A team of researchers from Georgia University in the US have been exploring how a particular protein found in GBM can be targeted and made less active, which may then cause the tumour cells to be more sensitive to radiotherapy and Temozolomide (TMZ). We unpack the research and it’s conclusions in this article.
What are the findings?
Glioblastoma is the most aggressive form of brain tumour, and accounts for half of all diagnosed malignant Gliomas. For this reason this team, like many others, is researching ways to improve outcomes.
The research focuses on the SAMHD1 protein, which is known to aid in the repair of DNA with a Glioblastoma. The study found that it was ‘highly expressed’, meaning it is found in large quantities, and therefore is a good target for treatment.
A viral protein known as ‘Vpx’ can target SAMHD1, making it less active and reducing it’s ability to effectively repair the tumour.
The results of the study showed that the SAMHD1 protein became less effective at recombining the DNA in the tumour, after being mediated with Vpx. As a consequence, it successfully caused the tumour to become more sensitive to both interventional radiological techniques (e.g. radiotherapy) and the effects of the immunotherapy drug, Temozolomide.
Ultimately, this means the standard of care for Glioblastoma has the potential to be more effective overall, providing better survivability and quality of life.
What’s next?
Further research would be useful, in a larger scale trial to test for efficacy, consistency and safety in large patient cohorts. If the outcomes were positive with little toxicity, we could see this method move into consideration for standard care.
To read more scientific information, click here.
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