What do hijacking, ancient viruses and insulin feedback have to do with glioblastoma?

4 min read

This week, the Tessa Jowell Brain Cancer Mission announced the appointment of Dr Morag Brothwell and Dr Sean Main to the inaugural Tessa Jowell Fellowship programme. The 12-month programme will train clinicians to appreciate the breadth of comprehensive brain tumour management and equip them with the research skills to lead high impact, practice- changing neuro-oncology clinical trials of the future. The new fellows will be hosted at two Tessa Jowell Centres of Excellence: King’s Health Partners and University College London Hospital. 


How Some Brain Tumors Hijack the Mind to Grow In a new study published in Nature, researchers have found that glioblastoma tumours can change the formation of new synapses to fuel their own growth. This neural redirection also appears to play a role in the devastating cognitive decline seen in many people with glioblastoma. The research team also pinpointed a protein that appears to be critical to the hijacking process and showed that it may be a potential target for new treatments. 

Insulin feedback is a targetable resistance mechanism of PI3K inhibition in glioblastoma  In this study, researchers demonstrated that efficacy of PI3K inhibition for cancer treatment is impaired by on-target insulin feedback that reactivates the PI3K signalling pathway.  

The study, published in Neuro-Oncology, demonstrates that PI3K inhibitors induce hyperglycaemia and hyperinsulinaemia in mice and that counteracting hyperglycaemia with metformin enhances therapeutic efficacy in a glioblastoma mouse model. Researchers also revealed that hyperglycaemias worsen progression-free survival in patients with glioblastoma treated with PI3K inhibition. Implementation of a rational anti-hyperglycaemia regimen along with PI3K inhibition may help translate these findings to improve PI3K targeting in patients with glioblastoma. 

Ancient Virus Awakening: Hidden Culprit in Glioblastoma Brain Cancer Aggressiveness  The reactivation of a dormant retrovirus, HML-2, may contribute to the aggressiveness of glioblastoma. Researchers discovered that the virus influences the stem-cell state of the tumours, thereby promoting a more resistant form of cancer. HML-2 was found to affect stem cell programming via a gene-regulating protein named OCT4. These findings present potential targets for developing more effective glioblastoma treatments. 

Glioblastoma cells found to have ‘critical point’ between order and disorder For years, scientists understood the cells in these tumours as static and relatively fixed. But recent studies have uncovered that glioblastomas contain active cells moving in complex patterns known as "oncostreams", which determine how aggressively the tumours grow. 

Research led by Michigan Medicine and the University of Michigan, published in Science Advances, suggest that glioblastoma cells possess some form of large-scale coordination throughout the whole tumour that allows them to respond in practical unison to attempts to kill tumour cells, such as chemotherapy or radiation. Disrupting the large-scale organisation of brain tumours may result in more powerful ways to treat and one day eliminate brain tumours. 

Back to Research & Campaigning News