COLUMBUS, Ohio — Glioblastoma remains one of the deadliest cancers, with limited treatment advances and tumors that often resist radiation and chemotherapy. New research from The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC - James) points to SET as a potential target for making glioblastoma cells more vulnerable to treatment. The goal is to make existing treatments more effective, not replace them. In preclinical models, researchers found that suppressing SET — one of the proteins involved — prevented tumors from forming. SET emerged as the most promising target because of its effect on tumor formation. Researchers also found that blocking related proteins helped glioblastoma cells become more sensitive to radiation. The results suggest the pathway may be one researchers can target with drugs. This OSUCCC – James research focused on PP2A, an enzyme that helps control signals that allow cancer cells to grow, survive and repair damage after treatment. Glioblastoma cells appear to block PP2A through proteins called ANP32A, CIP2A and SET. When researchers blocked these proteins in lab and animal models, cancer cell survival dropped and the cells became more sensitive to radiation. “Glioblastoma is hard to treat because it can adapt and survive,” said Arnab Chakravarti, MD, chair of radiation oncology at the OSUCCC – James. “Our findings suggest that restoring PP2A activity may make glioblastoma cells less able to survive treatment. That gives us a clear path to test whether this approach can make radiation and chemotherapy more effective for patients with GBM.” The findings are preliminary and have not been tested in patients. Researchers are now studying whether SET or related PP2A-blocking proteins can be targeted safely and whether that improves response to standard glioblastoma treatment. The team also tested an FDA-approved antipsychotic drug that can increase PP2A activity. Researchers say the finding supports further testing of drugs that act on this pathway. The drug is not ready for use in people with glioblastoma and should not be used for this purpose outside a clinical trial. “This is an important first step,” said Chakravarti. “By understanding how SET and related PP2A blockers help GBM survive treatment, we can test ways to block that protection and make current therapies more effective.” The study was published in the May 2026 issue of Cancer Letters, and supported by grants from The National Institues of Health, National Cancer Institute and The Ohio State University Comprehensive Cancer Center. ### MEDIA CONTACT: Amanda Harper amanda.harper2@osumc.edu | 614-685-5420 |