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News
Scientists have identified a metabolite called guanidinoacetate (GAA) that accumulates in high-grade gliomas and supercharges tumor growth by overstimulating nearby neurons. The discovery, published in Cell, opens the door to a potential dietary therapy already approved for a related metabolic disorder. Researchers are now planning clinical trials to test whether diet changes before surgery can reduce GAA levels in patients.
Scientists at UT Southwestern's Children's Medical Center Research Institute have uncovered a surprising driver of aggressive brain tumor growth: a metabolite called guanidinoacetate (GAA). Published in Cell, the study found that virtually all high-grade gliomas in adults accumulate GAA at levels 100 times higher than normal — and that excess GAA leaks out of cancer cells, activates nearby neurons, and triggers a cascade that fuels tumor proliferation.
The mechanism works like this: tumors hyperactivate the enzyme that produces GAA, but a downstream enzyme (GAMT) can't keep up to convert it into creatine. The overflow GAA floods the tumor microenvironment, binds to neuronal receptors, and stimulates neurons to release signals that drive cancer cell growth. Blocking GAA production slowed tumor growth in lab experiments.
Key Takeaways:
Why it matters: High-grade gliomas are among the deadliest cancers, with very few effective treatments. This discovery not only explains a long-standing mystery in cancer neuroscience but also points to a potentially fast-tracked therapeutic strategy — repurposing an already-approved dietary therapy — that could be tested in patients soon.
