Glioma

…The program spans neuron-glioma crosstalk, tumor-induced neurological dysfunction, cancer pain circuits, peripheral nervous-system structure, metabolism, and therapeutic targets.

In recent years, the interaction between glioma and brain cells has emerged as one important regulator of tumor progression. In order to investigate the molecular and physiologic alterations of the peritumoral neurons induced by glioma growth, we used two well-established glioma syngeneic cell lines: GL261 and CT-2A. We performed in vivo electrophysiological recordings of visual evoked potentials (VEPs) to longitudinally monitor the neural dysfunctions along with tumor progression. With respect to controls, glioma-bearing (GBM) mice showed a decay of visual responses that started from day 14 a

…cellular origin for many forms of glioma, suggests that dysregulated or “hijacked” mechanisms of myelin

Pediatric high-grade gliomas (pHGG) are a devastating group of diseases that urgently require novel therapeutic options. We have previously demonstrated that pHGGs directly synapse onto neurons and the subsequent tumor cell depolarization, mediated by calcium-permeable AMPA channels, promotes their proliferation. The regulatory mechanisms governing these postsynaptic connections are unknown. Here, we investigated the role of BDNF-TrkB signaling in modulating the plasticity of the malignant synapse. BDNF ligand activation of its canonical receptor, TrkB (which is encoded for by the gene NTRK2),