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. 2019 Nov 12;1(1):vdz025. doi: 10.1093/noajnl/vdz025

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© The Author(s) 2019. Published by Oxford University Press, the Society for Neuro-Oncology and the European Association of Neuro-Oncology.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Fig. 2. — VPA does not increase histone acetylation activity in tumor tissue from GBM patients. (A) Examples of immunohistochemical staining of glioblastoma sample on tissue microarray (TMA). The left panel displays hematoxylin and eosin staining, the middle panel shows immunostaining of acetylated histone H3, and the right panel displays immunostaining of acetylated histone H4 in the same patient. (B) Quantification of immunohistochemical staining on TMAs containing tumor tissue from glioblastoma patients. TMA’s were stained for acetylated histone H3K9 and H4K8. Boxes represent median and quartiles, whiskers represent data range. Results were analyzed by Mann–Whitney U test. (C) Quantification of western blot results for acetylated histone H3K9 and H4K8, relative to GAPDH expression, in fresh-frozen patient-derived glioblastoma tissue. Bars represent mean ± SD. VPA: patients that were treated with VPA for epileptic seizures, n = 8. No AED: patients had tumor-associated seizures but were not treated with any AED at the time of surgery, n = 6. Results were analyzed by Mann–Whitney U test. (D) Western blot results for acetylated histone H3K9 and H4K8, and GAPDH (loading control) in fresh-frozen GBM tissues. (E) Molecular subtype distribution in the patients with VPA and patients with epilepsy but without antiepileptic drugs treatment. Fisher exact test, P = 1.0. AED, antiepileptic drug; GBM, glioblastoma; VPA, valproic acid.