Stroke sped glioma invasion into injured tissue in human and mouse models
A peer-reviewed Baylor and Texas Children's study in Nature Cancer shows that stroke pushed tumors into injured regions in human and mouse glioma models and lowered survival in those models. Tumor-associated astrocytes with weaker calcium activity appeared at the invasive front, and microglia and macrophages accumulated. Restoring that calcium activity, or depleting those immune cells, suppressed the advance in the models.
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Tumors moved into injured tissue, and survival fell in the models
A peer-reviewed Baylor and Texas Children's study shows that stroke pushed tumors into injured brain regions in human and mouse glioma models and lowered survival in those models. Principal investigator Hyun Kyoung Lee of the Duncan Neurological Research Institute said the group worked with those models because the mechanism connecting brain injury and cancer had been unclear. The result comes from human and mouse glioma models, not from a count of patient diagnoses.[1], [2]
Astrocytes at the front had weaker calcium activity
Tumor-associated astrocytes with weaker calcium activity appeared at the invasive front, accompanied by remodeled microglia and macrophages that accumulated there. The paper identifies SLC4A4 in the astrocytes as a regulator of calcium activity and CCL2 as the signal that calls those immune cells in. Astrocytes are the brain's support cells; microglia are the brain's own immune cells, and macrophages are immune cells that arrive from the blood. The study is published in the peer-reviewed journal Nature Cancer.[1], [2]
Restoring calcium, or removing the immune cells, slowed the models
Restoring calcium signaling in the astrocytes, or depleting the microglia and macrophages, suppressed the stroke-linked glioma progression in the models. The findings are a lead for later work on people with a history of brain injury. They are not a treatment recommendation, and they do not measure how often stroke patients later receive a glioma diagnosis.[1], [2]
