A type of non-neuronal brain cell called a glial cell can give rise to a lethal cancer called glioblastoma. Half of the cells in the human brain are glial cells, which normally act to support the function and communication of neurons. Yet despite decades of research, there are no existing treatments for glioblastoma that substantially increase the survival time of people with such tumours. Writing in Nature, Yu et al. report their analysis of the effects on the brain of certain glioblastoma-associated mutations. These insights might open up new strategies for anticancer research.

Yu and colleagues’ work supports growing evidence that tumour cells interact with their neighbouring healthy cells to alter brain function. Recent work has revealed that cells of the glioblastoma itself can form a synapse with surrounding neurons (in such synapses, the tumour has postsynaptic structures and the neuron forms presynaptic structures), and that blocking this synaptic input to the glioblastoma decreases tumour growth. 

Yu et al. now reveal how a glioblastoma can remodel connections between its neighbouring neurons, and report that the underlying mechanism differs depending on the specific PIK3CA variant involved. It will be interesting to determine in future studies whether the same synapse-promoting signals are responsible for regulating the synapses that form between a tumour and its neighbouring neurons, and for regulating synapses that form between neurons surrounding the tumour. This is an intriguing matter, because glypicans regulate neuronal synapse formation through what are known as AMPA receptors, and the synapses that form between neurons and glioblastoma cells use AMPA receptors for signalling.


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