Deadly cancer invades the brain and cannot be treated on its own, study finds

Image for article Study shows deadly cancer invades the brain and cannot be treated on its own

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New research out this week shows that aggressive brain cancer cannot stop itself from invading the brain’s own circuitry and spreading further.. German scientists studied glioblastoma cells in the laboratory and found that these tumors use the same mechanisms behind the development and migration of normal neurons to 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. about 15% primary brain tumors. It is also one of the most dangerous cancers. It originates in cells called astrocytes, which support neurons, and spreads rapidly throughout the brain. Symptoms are initially nonspecific, including headache and nausea. Treaction is rarely successful, and cancer frequent resources, with average life expectancy less than a year.

One of the main reasons for its invulnerability is that the cancer has spread to the brain, making it much more difficult to remove accurately, surgically or otherwise. GBM tumors also contain a variety of cells, complicating any treatment. However, the precise role and function of these diverse populations of GBM cells remains enigmaticAccording to study author Varun Venkataramani, a brain tumor researcher at the University of Heidelberg in Germany.

To better understand GBM, Venkataramani and his colleagues combined several different methods to study these tumors at the molecular and cellular levels. One of these techniques, called chronic cranial windowing, even allowed the brain and GBM tumors in mice to be visualized while they were awake. They also sequenced the genetics of single cells, allowing them to see which genes were turned off or on.

Other studies have shown that GBM cells form a network connected to each other by long protrusions called microtubules, and these microtubules can further spread the cancer. But the team’s work found that other, unrelated GBM cells play an important role in the cancer’s spread. These cells seem to receive signals from neurons that encourage them to invade other parts of the brain. To accomplish this, the team’s work further suggests that cancer cells take advantage of the same processes that healthy brains use to create neurons early in our development. Neuronal signals also promote microtubule growth. the and, Over time, unattached GBM cells merge with the rest of the cancer. Perhaps most alarmingly, crayfish attacks may follow a Lévy-like movement pattern, a term used to describe the energy-efficient ways some predators hunt for food in a short amount of time.

“Taken together, we see that the mechanisms of immature neurons and neural progenitor cells are indeed hijacked during development to take over,” Venkataramani wrote in an email to Gizmodo. Team work published in the journal Cell.

These findings are confirmed by the ideal addn studies by other researchers. And there are always things to learn. The current study, for example, only looked at GBM cells that were allowed to proliferate unhindered, so it’s unclear how they behave in response to chemotherapy and other treatments.

ThBasic research is a type of research that is very important to make discoveries that may someday lead to new ones Therapy for GBM. Since neurons appear to be an important aspect of how cancer communicates with itself, one way to stop it may be to interfere with these signals. The team highlights some possible ways to disrupt these signals, but more work needs to be done before we get to this point.

“We believe these findings should best be tested in clinical trials, and we need to further develop clinical imaging to be able to accurately monitor the invasive nature of these brain tumors,” Venkataramani said. “Ultimately, this research provides a framework that can be used in all cancer subjects, and understanding how these mechanisms translate to other tumor types will be important.

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