Ancient Retrovirus Causes Aggressive Brain Tumors That Do Not Respond to Treatments

According to a recent study, some aggressive brain tumors that don't respond to treatments were triggered by an ancient retrovirus.

Ancient Retrovirus and Aggressive Tumors

More aggressive, difficult-to-treat brain tumors may be caused by a long-dormant virus.

An ancient retrovirus known as HML-2, which was discovered by researchers from the Sylvester Comprehensive Cancer Center at the University of Miami Miller School of Medicine, is a factor in the development of brain tumors.

Glioblastoma, an aggressive and quickly growing brain tumor, often has a 14-month life expectancy. But some cancers are a lot more dangerous than others.

These tumors that may not react as well to treatment may be caused in part by these ancient retroviruses.

This specific retrovirus, a type of virus that invades cells by using a DNA copy of its RNA genome, developed 6 million years ago and is largely dormant, however, it has been found to reactivate in some tumors.

Mostly Dormant

Then ancient retrovirus is a subtype of HERV-K, an endogenous retrovirus type that has been studied historically.

Since these viruses are typically dormant, they do not spread illness. In some malignancies, though, that is not the case.

With the help of her team, Ashish Shah, the director of Sylvester's Brain Tumor Initiative (BTI), was able to show for the first time how this virus, when it is reactivated, contributes to the stem-cell state of high-grade gliomas and fosters an aggressive form of cancer. Neurosurgeon Shah is the study's first author.

This team of researchers from Sylvester, Georgetown University, and the National Institutes of Health discovered that HML-2 activated the gene-regulatory protein OCT4, which changed the tumor's stem cell programming.

This ancient virus has previously been related to various diseases, but it has never before been connected to brain cancer.

The glioblastoma stem-cell niche is the microenvironment that supports stem cells and determines their fate, and according to the senior author of the study Dr. Avindra Nath, who is also the clinical director of the Division of Intramural Research, National Institute of Neurological Disorders and Stroke, their findings point to a fundamental contribution by HML-2 to this niche.

Futures of Cancer Treatment

The study group carried out a thorough translational analysis into the expression of HML-2 in glioblastoma and its function in preserving the cancer stem cell phenotype.

This discovery will support further research into this cancer, particularly when creating new treatments.

Their research may even be leading to future medicines for the treatment of severe brain cancers.

They discovered that antiretroviral medication dramatically decreased HML-2 activity.

According to Shah, one appealing strategy to avoid stem cell changes, lower the risk of tumor recurrence, and overcome treatment resistance is to target the glioblastoma stem cell niche, Newsweek reports.

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The study group carried out a thorough translational analysis into the expression of HML-2 in glioblastoma and its function in preserving the cancer stem cell phenotype.

This discovery will support further research into this cancer, particularly when creating new treatments.

Their research may even be leading to future medicines for the treatment of severe brain cancers.

They discovered that antiretroviral medication dramatically decreased HML-2 activity.

According to Shah, one appealing strategy to avoid stem cell changes, lower the risk of tumor recurrence, and overcome treatment resistance is to target the glioblastoma stem cell niche, according to Neuroscience News.

Shah and Nath, together with several colleagues, published their findings in the Journal of Clinical Investigation.

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