Resident Weekly

A Exclusive Current Affairs Platform


A Historical Retrovirus Could Be The Cause Of Severe Brain Tumours

The middle length of endurance after determination of glioblastoma is 14 months, yet a portion of these cerebrum growths are more forceful and impervious to therapy than others, and another review from Sylvester Far reaching Disease Center at the College of Miami Mill operator Institute of Medication proposes reactivation of an old retrovirus might be halfway to fault.

“Our lab discovered that HML-2, a subtype of HERV-K, a dormant retrovirus from 6 million years ago, plays a role in the development of brain tumors. Dr. Ashish Shah, a neurosurgeon and principal investigator at Sylvester’s Brain Tumor Initiative (BTI) and first author of a paper published in the Journal of Clinical Investigation, said, “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.”

A subset of cancer cells called cancer stem cells are responsible for tumor initiation and growth as well as determining how aggressive and resistant a cancer will be to treatment. Researchers from Sylvester, Georgetown, and the National Institutes of Health carried out this study, which found that HML-2 altered the programming of stem cells by activating a gene-regulating protein known as OCT4. This is thought to be the first study to demonstrate the effects of HML-2 on gliomas and to describe the molecular and cellular mechanisms involved. Although HML-2 has previously been linked to the onset and progression of other types of cancer, this one is believed to be the first.

Senior author Nath stated, “We conducted a comprehensive translational investigation of HML-2 expression in glioblastoma and its role in maintaining the cancer stem cell phenotype.” Results depended on investigations of patient-inferred glioblastoma cells and mouse model examinations.

The findings of the team provide researchers with therapeutic targets; also, in their work, an enemy of retroviral drug fundamentally diminished HML-2 action and decreased growth undifferentiated cell markers, said Shah, head of clinical preliminaries and translational exploration and head specialist in the Segment of Virology and Immunotherapy at Sylvester Exhaustive Disease Place’s Cerebrum Cancer Drive (BTI).

He stated, “Targeting the glioblastoma stem cell niche is an attractive option to prevent stem cell alterations, reduce tumor recurrence, and reduce treatment resistance.”

One of the many human endogenous retroviruses (HERVs) is HML-2, which is a subtype of HERV-K. These HERVs are the ancestors of retroviral infections that occurred in the past and led to the integration of viral sequences into the human genome. HERVs, which make up about 8% of the human genome, typically remain silent and are incapable of causing infection; however, researchers have recently discovered that some of them can be reactivated in particular types of cancer.

First author Shah, Vaidya Govindarajan, Dr. Jay Chandar, Deepa Seetharam, PhD, Jelisah Desgraves, Dr. Michael Ivan, and Dr. Ricardo Komotar are University of Miami authors. In the article, you can find a comprehensive list of authors and affiliations.

error: Content is protected !!