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. Author manuscript; available in PMC: 2020 May 13.
Published in final edited form as: Cancer Cell. 2019 May 13;35(5):782–797.e8. doi: 10.1016/j.ccell.2019.04.004

Figure 8. Schematic summary of findings resulting from this study.

Figure 8.

The global loss of H3K27me3 by H3.3K27M leads to pervasive gain of H3K27ac across broad regions of chromatin, including repeat elements and endogenous retroviruses. This state primes them for activation by DNA demethylation and HDAC inhibition, a therapeutic vulnerability caused by this mutation.