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A new study reveals that the healing process following a brain injury could trigger the development of glioblastoma cancers. According to the researchers, the new cells generated to replace those lost following a brain injury can be derailed by mutations, which then gives rise to a tumor. The team reportedly said their findings could lead to a new therapy for glioblastoma, the most common high grade primary brain tumor in adults.
Highly aggressive and with limited treatment options, glioblastoma is the second most common brain tumor. Because of this, the average lifespan is 15 months after diagnosis.
Dr Peter Dirks, the Head of the Division of Neurosurgery and a Senior Scientist in the Developmental and Stem Cell Biology program at The Hospital for Sick Children (SickKids) in Canada, and leader of the pan-Canadian Stand Up To Cancer Canada Dream Team that focuses on glioblastoma described glioblastoma as “a wound that never stops healing.” “Our data suggest that the right mutational change in particular cells in the brain could be modified by injury to give rise to a tumour,” he said.
Brain injuries are extremely serious — even a minor concussion can lead to permanent cognitive and behavioral issues. In 2017, there were 61,131 cases of traumatic brain injury-related deaths in the U.S., according to data quoted by Statista. And in the case of those victims who survive, about 2% of the American population — or approximately 5.3 million people — require lifelong assistance with daily tasks because of a traumatic brain injury.
Published in “Nature Cancer”, the study’s researchers applied the latest single-cell RNA sequencing and machine learning technologies to map the molecular make-up of the glioblastoma stem cells (GSCs), which are responsible for tumor initiation and recurrence after treatment. What the study showed was that the tumours were highly diverse, containing multiple subpopulations of cancer stem cells, and that each tumor had two potential molecular states – termed “Developmental” and “Injury Response” – or existed on a gradient between the two. This makeup makes cancer recurrence more likely, as existing therapies are unable to wipe out all the different “subclones.”
The second state was as a surprise to the team, named “Injury Response” because these GSCs showed an upregulation of immune pathways and inflammation markers, which are indicative of wound healing processes. According to Dirks, what this suggests is that some glioblastomas start to form when the normal tissue healing process is disrupted by mutations, possibly even many years before patients become symptomatic.
Once a mutant cell becomes engaged in wound healing, it doesn’t stop multiplying — with all normal controls broken — spurring tumour growth, the team reportedly said. ‘The goal is to identify a drug that will kill the glioblastoma stem cells,’ said paper author and molecular geneticist Gary Bader of the University of Toronto.
The team said the relative mix of the two states was patient-specific. They are now looking for medication that are effective on different points of this gradient for tailored therapies.