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. Author manuscript; available in PMC: 2016 Jan 1.
Published in final edited form as: Cell Tissue Res. 2014 Nov 23;359(1):225–254. doi: 10.1007/s00441-014-2046-y

Figure 1. Deregulation of neuronal and glial differentiation as a priming step in GBM formation.

Figure 1

Schematics of frontal lobes and lateral ventricles in the anterior regions of the adult cerebrum. Genetic alterations in SVZ neural precursors in the RAS/ERK pathway induce a NEUROG2-ASCL1 switch that induces gliomagenesis (Li, et al., 2014). The inability of IDH1R132H mutation to transform nestin-expressing NSCs, the high frequency of IDH1R132H mutation in oligodendroglioma (shown to originate from white matter OPCs), and the association of these tumors to the frontal cortex suggest that expression of IDH1R132H mutation in white matter (WM) progenitors inhibits differentiation and drive formation of proneural gliomas (Phillips, et al., 2006, Sturm, et al., 2012). Similarly, childhood GBMs displaying G34R/V mutation in the H3F3A gene express high levels of FOXG1 and MYC, but low/no levels of the OPC-related gene OLIG2, implicating a NSC origin. Misexpression (activation/upregulation (*) or (loss) of important cancer genes is shown in black.