Stroke may change brain cells in ways that help gliomas grow
· Medical Xpressedited by Sadie Harley, reviewed by Robert Egan
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Researchers at Texas Children's Duncan Neurological Research Institute (Duncan NRI), Baylor College of Medicine and collaborating institutions report in Nature Cancer that stroke promotes glioma growth. They also identified cellular and molecular mediators involved in the process, linking brain injury to malignant brain tumors.
"Epidemiological and clinical studies suggest that patients with a history of stroke or traumatic brain injury are at increased risk of developing brain tumors. The risk can be about threefold to sevenfold, depending on the age and sex of the patient," said corresponding author Dr. Hyun Kyoung Lee, principal investigator at the Duncan NRI. Lee is also an associate professor of pediatrics and neurology and a member of the Dan L Duncan Comprehensive Cancer Center at Baylor.
"Despite these clinical observations, the mechanism that connects brain injury and cancer remains unclear. In the current study, we worked with human and mouse models to investigate whether stroke promotes glioma growth and the factors mediating the connection," Lee said.
Stroke draws glioma into injured tissue
The study's first authors, Dr. Qi Ye and graduate student Christine Madamba of Lee's lab, focused on stroke as one type of brain injury and glioma as a specific type of brain tumor. Glioma is the most prevalent and aggressive malignant brain tumor in adults. The researchers also considered its five-year survival rate.
"We show that stroke promoted tumor infiltration into injured brain regions in human and mouse glioma models, and reduced overall survival," Lee said. "Looking closer into the cellular and molecular makeup of the tumors, we found that stroke triggers remodeling of the tumor microenvironment."
Astrocytes and immune cells drive growth
The team discovered the emergence of a distinct population of brain cells—tumor-associated astrocytes (TAAs)—with distinct physiological and molecular characteristics, including diminished calcium activity. TAAs were accompanied by the accumulation of two other cell types: remodeled tumor-associated microglia and immune cells called macrophages (TAMs).
Restoring TAA calcium signaling or removing TAMs suppressed stroke-induced glioma progression, identifying both populations as critical mediators of the stroke response.
The findings suggest that these injury-induced, tumor-promoting pathways are potential therapeutic targets and support continued research into strategies that could reduce the risk of glioma growth in patients with a history of brain injury.
"Our study supports the idea that brain injury can be a risk factor for brain cancer. In addition, our findings contribute to growing evidence pointing to a role of astrocytes in brain tumor growth," Lee said.
"Neuron-tumor interactions have been shown to contribute to cancer growth. We show that other brain cells, astrocytes, also seem to communicate with brain cancer cells and influence their behavior. They should be considered when studying cancer mechanisms and therapies."
Publication details
Stroke drives glioma progression through the emergence of tumor-associated astrocytes with reduced Ca2+ activity, Nature Cancer (2026). DOI: 10.1038/s43018-026-01238-8
Journal information: Nature Cancer
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Sadie Harley
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