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. Author manuscript; available in PMC: 2015 Apr 24.
Published in final edited form as: Cell. 2014 Apr 10;157(3):580–594. doi: 10.1016/j.cell.2014.02.030

Figure 1. Epigenetic landscapes distinguish functionally distinct GBM models.

Figure 1

(A) GBM cells (MGG8) grown as gliomaspheres in serum-free conditions propagate tumor in vivo while serum-differentiated cells fail to do so. (B) Flow cytometry of MGG8 TPCs shows positivity for the GBM stemlike markers SSEA-1 and CD133, while serum-differentiated cells do not. (C) Cells grow in serum as adherent monolayers and express the differentiation markers GFAP (astroglial), beta III tubulin (neuronal), MAP-2 (neuronal) and GalC (oligodendroglial). (D) Xenografted tumors from MGG8 TPCs (left) are invasive, crossing the corpus callosum (boxed region), infiltrating along white matter tracks (arrowhead). At high magnification, the cells are atypical and mitotic figures are evident (arrow). Xenografted tumors from MGG4 TPCs (right) are more circumscribed but also infiltrate adjacent parenchyma (boxed region, arrowhead). At high magnification areas of necrosis (*) and mitotic figures (arrow) are readily identified. LV: lateral ventricle. (E) TPC-specific, DGC-specific and shared regulatory elements. Shared elements tend to be located proximal to promoters, while the vast majority of TPC- and DGC-specific elements are distal. Motif analyses predict binding sites for TF families within each set of sites. See also Supplemental FigureS1.