EZHIP's role in diffuse midline glioma: echoes of oncohistones?
- Publisher:
- CELL PRESS
- Publication Type:
- Journal Article
- Citation:
- Trends Cancer, 2024, 10, (12), pp. 1095-1105
- Issue Date:
- 2024-12
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Full metadata record
| Field | Value | Language |
|---|---|---|
| dc.contributor.author | Cassim, A | |
| dc.contributor.author | Dun, MD | |
| dc.contributor.author | Gallego-Ortega, D | |
| dc.contributor.author | Valdes-Mora, F | |
| dc.date.accessioned | 2025-04-02T06:08:28Z | |
| dc.date.available | 2024-09-03 | |
| dc.date.available | 2025-04-02T06:08:28Z | |
| dc.date.issued | 2024-12 | |
| dc.identifier.citation | Trends Cancer, 2024, 10, (12), pp. 1095-1105 | |
| dc.identifier.issn | 2405-8033 | |
| dc.identifier.issn | 2405-8025 | |
| dc.identifier.uri | http://hdl.handle.net/10453/186502 | |
| dc.description.abstract | The enhancer of zeste inhibitory protein (EZHIP) is typically expressed during germ cell development and has been classified as a cancer-testis antigen (CTA) in various cancers. In 2020, 4% of diffuse midline gliomas (DMGs) were shown to aberrantly express EZHIP, mirroring the DMG hallmark histone H3 K27M (H3K27M) oncohistone mutation. Similar to H3K27M, EZHIP is a negative regulator of polycomb repressive complex 2 (PRC2), leading to global epigenomic remodeling. In this opinion, we explore the similarities and disparities between H3K27M- and EZHIP-DMGs with a focus on their shared functional hallmark of PRC2 inhibition, their genetic and epigenomic landscapes, plausible differences in the cell of origin, and therapeutic avenues. Upcoming research on EZHIP will help better understand its role in gliomagenesis and DMG therapy. | |
| dc.format | Print-Electronic | |
| dc.language | eng | |
| dc.publisher | CELL PRESS | |
| dc.relation | National Breast Cancer FoundationIIRS- 21-096 | |
| dc.relation.ispartof | Trends Cancer | |
| dc.relation.isbasedon | 10.1016/j.trecan.2024.09.002 | |
| dc.rights | info:eu-repo/semantics/openAccess | |
| dc.subject | 1112 Oncology and Carcinogenesis | |
| dc.subject.classification | 3211 Oncology and carcinogenesis | |
| dc.subject.mesh | Humans | |
| dc.subject.mesh | Glioma | |
| dc.subject.mesh | Histones | |
| dc.subject.mesh | Brain Neoplasms | |
| dc.subject.mesh | Mutation | |
| dc.subject.mesh | Polycomb Repressive Complex 2 | |
| dc.subject.mesh | Gene Expression Regulation, Neoplastic | |
| dc.subject.mesh | Repressor Proteins | |
| dc.subject.mesh | Epigenesis, Genetic | |
| dc.subject.mesh | Oncogene Proteins | |
| dc.subject.mesh | Humans | |
| dc.subject.mesh | Glioma | |
| dc.subject.mesh | Brain Neoplasms | |
| dc.subject.mesh | Oncogene Proteins | |
| dc.subject.mesh | Histones | |
| dc.subject.mesh | Repressor Proteins | |
| dc.subject.mesh | Epigenesis, Genetic | |
| dc.subject.mesh | Gene Expression Regulation, Neoplastic | |
| dc.subject.mesh | Mutation | |
| dc.subject.mesh | Polycomb Repressive Complex 2 | |
| dc.subject.mesh | Humans | |
| dc.subject.mesh | Glioma | |
| dc.subject.mesh | Histones | |
| dc.subject.mesh | Brain Neoplasms | |
| dc.subject.mesh | Mutation | |
| dc.subject.mesh | Polycomb Repressive Complex 2 | |
| dc.subject.mesh | Gene Expression Regulation, Neoplastic | |
| dc.subject.mesh | Repressor Proteins | |
| dc.subject.mesh | Epigenesis, Genetic | |
| dc.subject.mesh | Oncogene Proteins | |
| dc.title | EZHIP's role in diffuse midline glioma: echoes of oncohistones? | |
| dc.type | Journal Article | |
| utslib.citation.volume | 10 | |
| utslib.location.activity | United States | |
| utslib.for | 1112 Oncology and Carcinogenesis | |
| pubs.organisational-group | University of Technology Sydney | |
| pubs.organisational-group | University of Technology Sydney/Faculty of Engineering and Information Technology | |
| pubs.organisational-group | University of Technology Sydney/Faculty of Engineering and Information Technology/School of Biomedical Engineering | |
| utslib.copyright.status | open_access | * |
| dc.rights.license | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND 4.0). To view a copy of this license, visit https://creativecommons.org/licenses/by-nc-nd/4.0/ | |
| dc.date.updated | 2025-04-02T06:08:26Z | |
| pubs.issue | 12 | |
| pubs.publication-status | Published | |
| pubs.volume | 10 | |
| utslib.citation.issue | 12 |
Abstract:
The enhancer of zeste inhibitory protein (EZHIP) is typically expressed during germ cell development and has been classified as a cancer-testis antigen (CTA) in various cancers. In 2020, 4% of diffuse midline gliomas (DMGs) were shown to aberrantly express EZHIP, mirroring the DMG hallmark histone H3 K27M (H3K27M) oncohistone mutation. Similar to H3K27M, EZHIP is a negative regulator of polycomb repressive complex 2 (PRC2), leading to global epigenomic remodeling. In this opinion, we explore the similarities and disparities between H3K27M- and EZHIP-DMGs with a focus on their shared functional hallmark of PRC2 inhibition, their genetic and epigenomic landscapes, plausible differences in the cell of origin, and therapeutic avenues. Upcoming research on EZHIP will help better understand its role in gliomagenesis and DMG therapy.
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