Core Concept Neuroscience and Psychology Collection Article Published: June 4, 2026

A New Hope for Treating Childhood Brain Cancer

Abstract

The brain is full of billions of healthy cells—but sometimes a few of them can start growing out of control and become cancerous. The cells that “go bad” can form brain tumors called gliomas. We discovered that glioma cells actually connect directly with healthy brain cells and “hijack” the brain’s normal communication system. They use the same electrical signals and chemical messengers that usually help the brain grow and learn to fuel their own growth instead. In this article, I will explain what we currently know about how glioma cells communicate with healthy brain cells, and how this understanding is helping scientists design better treatments to stop tumors from hijacking the brain. Our findings could help thousands of children and adults who are living with brain cancer.

Professor Michelle Monje won the Brain Prize in 2025, together with Prof. Frank Winkler for “pioneering the field of Cancer Neuroscience.”

The Brain Prize is an international award that recognizes and celebrates highly original and groundbreaking advances in any area of brain research, from basic neuroscience to applied clinical research. Since it was founded in 2011 and up until 2025, The Brain Prize has been awarded to 49 scientists from 11 countries.

Brain Cancer: When Good Cells Go Bad

Cancer happens when some of the body’s cells grow out of control. This can occur in various organs including the lungs, the stomach, and the brain. A cell becomes cancerous due to changes in its DNA, which are called mutations. DNA is like the instruction manual for how cells should behave (Figure 1). When this manual gets damaged, cells can “go bad” and grow uncontrollably.

Illustration showing three labeled elements: A is a book with DNA motifs and a cluster of cells, suggesting genetic information; B is a broken DNA double helix strand, indicating DNA damage or mutation; C is a cluster of abnormal cells, likely representing tumor or cancerous growth.
  • Figure 1 - How a cancerous tumor can begin from changes in DNA.
  • (A) DNA is like an instruction book that tells cells how to grow and behave. (B) Sometimes a piece of these DNA instructions gets damaged or changed—this is called a mutation. (C) A harmful mutation can cause cells to grow when they should not, which may lead to the formation of a cancerous tumor.

In adults, mutations often happen because their cells have been exposed to harmful things—like chemicals or radiation—for many years. But in children and teenagers, most mutations happen for a different reason. Their bodies are still growing, so their cells divide very quickly. Each time a cell divides, it has to copy its DNA, and sometimes a tiny copying mistake—called a random mutation—can happen. Even one or two of these mistakes can make a cell stop following the rules and start growing out of control, which can lead to a tumor (Figure 1C).

Childhood cancer is relatively rare. Out of the millions of children in the United States, about 4,000 develop brain tumors each year—and this same rate is true globally (less than 1 kid per 10,000 kids). Even though it is a relatively rare disease, childhood cancer is often very hard to treat and has devastating outcomes. This is why we urgently need to better understand how these cancers form and how we can treat them more effectively.

Glioma: The Most Common Brain Cancer in Kids

The most common type of brain tumor in children is called a glioma, and it is the focus of my lab’s research [1]. Your brain contains billions of cells called neurons that communicate via electrical signals. These neurons are like wires, and just like the electrical wires in your home need insulation, neurons need insulation too. This insulation is called myelin, a fatty substance that wraps around neurons and helps signals travel faster and more efficiently [2].

The process of adding this myelin insulation—called myelination—takes about 30 years to complete! It starts with the most basic groups of neurons in your brain, like those that help you see and move. But the brain areas involved in complex processes like thinking, planning, and decision making (often called executive functions) get myelinated much later. In fact, your brain is still myelinating right now, and it will continue through the next two decades of your life.

The brain cells responsible for myelination are called oligodendrocytes (Figure 2). Oligodendrocytes develop from “younger” cells called oligodendrocyte precursor cells (OPCs). OPCs are very important because they travel to the places in the brain where myelination needs to occur next, and then they mature into oligodendrocytes that wrap myelin around neurons. The problem is that OPCs, which are so important for normal brain development, are also the cells that most commonly turn into gliomas when they get a mutation.

