Brain tumors “hack” communications between neurons, causing symptoms unconnected to the size of the cancer, a new study claims.
And the discovery could lead to ways to detect early on whether a brain tumor is spreading and how to stop it.
It was thought that impairment from brain cancer was due to the size of the tumor and where it was pressing on the brain.
But a groundbreaking study, featured on the cover of the journal Cancer Cell, shows that the cancer metastasis, or spread, changes the brain’s chemistry and disrupts neuronal communication.
Researchers from the Spanish National Research Council (CSIC) and the Spanish National Cancer Research Center (CNIO) used artificial intelligence to detect the effects of cancer in other parts of the brain.
They set out to investigate why small tumors can cause significant changes and large tumors can produce only mild effects.
Nearly half of all patients with brain metastasis experience cognitive impairment and the study shows that this is caused when neurons, which communicate through electrical impulses generated and transmitted by biochemical changes in the cells and their surroundings, are disrupted.
Dr. Manuel Valiente, head of the CNIO’s Brain Metastasis Group said: “Our multidisciplinary study challenges the hitherto accepted assumption that neurological dysfunction, which is very common in patients with brain metastasis, is due solely to the mass effect of the tumor.
“We suggest that these symptoms are a consequence of changes in brain activity resulting from tumor-induced biochemical and molecular alterations.
“This is a paradigm shift that could have important implications for diagnosis and therapeutic strategies.”
The researchers have begun to explore the biochemical changes that might explain this alteration and have identified a molecule, EGR1, that may play an important role in this process.
The finding opens up the possibility of designing a drug to prevent or alleviate the neurocognitive effects of brain tumor metastasis.
The team measured the electrical activity of the brains of mice with and without metastases and saw the electrophysiological recordings of the two groups were different.
They then trained an automatic algorithm with numerous electrophysiological recordings, and the model was indeed able to identify the presence of metastases.
The results show that metastasis does indeed affect the brain’s electrical activity in a specific way, leaving clear and recognizable signatures.
“This computational approach may even be able to predict subtypes of brain metastases at an early stage.
“It is a completely pioneering work that opens up an unexplored path.”
Dr. Valiente added: “We will look for molecules involved in metastasis-induced changes in neuronal communication, and evaluate them as possible therapeutic targets.”
Produced in association with SWNS Talker
