New Study Shows ‘Viral Mimicry’ Could Transform Glioblastoma Treatment

Glioblastoma continues to be one of the most challenging cancers to treat as it resists even the latest innovations in immunotherapy. Now, a new study conducted by a team at the Sylvester Comprehensive Cancer Center at the University of Miami suggests that, when a specific protein is suppressed, an antiviral immune response increases the effectiveness of immune checkpoint inhibitors.

This discovery not only opens the door to a novel way to treat glioblastoma but also suggests that the protein in question, ZNF638, could be a valuable biomarker as treatment teams customize immunotherapy for specific patients. The research findings appeared in the Journal of Clinical Investigation on March 17 this year.

Over the past two decades, the clinical outcomes for people diagnosed with glioblastoma haven’t changed meaningfully despite approximately 12,000 cases being diagnosed in America annually. The need to find effective ways to treat this cancer is therefore urgent.

Immune checkpoint inhibitors have transformed how different forms of cancer are treated, but this approach has had dismal results in brain cancers because of the strong immune-suppressive conditions within the brain. Learning how to increase the efficacy of immunotherapies could help in understanding how brain cancer patients can be treated, says Ashish Shah, the study’s senior author.

The technique that the researchers wanted to test with regard to making immunotherapy more effective against brain cancers is called ‘viral mimicry.’ This approach entails activating dormant viral fragments inside the brain. These endogenous retroviruses have been collected over millennia and stored in the genome. The body has numerous mechanisms through which these retroviruses are kept dormant.

Over the past few years, scientists have learned that activating those retroviruses causes the body to initiate an immune response, which then helps immunotherapies to work better. The study was aimed at finding out whether using this approach could result in making immunotherapy effective against malignant brain tumors.

It should be noted that the activation of these retroviruses doesn’t cause an actual infection in the brain since the retroviruses are too weak to trigger infection.

Shah and his team focused on ZNF638 and suppressed this regulator which is one of many others engaged in keeping retroviruses inactive. Suppressing this regulator allowed the retroviruses to become active in preclinical trials. This activation caused an anti-viral response within the cancer tumor, suppressed tumor growth, increased immune cell activity with the malignant tissues and increased survival times.

The team was glad to find that when they examined the clinical data of patients who had undergone immunotherapy, those who fared better exhibited minimal ZNF638 expression. This confirmed that suppressing this regulator could indeed improve the efficacy of immunotherapies.

This study could be a game-changer in brain cancer treatment since it opens the possibility of developing drugs that can penetrate the brain and silence ZNF638 proteins. With companies like Calidi Biotherapeutics Inc. (NYSE American: CLDI) heavily investing in developing oncolytic viruses targeting brain cancers and other solid tumors, a time may soon come when glioblastoma and other brain malignancies can be treated effectively.

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