Illustration showing three labeled panels: panel A displays healthy neurons with intact myelin sheaths; panel B zooms in on cross-sections of myelinated nerve fibers numbered one to three; panel C depicts damaged neurons and myelin loss in the brain, indicated by reddish lesions.
  • Figure 2 - Myelination in the brain and how it relates to brain cancer.
  • (A) In the brain, special support cells called oligodendrocytes help neurons work properly by wrapping them with layers of a fatty material called myelin (blue sheath). (B) Oligodendrocytes wrap axons in layers of a fatty material called myelin, which speeds up electrical signals and keeps them from “leaking” out. (C) The younger cells that grow up to become oligodendrocytes, called OPCs, are the cells that most often turn into brain tumors called gliomas when they get a mutation.

The Flexibility Tradeoff

OPCs are powerful cells—they can divide, move around, and change into different types of cells. They are not fully specialized yet, which means they have lots of potential for growth and change. This provides the brain with the adaptability and plasticity that it needs to develop properly. Unfortunately, this same flexibility and power to grow makes OPCs—as well as other precursor cells in the brain and body—more vulnerable to becoming cancerous.

A New Understanding of Brain Cancers

For many years, scientists studied brain tumors the same way they studied other cancers—as groups of cells that grew out of control because of mutations. But trying to treat them with the same treatments that work for cancers elsewhere in the body did not work very well in the brain, especially in the case of gliomas. This suggested that something was different about these types of cancers.

Healthy neurons in the brain create connections called synapses, which they use to communicate with each other through electrical and chemical messages. My colleagues and I discovered that glioma cells also form synapses with neurons [3]. They hijack this normal communication system and use the brain’s own signals to fuel their growth. Any time an electrical signal is created in the synapse where a glioma cell and neuron meet, it triggers the glioma cell to divide, which helps the tumor to grow and spread within the brain. Additionally, when neurons are active, they release molecules called growth factors that tell nearby support cells to grow. Glioma cells, which come from those same support cells, also “listen” to the growth factors and grow in response to their signals [4]. In other words, the tumor literally uses the brain’s activity as fuel for its own growth.

This was a surprising discovery because it meant that brain tumors do not behave in the way we thought that cancers behave. Instead of acting like “foreign” cells, they blend into the surrounding brain tissue and behave as if they are normal cells, using the brain’s own signals and processes to help themselves grow and spread.

The Door is Open to New Treatments

Now that we better understand how gliomas hijack the brain’s processes, we can develop more efficient treatments (Figure 3). This is the exciting part—we are finding ways to disrupt the tumor’s connection to healthy brain cells.

Cartoon illustration divided diagonally into two panels. Panel A shows a neural structure with a labeled cluster releasing molecules, symbolizing communication or chemical signaling. Panel B features a similar cluster under a shower of particles from containers, alongside icons indicating no wireless signal, an item being removed from a cart, and a reduction in cluster size.
  • Figure 3 - Using existing drugs to treat brain cancer.
  • (A) Brain tumors grow by using the electrical signals and helpful molecules that healthy neurons normally send out to talk to each other. (B) Some medicines already used for other brain conditions can block tumor cells from using these signals. They reduce communication between cells (top circle) and limit the release and availability of helpful molecules (middle circle), which together slows the growth of tumor cells (bottom circle). Because cancer cells cannot adapt as well as healthy cells, they struggle to keep growing when these signals are blocked—while healthy brain cells can adjust and continue working.

One promising approach is to repurpose existing medicines [5]. Many drugs already used to treat brain conditions like epilepsy, pain, or anxiety act on the same kinds of brain signals that glioma cells hijack to grow. In some cases, medicines that slightly disrupt brain activity can hurt cancer cells much more than healthy brain cells (which are more adaptable), offering a potent way to treat the tumor.

