Blocking a protein that hijacks the immune system's checkpoints to allow tumour growth shows potential of an anti-body-based treatment for brain cancer.
The researchers found that the protein FGL2 acted as a key "switch" to prevent tumours from being detected by the immune system and neutralised it by using anti-FGL2 antibody, curing four of the 17 infected mice.
"It is well-known that cancer evades immune surveillance by exploiting a series of editing mechanisms to avoid immune detection and eradication," said Shulin Li, professor at the University of Texas MD Anderson Cancer Center.
"One such mechanism is to hijack an immune cell's checkpoints, subverting the immune system and allowing tumour growth," Li noted.
FGL2 modulates the immune system's "brakes" called checkpoints, as well as immune suppressive cells that stop the immune system's natural attack on cancer cells, the findings showed.
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The study found that FGL2 increased tumour growth in mice by enhancing immune checkpoint gene expression.
The research team neutralised the protein by using an anti-FGL2 antibody.
"The average survival time in mice treated with the antibody was significantly longer than those receiving an alternative control antibody," Heimberger noted.
"Interestingly, four of 17 mice treated with FGL2 antibody were completely tumour free," Heimberger said.
The study team also found an association between levels of FGL2 expression and tumour aggressiveness. The results revealed that patients who had higher levels of FGL2 expression experienced a lower overall survival rate than patients with less FGL2 expression.
The results were published in the Journal of the National Cancer Institute.
