Skip to main content
Fig. 6 | Genome Biology

Fig. 6

From: Pediatric glioma histone H3.3 K27M/G34R mutations drive abnormalities in PML nuclear bodies

Fig. 6

Arsenic trioxide treatment of H3.3 K27M mutated patient-derived glioma cells. A Phase-contrast microscopy of DIPG XIII H3.3 WT (K27M KO) and H3.3 K27M pediatric glioma cells treated with 1 µM of arsenic trioxide for 1, 4, and 8 days. Untreated cells are shown as controls. Cell counts of B H3.3 WT (K27M KO) and C H3.3 K27M pediatric glioma cells treated with 1 µM of arsenic trioxide for 0, 4, and 8 days compared to untreated controls. D–F Experiments were repeated in an independent BT245 H3.3 WT (K27M KO) and H3.3 K27M pediatric glioma cell line. Points and error bars represent the mean average and standard deviation of three independent experiments. P-values were calculated using two-tailed Student’s t test (*P < 0.05 **P < 0.005)

Back to article page