One reason this approach is so exciting is that we have been using these medicines safely for other conditions for years, so we already know they can reach the brain and that people can tolerate them. By testing these medicines in laboratory mice with gliomas, we found that some of them can significantly slow tumor growth. For example, there is an anti-seizure medicine called perampanel that blocks a type of synapse commonly used by tumor cells. When we give this medicine to mice with gliomas, their tumors grow more slowly.

However, we must be careful. Not all brain medicines are helpful for cancer patients. In fact, we discovered that some commonly used medicines, like certain anti-anxiety drugs called benzodiazepines, might actually speed up the growth of specific types of brain cancer. This is why we need to conduct very careful scientific studies in patients, to test which medicines might be good cancer treatments and which might harm the patient.

The Future of Brain Cancer Research

I became a pediatric neuro-oncologist—a doctor who treats children with brain tumors—because when I first encountered this disease, I knew I could not turn away. These tumors are devastating, and we definitely need better treatments. Now that we understand how important the interaction between tumors and healthy brain cells is, we can find new treatments for these complex cancers.

But there is still an enormous amount of work to do. To really understand what happens to make cancer cells go bad, we must also understand in great detail the healthy processes that happen when everything is functioning properly. To accomplish this, we need many more scientists with broad knowledge in biology, neuroscience, cancer research, and immunology. The most exciting discoveries often happen at the intersection of different fields, and I would therefore recommend that you choose the field you are most interested in and focus on that, while also trying to have at least a general understanding of other fields.

Brain tumors may have learned to hijack the healthy brain, but now we are onto them—we are on the right track to effectively neutralize these dangerous cancers. With the help of talented young people like you, I am sure we can reach this critical goal.

Acknowledgments

I wish to thank Or Raphael for conducting the interview that served as the basis for this paper, and for co-authoring the paper, Iris Gat for providing the figures, and Susan Debad for copyediting the manuscript.

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Glossary

Mutations: Changes in a cell’s DNA that can alter how the cell behaves, sometimes leading to cancer.

Tumor: A group of cells that start growing when they are not supposed to.

Glioma: A type of brain tumor that resembles support cells in the brain called glial cells.

Myelin: A fatty substance that wraps around neurons like insulation on a wire, helping electrical signals travel faster.

Oligodendrocyte Precursor Cells (OPCs): Immature/developing cells that eventually form oligodendrocytes, the glial cells that create myelin in the brain.

Plasticity: The brain’s ability to change its structure and connections when we learn.

Synapses: Connection points where one neuron communicates with another cell using electrical and chemical signals.

Growth Factors: Molecules that send messages to cells, telling them when to grow, divide, or repair themselves.

Conflict of Interest

The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


References

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[2] Gibson, E. M., Purger, D., Mount, C. W., Goldstein, A. K., Lin, G. L., Wood, L. S., et al. 2014. Neuronal activity promotes oligodendrogenesis and adaptive myelination in the mammalian brain. Science 344:1252304. doi: 10.1126/science.1252304

[3] Venkatesh, H. S., Morishita, W., Geraghty, A. C., Silverbush, D., Gillespie, S. M., Arzt, M., et al. 2019. Electrical and synaptic integration of glioma into neural circuits. Nature 573:539–45. doi: 10.1038/s41586-019-1563-y

[4] Venkatesh, H. S., Johung, T. B., Caretti, V., Noll, A., Tang, Y., Nagaraja, S., et al. 2015. Neuronal activity promotes glioma growth through neuroligin-3 secretion. Cell 161:803–16. doi: 10.1016/j.cell.2015.04.012

[5] Winkler, F., Venkatesh, H. S., Amit, M., Batchelor, T., Demir, I. E., Deneen, B., et al. 2023. Cancer neuroscience: state of the field, emerging directions. Cell 186:1689–707. doi: 10.1016/j.cell.2023.02.002