New research suggests this week that aggressive brain cancer can hijack brain circuits to spread further and make itself unstoppable. Researchers in Germany studied glioblastoma cells in mice and in the lab, and found that these tumors use some of the same mechanisms behind the normal development and migration of neurons to systematically invade the brain. The research may one day allow scientists to develop better treatments for the almost always fatal condition.
Although brain cancer is relatively rare, glioblastoma (also called glioblastoma multiforme, or GBM) is the most common type, accounting for about 15% of primary brain tumors. It is also one of the most dangerous types of cancer out there. It is formed from cells known as astrocytes, which support neurons, and then rapidly spread throughout the brain. Symptoms tend to be nonspecific at first, including headache and nausea. Treatment is seldom successful, Cancer often recurs, with Average survival time be less than a year old.
One of the main reasons for its immunity is that cancer can implant itself extensively throughout the brain, making precise removal by surgery or other methods more difficult. GBM tumors also appear to contain a diverse population of cells, which further complicates any treatment. But the exact role and function of these different groups of GBM cells has remained enigmaticAccording to study author Varun Venkataramani, a researcher in brain tumors at the University of Heidelberg in Germany.
To better understand GBM, Venkataramani and colleagues combined several different approaches to studying these tumors at the molecular and cellular level. One of these techniques, known as the chronic cranial window, even allowed them to view brain tumors and GBM tumors in mice while they were awake. They also sequenced the genes of single cells, allowing them to see which genes were turned off or on.
Other research showed that GBM cells form a kind of network with each other, connected by long protrusions known as microtubules, and that these microtubules increase the spread of cancer. But the team’s work found that other, unconnected GBM cells appeared to play a vital role in the spread of cancer. These cells appear to receive a signal from neurons that prompt them to invade other parts of the brain. To achieve this, the team’s work further suggests, that cancer cells benefit from the same processes that a healthy brain normally uses to form neurons early in our development. Neural signals also seem to fuel the growth of microtubules, And the, Over time, the unconnected GBM cells combine with the rest of the cancer. Perhaps most terrifyingly, the crab invasion may follow a fibrous-like movement pattern, a term that describes the energy-efficient ways some predators will hunt food on rare occasions.
“Taken together, we already see that the mechanisms of immature neurons and neural progenitor cells during development are hijacked for invasion,” Venkataramani said in an email to Gizmodo. Team work is published in Cell Journal.
These results will ideally be validated by additional Studies from other researchers. There is always more to be learned. The current study, for example, only looked at GBM cells that were allowed to proliferate unimpeded, and it’s not clear how they would behave in response to chemotherapy and other treatments.
The tenthThe kind of basic research is crucial to making discoveries that might one day lead to new ones. GBM treatments. Since neurons seem to be an important aspect of how cancer communicates with itself, one way to stop it could be by interfering with these signals. The team highlights some potential ways these signals could be interrupted, although there is a lot of work to be done before we can get to this point.
“We believe these results should be better tested in clinical trials and we will need to further develop clinical imaging so that we can monitor the invasive nature of these brain tumors more specifically,” said Venkataramani. “Finally, this study establishes a framework that can in principle be used across all cancer entities, It will be important to understand how these mechanisms translate to other types of tumors.”
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