During Glioblastoma (GBM) Awareness Week, we highlighted an exciting discovery from our Centre of Excellence at Queen Mary University of London which could pave the way to new treatments to combat the disease.
Our researchers have described for the first time how a gene – already known to be overactive in a number of cancers including low-grade glioma – is essential in regulating the growth of GBM tumours.
The study, published in Cell Reports, has helped our understanding of how GBM tumours grow. It has opened up new avenues of research to find treatments which exploit this vulnerability and improve outcomes for patients.
How did our researchers find this gene?
Using their world-leading SYNGN platform, researchers compared GBM stem cells with normal neural stem cells and in doing so, discovered that a gene called METTL7B was overactive in GBM cells.
The SYNGN platform is unique because it compares GBM cells and healthy cells from the same patients, unlike other comparison platforms where cells are likely from different patients. This ensures that any differences found are due to the tumour and not due to the cells being from different individuals.
How does this help us understand how GBM tumour grow?
To explore more about the function of this overactive gene, Dr Myrianni Constantinou silenced METTL7B and found that the resultant tumours were significantly smaller, which is good news. However, the tumour cells travelled more into the surrounding areas of the brain, making the tumour more invasive.
The paper explains that the METTL7B gene causes GBM stem cells (these are cells which have the potential to become any cell within a GBM tumour) to preferentially develop into the cells that are more densely located in the core of a tumour. These cells have little connection to the cells outside the tumour, and therefore are less likely to migrate into surrounding tissue.
When the METTL7B gene is silenced, the GBM stem cells stop progressing into these ‘core’ cells. Instead, they progress into cells that are more like neurones. This cell type makes more connections to cells outside the tumour, and therefore supports its travel into the areas surrounding the tumour. As result, the tumour is smaller as there is less ‘core’, but more invasive.
What does this mean for brain tumour patients?
Although still very early-stage science, the paper has unravelled one of the mechanisms that regulates the growth of GBM tumours. This is important because understanding how GBM tumours grow could provide researchers with new insights on how to treat these tumours.
In fact, researchers could exploit this vulnerability and use a potential combination therapy to produce smaller, less aggressive tumours. They could use one type of drug to target METTL7B and stall tumour growth, alongside a drug which targets invasiveness. This two-pronged approach could improve patient outcomes in the future.
Research like this is only possible with your support. By making a one-off or regular donation, taking on a fundraising challenge or campaigning with us, you can help to find a cure for all types of brain tumours.
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