSCs) that can make it harder for the immune system to recognize and destroy tumors.

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