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An ancient, dormant virus may be to blame for more aggressive, hard-to-treat brain tumors.
Scientists from the Sylvester Comprehensive Cancer Center at the University of Miami Miller School of Medicine discovered that an ancient retrovirus—known as HML-2—contributes to the formation of brain tumors. They published their findings in a new Journal of Clinical Investigation study.
The life expectancy for glioblastoma—a fast developing and aggressive brain tumor—is usually around 14 months. However some tumors are far more severe than others.
These ancient retroviruses may be partly to blame for these aggressive tumors that may not respond as well to treatment.
"We were certainly surprised by our findings as studies in endogenous retroviruses in gliomas have been largely neglected in neuro-oncology since they were considered junk DNA," neurosurgeon Ashish Shah, principal investigator at Sylvester's Brain Tumor Initiative (BTI) and first author of the study, told Newsweek. "The next step is to translate our findings into a clinical trial for targeted antiretroviral therapy for glioblastoma and to develop viral biomarkers that may predict clinical responses."
This particular retrovirus—a type of virus that uses a DNA copy of its RNA genome to infect the cells it invades—evolved 6 million years ago and is mostly dormant, although it has been known to reactivate in certain cancers.
It is a subtype of HERV-K—a type of endogenous retrovirus that can be tracked throughout history.
These types of viruses are usually dormant and therefore do not cause infection. However that is not the case in some cancers.
"We demonstrated for the first time that this virus, when reactivated, plays a role in defining the stem-cell state of high-grade gliomas, promoting an aggressive form of cancer," Shah said in a press release.
During their research, scientists from Sylvester, and also Georgetown University and the National Institutes of Health, found that HML-2 activated a gene-regulating protein called OCT4, which affected the stem cell programming of the tumor.
Although this ancient virus has previously been linked to other cancers, this is the first time it was found to be associated with brain cancer.
"Our results suggest that HML-2 fundamentally contributes to the glioblastoma stem-cell niche, the microenvironment that supports stem cells and determines their fate," Dr. Avindra Nath, senior author of the study and clinical director of the Division of Intramural Research at the National Institute of Neurological Disorders and Stroke at the National Institutes of Health, said in a press release. "We conducted a comprehensive translational investigation of HML-2 expression in glioblastoma and its role in maintaining the cancer stem cell phenotype."
This finding will help future research into the study of this cancer, especially when developing future treatments.
In fact, their findings may already be pointing to potential therapies to help treat aggressive brain tumors.
They found that an antiretroviral drug reduced HML-2 activity significantly.
"Targeting the glioblastoma stem cell niche is an attractive option to prevent alterations in stem cells and reduce tumor recurrence and treatment resistance," Shah said.
Update 7/5/23, 2:49 a.m. ET : This article has been updated to include direct quotes.
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About the writer
Robyn White is a Newsweek Nature Reporter based in London, UK. Her focus is reporting on wildlife, science and the ... Read more