Researchers from the Institute of Cancer Research discovered that tumour cells in paediatric high-grade gliomas work together to invade other structures of the brain
Paediatric glioblastoma and diffuse midline glioma, formerly known as diffuse intrinsic pontine glioma (DIPG)*, are two of the most fatal types of childhood brain tumour, with less than 1% of children with diffuse midline glioma surviving beyond five years.
Part of the poor prognosis is due to intra-tumour heterogeneity: the tumours are made up of lots of different cell types that have different characteristics and respond differently to therapy. As a result, a particular treatment may kill some of the tumour cells, while others cells continue to grow.
The study published in Nature Medicine shows that the different cells work together, enabling them to leave the tumour and infiltrate other structures of the brain.
The researchers showed that there is one particular type of cell that leaves the tumour and migrates to other structures of the brain early on in tumour development. As this cell migrates, it signals for other cells from the tumour to follow, resulting in rapid spread of the tumour.
“This is the first time we've observed this sort of interaction between different tumour cells in DIPG. The idea that the cells are working together to make the disease grow and become aggressive is new and surprising.
Childhood cancers were thought to be very simple but this shows us that isn't always the case. Crucially, this gives us hope that we can develop new treatments," says Professor Chris Jones, who led the study.
These findings are important as they increase our knowledge on how childhood tumour grow and why some of them are resistant to treatment.
They also serve as a foundation upon which treatments targeting the different types of cells in the tumour and/or the cooperation between these cell types can be developed.
*Following the 2016 revision to WHO classification, this tumour is now known clinically as “Diffuse Midline Glioma- Pontine Location H3 K27M.