23rd September 2019

Brain tumour cells 'talk' to neurons
allowing them to proliferate:
insights could mean new
treatment targets

Exciting new research is shedding light on how brain tumours grow, with important implications for other cancers and how they might be treated in the future.1

Brain tumours can be benign or cancerous but until now it was unclear why they progress so rapidly. Symptoms can vary from headaches to cognitive deficits, progressive weakness on one side of the body, speech problems or seizures depending on size, location and type of tumour. Ultimately, they can be fatal. More than 11,000 people are diagnosed with a brain tumour in the UK every year, and the numbers are rising.2 One of my brothers suffered a brain tumour at the age of two, and despite being one of the luckier ones with benign disease, he’s been living with the consequences of the resulting brain damage ever since. A better understanding of what determines the growth rate of brain tumours could potentially lead to the development of new treatments that could slow tumour progression and prolong the life of patients. 

Preclinical research published in Nature this week3-5 shows that brain tumours form connections with neurons (brain cells) in the same way that neurons connect with each other in order to communicate, and it’s these connections that enable tumour cells to proliferate. Neurons ‘talk’ to each other across synapses: small gaps across which neurotransmitters flow from one neuron to the neighbouring neuron, turning chemical messages into electrical information. Cancer cells in the brain hijack this process, forming synapses with neurons to enable them to accelerate tumour growth.3,4 

The most common type of brain tumour, glioma, occurs in supporting non-neuronal cells in the brain called glial cells, and is a major cause of death due to brain cancer. Glial cells regulate neuronal signal transmission at synapses.1 As well as forming synaptic connections with neurons, glioma cells produce long, thin, tendril-like protrusions called tumoural microtubes which infiltrate the surrounding tissue and help them proliferate.1,3,4 

The latest findings also show that breast cancer cells – which often migrate (metastasize) to the brain – also exploit the methods that neurons use to create synapses in the brain. Breast cancer cells produce a protein that enables them to stick together, which is also used by neurons to form the scaffolding at synapses.5 

This research suggests that targeting the mechanisms used by neurons and cancer cells to communicate may provide future treatment opportunities, for those with brain tumours and possibly other cancers such as breast cancer that also show similar biochemical properties. By slowing or halting brain tumour proliferation, we may be able to improve the quality of life of patients and prolong their survival.    

For a good overview of the research described, read the editorial in this week’s issue of Nature1, available at: https://www.nature.com/magazine-assets/d41586-019-02746-7/d41586-019-02746-7.pdf  

For more information on brain tumours including symptoms, visit the NHS website: https://www.nhsinform.scot/illnesses-and-conditions/cancer/cancer-types-in-adults/brain-tumours  

References

1. Barria A. Dangerous liaisons as tumour cells form synapses with neurons. Nature 2019; Sept 18. doi: 10.1038/d41586-019-02746-7 [Epub ahead of print].

2. Cancer Research UK. Available at: https://www.cancerresearchuk.org/about-cancer/brain-tumours/about 

3. Venkataramani V, Tanev DI, Strahle C, et al. Glutamatergic synaptic input to glioma cells drives brain tumour progression. Nature 2019; Sep 18. doi: 10.1038/s41586-019-1564-x [Epub ahead of print].

4. Venkatesh HS, Morishita W, Geraghty AC, et al. Electrical and synaptic integration of glioma into neural circuits. Nature 2019; Sep 18. doi: 10.1038/s41586-019-1563-y [Epub ahead of print].

5. Zeng Q, Michael IP, Zhang P, et al. Synaptic proximity enables NMDAR signalling to promote brain metastasis. Nature 2019; Sep 18. doi: 10.1038/s41586-019-1576-6 [Epub ahead of print].