New Research Identifies Potential Target in One of the Deadliest Brain Tumours

Glioblastoma may have an unexpected weakness that could help existing treatments work better, after researchers identified a protein that appears to protect tumour cells from therapy.

Scientists at The Ohio State University Comprehensive Cancer Center found that a protein called SET could be a potential target for making glioblastoma cells more vulnerable to radiation and chemotherapy. The findings, published in Cancer Letters, are still based on laboratory and animal experiments and have not been tested in patients.

The researchers focused on PP2A, an enzyme that helps control signals involved in cell growth, survival and responses to treatment. Glioblastoma cells appear to suppress PP2A using three proteins: SET, ANP32A and CIP2A.

When researchers blocked these proteins in laboratory and animal models, fewer glioblastoma cells survived. The remaining cells also became more sensitive to radiation, suggesting that restoring PP2A activity could weaken the tumour's ability to withstand treatment.

SET stood out as particularly promising because suppressing it prevented tumours from developing in the preclinical models. Researchers say this could eventually lead to treatments designed not to replace standard therapies, but to help them work more effectively.

The team also investigated an already approved antipsychotic medicine that can increase PP2A activity. However, researchers stressed that this drug is not currently a treatment for glioblastoma and should not be used for this purpose outside a clinical trial.

Glioblastoma is difficult to treat because tumour cells can adapt to treatment and repair damage caused by radiation and chemotherapy. Finding ways to interfere with these survival mechanisms could therefore provide a new strategy against the disease.

Researchers are now studying whether SET, ANP32A, CIP2A or other PP2A-regulating proteins can be safely targeted and whether blocking this pathway can improve standard treatments.

Clinical trials will be needed to determine whether targeting PP2A can improve treatment outcomes for people with glioblastoma.

REFERENCE: John Ryan Jacob, Shahid M. Nimjee, J. Bradley Elder, Arnab Chakravarti, Kamalakannan Palanichamy. Endogenous inhibitors of PP2A activate oncogenic and DNA damage response kinases in glioblastoma. Cancer Letters, 2026; 645: 218325 DOI: 10.1016/j.canlet.2026.218325