Enabling epigenetic therapies by exploring DIPG chromatin sensitivities
Background: Recently, driver mutations in histone H3 have been found to correlate with particularly malignant forms of DIPG. These mutations change lysine 27 of H3 to methionine (K27M), abrogating methylation and acetylation at this site, both of which are epigenetic marks that influence chromatin architecture and are important for regulating ...