Researchers identify a protein that could help prevent glioblastoma spreading

Published today in the journal eLife, the research targeted the ephrin-B2 protein and results demonstrate it halts the division of cancer cells and then stops them spreading.

The study was carried out by researchers at the Medical Research Council (MRC) Clinical Sciences Centre based at Imperial College London.

The researchers used a cutting-edge technique called intravital imaging to watch this invasion within a mouse brain in real time. They observed that when healthy cells first develop non-cancerous mutations, blood vessels within the brain keep them in a compartment so that they cannot spread and cause damage.

They found that the vessels do this by producing ephrin-B2, which appears to immobilise the cells and hold them in place. However, when the cells become cancerous, they are able to override this signal and escape.

The team showed that the cancerous cells do this by producing their own ephrin-B2, which makes them insensitive to the ephrin-B2 already in the blood vessels stopping the cells from spreading.

“These types of brain tumours are not only the most common but also the most difficult to treat,” said Dr Adam Babbs, programme manager for cancer research at the MRC.

“The MRC's investment in high quality brain tumour research is advancing our knowledge of how the disease works and could help in the search for a more effective treatment.”

David Jenkinson, chief scientific officer of The Brain Tumour Charity, said: “This is an encouraging discovery which we hope will lead to further positive developments in the quest for effective glioblastoma treatments.

“A key part of research is to identify the proteins that are important in the development of brain tumours, so that we can work towards targeting those proteins with new therapies.

“By harnessing groundbreaking technology and pioneering research techniques, as the MRC team have done, we can make real progress together towards our goal of doubling brain tumour survival.”

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