Figure 7. CPE is heterogeneously expressed in human gliomas.

(A-F) HE stainings (left) and CPE immunohistochemistry (right) of human glial tumors. (A) Human IDH wild-type glioblastoma displaying absent to very weak CPE expression. (B) In IDH1-mutant (IDH1_R132H) glioblastoma samples, a weak to partially moderate CPE expression was observed while on very few cells (arrows) morphologically resembling reactive astrocytes showed slightly stronger CPE expression. (C) In recurrent GBM, CPE was strongly accumulating in a perivascular distribution (arrows) in areas with prominent astrogliotic changes. Presumably, the respective CPE expression is at least partly localized to reactive perivascular astrocytes. (D) In vital tumor areas of recurrent GBM, CPE was also most strongly expressed by cells with reactive astrocytic morphology. (E-F) Of note, a strong heterogeneity in CEP expression was also observed within distinct tumor specimens. While areas with an (E) epitheloid differentiation displayed strong CPE expression in gliosarcoma, its counterparts with (F) sarcomatous morphology remained largely CPE-negative. (A-F: scale bars = 100μm). (G) A representative immunoblot for detection of CPE and RPS6 in lysates of WHO°I to WHO°IV gliomas as well as normal appearing grey (GM) and white matter (WM). α-tubulin and β-actin were used as loading controls. (H) Correlation analysis of densitometric measurements of immunoblotting results in the WHO setting between CPE and RPS6. Pearson coefficient and exact p-value is shown (*p<0.05).