1. Nat. Rev. Neurol. doi:10.1038/nrneurol.2016.173
Figure 2 Molecular genetic pathways affected in low-grade epilepsy-associated neuroepithelial tumours
Figure 2 | Molecular genetic pathways affected in low-grade epilepsy-associated neuroepithelial tumours. Genetic alterations detected in low-grade epilepsy-associated neuroepithelial tumours (LEATs) connect two major signalling pathways, the RAS–RAF–MAPK (green) and PI3K–AKT–mTOR (blue). Upstream in receptor signalling, FGFR1 mutations have been described in dysembryoplastic neuroepithelial tumours. B-Raf is a component further downstream in the RAS–RAF–MAPK signalling cascade. Activation of this pathway by the Val600Glu mutation detected in gangliogliomas leads to phosphrylation of MAPKs, which phosphorylate and regulate transcriptions factors for cell proliferation and differentation, such as CREB, c-fos. B-Raf and MEK1/2 are pharmacological targets for therapy (pink). MAP kinase activation is regulated by substrates of the PI3K–AKT–mTOR signalling cascade (red links). One of the regulated transcription factors, c-MYB/MYBL1 (purple), is altered in angiocentric gliomas. Genetic alterations described in LEAT are indicated by a lightning bolt. Dashed lines indicate weak interaction employing additional pathways (Akt–CMYB/MYBL1) or direct, but weak interactions (all other dashed lines).
Blümcke, I. et al. (2016) Low-grade epilepsy-associated neuroepithelial tumours — the 2016 WHO classification
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