National brain tumour research funding needs to increase to £35 million a year
Our Plymouth centre’s work on high grade Meningioma published plus your worldwide research update.
We are always delighted to bring you news from our centres and work has been published this week from our Plymouth centre on a potential novel therapeutic target and biomarker for high-grade meningioma.
The paper’s title is “GATA-4, a potential novel therapeutic target for high-grade meningioma, regulates miR-497, a potential novel circulating biomarker for high-grade meningioma”
Using meningioma tissues and in vitro (in glass) models, our Plymouth team investigated microRNA levels in meningioma samples of different grades, as well as their regulation (the way they responded to different stimulus).
Based on this, they also investigated microRNAs expression in serum (basically blood without any clotting agents), and their potential as biomarkers.
Data contained in the paper suggests that GATA-4 ( a binding protein involved in regulating gene expression) that has been found to be greater in malignant Meningioma is a novel potential therapeutic target for high-grade meningioma, and regulates miR-497 ( an RNA gene), a potential novel circulating, non-invasive biomarker for high-grade meningioma.
Understanding of Meningioma at the discovery science level is the starting point before clinical trials can begin from which new therapeutics can be developed.
Principal investigator Professor Oliver Hanemann told us “I am very pleased that this work has now been published – there is a clear need for better therapeutic options for high grade meningioma patients and this research marks a step in the right direction to better understanding the disease and how we can improve outcomes for patients”
In the US researchers at the University of Michigan and their collaborators are excited a potential treatment approach that simultaneously targets two energy-production pathways within the cancer cells and could help overcome the effects of a cancer-causing mutation that is one of the hallmarks of DIPG. Although these are still early stage, pre-clinical results treatments for DIPG are so desperately needed that is a welcome update.
Results of a phase I clinical trial have been published and Australian researchers have found that patients who received a cellular immunotherapy for glioblastoma multiforme (GBM) in the trial on average survived longer than would have been expected without the treatment. The team also found the treatment was safe and identified clues that will help them improve it in future.
Could this drug lead to a potential treatment for brain cancer – including GBM? Researchers claim the drug could be even more effective than conventional chemotherapy temozolomide. The drug, known as AZ10606120, inhibits a particular protein called P2X7R that enhances tumour growth.
A protein that may protect against Alzheimer’s disease has been discovered by scientists. The newly identified pathway could also yield strategies for unleashing the immune response against malignant brain tumours.
Experimental drugs designed to lower the body’s natural production of alpha-ketoglutarate extended the lives of mice harbouring DIPG tumours by slowing the growth of the cancer cells. So could drugs against alpha-ketoglutarate combat DIPG? Researchers also found that artificially raising alpha-ketoglutarate levels with DIPG-causing genes may slow the growth of other brain tumours.
Suppressing the OSMR gene can improve the effectiveness of radiation therapy and in preclinical models the deletion of the OSMR gene resulted in a significant improvement of tumour response to therapy. By suppressing OSMR energy production in cancer stem cells was halted, essentially starving them to death. This study provides evidence that targeting OSMR gene, in combination with radiation therapy, can pave the way for future clinical trials that better treat GBM. Clinical trials are the next step.
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