Histone H3 K27M mediated Regulation of Cancer Cell Stemness and Differentiation in Diffuse Intrinsic Pontine Glioma (DIPG) [ChIP-seq]

Diffuse intrinsic pontine glioma (DIPG) is a rare pediatric brain tumor with a median survival of 10-15 months. Histone H3 is mutated in 80% of DIPGs, dictating tumor location, onset, and outcome. Therapeutic resistance remains a major obstacle to preventing tumor recurrence and is in part driven by cancer stem cells (CSCs), which exhibit self-renewal properties and tumorigenic potential. In previous studies, we have identified these proliferative and tumorigenic features in aldehyde dehydrogenase positive (ALDH+) CSCs in H3K27M mutant DIPG. We hypothesize that ALDH-mediated cancer stemness and resistance may in part be driven by H3K27M. Histone H3 K27 acetylation was assayed by chromatin immunoprecipitation and sequencing (ChIP-seq). SU-DIPG-XIII cells (here also "DIPG13") were treated with PI3K/mTOR inhibitor GSK458 or DMSO (one sample each). ChIP DNA was obtained using anti-H3K27Ac antibodies, as well as IgG IP and input DNA for a total of 6 ChIP-seq libraries.