Skip to main content
. 2020 Jan 28;11:550. doi: 10.1038/s41467-020-14312-1

Fig. 2. Histology of iHGGs.

Fig. 2

H&E staining of PTEN−/−;NF1−/− iHGGs showing a region of hypercellularity infiltrated by irregular, elongated to angulated tumor cells with occasional mitoses (a), scale bars, 50 μm (left) and 10 μm (right), biphasic dense (glial) and loose (mesenchymal/sarcoma) morphologies, typical of gliosarcoma (b), necrosis (central pink zone) with peripheral “pseudopalisading” of cells around the necrotic center (c), scale bars, 200 μm (b, c), vascular endothelial proliferation (d), scale bar, 100 μm, rupture through the pial surface, and consequently subarachnoid spread (upper right) (e), scale bar, 200 μm, and “secondary structures” typical of glioma, including perineuronal satellitosis and subpial accumulation of tumor cells (f), scale bar, 50 μm. GFAP (g), Olig2 (h), Ki-67 (i) staining of PTEN−/−;NF1−/− iHGGs, scale bars, 100 μm (g–i). H&E staining of TP53−/−;PDGFRAΔ8–9 iHGGs showing nodular growth of a primitive neuronal component (dark purple) intermingled with glial component (pink) (j), scale bar, 200 μm, rosettes with neuropil-like texture in a primitive neuronal component (k), scale bar, 50 μm, a serpiginous zone of pseudopalisading necrosis (l), scale bar, 200 μm, and a tumor rupture through ependyma illustrating intraventricular growth (m), scale bar, 500μm. GFAP (n), Olig2 (o), Ki-67 (p) staining of TP53−/−;PDGFRAΔ8–9 iHGGs, scale bars, 100 μm (n–p).