Lethal Brain Cancer: Breakthrough as SET EIP Is Targeted to Prevent Glioblastoma Tumours

By Hassan Wekesa - Editor

U.S., 6 September 2026 - Researchers in the medical field have achieved a major breakthrough after preclinical models showed that it is possible to weaken glioblastoma (GBM), a cancer that has for decades resisted chemotherapy and radiation, Science Daily reported on Sunday.

On 31 August 2026, researchers at the Ohio State University Comprehensive Cancer Center (OSUCCC) – James and The Ohio State University Wexner Medical Center published a report in the journal Cancer Letters.

They highlighted that glioblastoma can survive radiation and chemotherapy and protect itself against future treatment.

With this understanding, the team set out to identify key weak points and silence the main drivers of that protection.

The World Health Organization (WHO) classifies glioblastoma as a grade 4 astrocytoma, meaning it contains abnormal cells that multiply rapidly and invade nearby healthy brain tissue.

Using human and animal cell lines, human tissues and the gene-editing technology CRISPR-Cas9, the researchers demonstrated that silencing natural inhibitors of the protein phosphatase 2A (PP2A) enzyme frees PP2A to perform its antitumor functions.

The research team, led by Arnab Chakravarti, MD, worked with corresponding author Kamalakannan Palanichamy, PhD, who oversaw study design and implementation.

The study points to the possibility of administering drugs that target at least three endogenous inhibitors of PP2A (EIPs) in order to outsmart the cancer cells’ evasion mechanisms.

The three EIPs examined were ANP32A, CIP2A and SET. Researchers found that tumour cell survival dropped significantly when ANP32A and CIP2A were inhibited and ceased altogether under SET inhibition.

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When these three EIPs were blocked in laboratory and animal models, fewer cancer cells survived and the remaining cells became more vulnerable to radiation.

PP2A is an enzyme that regulates signals cancer cells use to grow, survive and recover from treatment-related damage.

Glioblastoma cells appear to interfere with PP2A using the three proteins ANP32A, CIP2A and SET. Blocking those proteins reduced cancer-cell survival and increased sensitivity to radiation.

The findings remain preliminary. Researchers emphasise the need to restore PP2A activity by targeting inhibitors such as SET that suppress the enzyme.

“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,” Chakravarti said.