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Diffuse midline glioma: review of epigenetics
Tabitha M Cooney1, Evan Lubanszky2,3, Rachna Prasad4
1Dana Farber Cancer Institute, Boston, MA, USA.
Journal of Neuro-Oncology
|August 18, 2020
Summary
Diffuse midline glioma (DMG), including H3 K27M-mutant tumors, is increasingly understood through its epigenetic alterations. Research is rapidly advancing epigenetic modifiers for clinical trials to improve patient outcomes.
Area of Science:
- Neuro-oncology
- Epigenetics
- Molecular Biology
Background:
- Diffuse midline glioma (DMG) and diffuse intrinsic pontine glioma (DIPG) are aggressive brain tumors.
- Histone H3 mutations (H3 K27M) have led to reclassification and a deeper understanding of DMG biology.
- Recent years have seen significant advancements in basic, translational, and clinical research on DMG.
Purpose of the Study:
- To review the current understanding of the epigenetics of diffuse midline glioma.
- To consolidate recent findings on H3 K27M mutations and their impact on DMG.
- To highlight the translational development of epigenetic modifiers for DMG treatment.
Main Methods:
- A comprehensive literature review was conducted.
- PubMed database was searched for studies from 1989 to 2019.
- Keywords included "diffuse intrinsic pontine glioma", "pontine glioma", and "midline glioma".
Main Results:
- H3K27M mutations significantly impact the chromatin landscape and DNA modification in DMG.
- Epigenetic modifiers are rapidly progressing through translational development, with several inhibitors in clinical trials.
- Ongoing research focuses on understanding the effects, tumor penetration, and immune microenvironment changes of epigenetic modifications.
Conclusions:
- Continued research is crucial for a comprehensive understanding of chromatin dysregulation and DNA modification in DMG.
- Clinical trials of epigenetic modifiers are advancing treatment strategies.
- Bench-to-bedside efforts and collaboration are essential for improving outcomes for DMG patients.
