Brain cancer, tumour can be triggered by healing process that follows stroke, brain injury
The human body is amazing, and even when the body only intends to do good, heal, and recover from certain health issues it is faced with, sometimes the healing processes can backfire. One such incidence is seen in auto-immune diseases, where the body's immune response can also target the healthy cells. As per the latest study, for instance, the healing process that follows a stroke, trauma, brain infection, or brain injury can trigger the development of cancer, a study has found.
According to researchers from Canada, when they analysed cells from tumours of 26 patients with a common but aggressive form of brain cancer known as glioblastoma, it was found that mutations can derail the process which is supposed to create new cells to replace those that have been lost, and spike tumour growth.
The team hopes that the research will help in developing more tailored therapies for individual brain cancer patients. As per researchers, the findings could lead to new therapies for glioblastoma patients, who currently have limited treatment options and an average lifespan of only 15 months after diagnosis.
'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,' said paper author and neurosurgeon Peter Dirks of The Hospital for Sick Children in Toronto.
'Glioblastoma can be thought of as a wound that never stops healing,' Dr Dirks said.
'We're excited about what this tells us about how cancer originates and grows and it opens up entirely new ideas about treatment by focusing on the injury and inflammation response.'
The researchers used single-cell RNA sequencing and machine learning technologies to map out the molecular make-up of glioblastoma stem cells – the one that is responsible for tumour initiation and recurrence after treatment.
The team found new subpopulations of glioblastoma stem cells which bear the molecular hallmarks of inflammation and are comingled with other cancer stem cells inside patients' tumours.
These findings, as per Dr Dirks, suggest that some cancer start to form when the normal tissue healing process begins, which is actually supposed to generate new cells to replace those lost to injury, gets derailed by mutations.
This, he added, might happen many years before a patient becomes 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 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.
'But we first needed to understand the molecular nature of these cells in order to be able to target them more effectively.'
The findings of the study were published in the journal Nature Cancer.
As the initial study is now complete, researchers are now looking to target these biases for tailored therapies.
'We're now looking for drugs that are effective on different points of this gradient,' said paper author and cancer genomicist Trevor Pugh of the Princess Margaret Cancer Centre in Toronto.
'There's a real opportunity here for precision medicine — to dissect patients' tumours at the single-cell level and design a drug cocktail that can take out more than one cancer stem cell subclone at the same time.'