• Profile
Close

Researchers find HIV drugs may treat low-grade brain tumours

ANI Dec 25, 2021

A new research has found that the drugs used to treat HIV/AIDS patients could be used to treat patients diagnosed with the most common form of primary brain tumour.


The study has been published in the Cancer Research Journal. The breakthrough, co-funded by the charity Brain Tumour Research, is significant because, if further research is conclusive, the anti-retroviral drugs could be prescribed for patients diagnosed with meningioma and acoustic neuroma brain tumours (also known as schwannoma). More effective approaches are urgently needed as there are very few treatment options for these tumour types which frequently return following surgery and radiotherapy.

Meningioma is the most common form of primary brain tumour. Mostly low-grade, it can become cancerous over time and develops from cells located in the meninges which protect the brain and spinal cord. Acoustic neuroma is a different type of low-grade, or non-cancerous brain tumour, which develops in nerve-protecting cells called Schwann cells. Both tumours may occur spontaneously, usually in adulthood, or in the hereditary disease Neurofibromatosis type 2 (NF2) in childhood/early adolescence.

Researchers at the Brain Tumour Research Centre at the University of Plymouth showed previously that a tumour suppressor, named Merlin, contributed to the development of meningioma, acoustic neuroma and ependymoma tumours. It can also contribute to neurofibromatosis type 2 (NF2).

Tumour suppressor genes play important roles in normal cells by controlling division or repairing errors in DNA. However, when tumour suppressors do not work properly or are absent, cells can grow out of control, leading to cancer. In this latest study Dr Sylwia Ammoun, Senior Research Fellow, and her collaborator, Dr Robert Belshaw investigated the role that specific sections of our DNA play in tumour development. Named 'endogenous retrovirus HERV-K', these sections of DNA are relics of ancient infections that affected our primate ancestors, which have become stable elements of human DNA.

Dr Ammoun said, "High levels of proteins produced by HERV-K DNA have previously been linked to the development of different tumours. In this study, the team showed that high levels of HERV-K proteins were present in meningioma and schwannoma cells obtained from patients. The team was also able to identify molecular events that may enable HERV-K proteins to stimulate the growth of these tumours. Furthermore, several drugs have identified that target these proteins, reducing the growth of schwannoma and grade I meningioma cells in the laboratory."

Professor Oliver Hanemann, Director of the Brain Tumour Research Centre of Excellence, added, "Significantly, these drugs - the retroviral protease inhibitors ritonavir, atazanavir, and lopinavir - have already been approved by them for use in the treatment of HIV/AIDS in the USA and are also available in the UK. These results revealed HERV-K proteins to be critical regulators of growth in tumours that are deficient in Merlin."

Hugh Adams, the spokesman for Brain Tumour Research, said, "These findings are extremely significant as drug repurposing is a valuable way to accelerate the testing of new approaches into clinical trials which, if successful, could reach patients sooner.
"This is particularly critical for patients with brain tumours as many of them do not have the luxury of time," he added. 

Only Doctors with an M3 India account can read this article. Sign up for free or login with your existing account.
4 reasons why Doctors love M3 India
  • Exclusive Write-ups & Webinars by KOLs

  • Nonloggedininfinity icon
    Daily Quiz by specialty
  • Nonloggedinlock icon
    Paid Market Research Surveys
  • Case discussions, News & Journals' summaries
Sign-up / Log In
x
M3 app logo
Choose easy access to M3 India from your mobile!


M3 instruc arrow
Add M3 India to your Home screen
Tap  Chrome menu  and select "Add to Home screen" to pin the M3 India App to your Home screen
Okay