Oncohistones and disrupted development in pediatric-type diffuse high-grade glioma.
Diffuse hemispheric glioma
Diffuse midline glioma
Epigenetic
H3 K27M
H3G34-mutant
H3K27-altered
Oncohistones
Pediatric diffuse glioma
Journal
Cancer metastasis reviews
ISSN: 1573-7233
Titre abrégé: Cancer Metastasis Rev
Pays: Netherlands
ID NLM: 8605731
Informations de publication
Date de publication:
06 2023
06 2023
Historique:
received:
13
01
2023
accepted:
05
04
2023
pmc-release:
01
06
2024
medline:
17
7
2023
pubmed:
29
4
2023
entrez:
29
4
2023
Statut:
ppublish
Résumé
Recurrent, clonal somatic mutations in histone H3 are molecular hallmarks that distinguish the genetic mechanisms underlying pediatric and adult high-grade glioma (HGG), define biological subgroups of diffuse glioma, and highlight connections between cancer, development, and epigenetics. These oncogenic mutations in histones, now termed "oncohistones", were discovered through genome-wide sequencing of pediatric diffuse high-grade glioma. Up to 80% of diffuse midline glioma (DMG), including diffuse intrinsic pontine glioma (DIPG) and diffuse glioma arising in other midline structures including thalamus or spinal cord, contain histone H3 lysine 27 to methionine (K27M) mutations or, rarely, other alterations that result in a depletion of H3K27me3 similar to that induced by H3 K27M. This subgroup of glioma is now defined as diffuse midline glioma, H3K27-altered. In contrast, histone H3 Gly34Arg/Val (G34R/V) mutations are found in approximately 30% of diffuse glioma arising in the cerebral hemispheres of older adolescents and young adults, now classified as diffuse hemispheric glioma, H3G34-mutant. Here, we review how oncohistones modulate the epigenome and discuss the mutational landscape and invasive properties of histone mutant HGGs of childhood. The distinct mechanisms through which oncohistones and other mutations rewrite the epigenetic landscape provide novel insights into development and tumorigenesis and may present unique vulnerabilities for pHGGs. Lessons learned from these rare incurable brain tumors of childhood may have broader implications for cancer, as additional high- and low-frequency oncohistone mutations have been identified in other tumor types.
Identifiants
pubmed: 37119408
doi: 10.1007/s10555-023-10105-2
pii: 10.1007/s10555-023-10105-2
pmc: PMC10441521
mid: NIHMS1920087
doi:
Substances chimiques
Histones
0
Types de publication
Journal Article
Review
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
367-388Subventions
Organisme : NCI NIH HHS
ID : F30 CA271570
Pays : United States
Organisme : NCI NIH HHS
ID : F31 CA265285
Pays : United States
Organisme : NCI NIH HHS
ID : P01 CA096832
Pays : United States
Informations de copyright
© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
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