In this Northwestern study, researchers found that glioblastoma (GBM) tumors 'hijack' microglia metabolism by exploiting a fructose transporter called GLUT5, causing the microglia (the brain's resident immune cells) to take up and metabolize fructose in a way that suppresses anti-tumor immunity. To test its role, they used genetically engineered mice lacking GLUT5.
In multiple mouse GBM models, GLUT5-deficient mice showed significantly reduced tumor growth and improved survival, indicating this pathway is required for tumor progression. The microglia became more inflammatory and less immunosuppressive, and there was greater activation of a broader immune response, including increased antigen presentation, higher inflammatory signaling, and shifts toward more active T cell responses (including CD8+ T cells).