Histone-Mutant Glioma: Molecular Mechanisms, Preclinical Models, and Implications for Therapy

Histone-Mutant Glioma: Molecular Mechanisms, Preclinical Models, and Implications for Therapy

Pediatric high-grade glioma (pHGG) is the leading cause of cancer death in children. Despite histologic similarities, it has recently become apparent that this disease is molecularly distinct from its adult counterpart. Specific hallmark oncogenic histone mutations within pediatric malignant gliomas...

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Main Authors: Maya S. Graham, Ingo K. Mellinghoff
Format: Article
Language:English
Published: MDPI AG 2020-09-01
Series:International Journal of Molecular Sciences
Subjects:
pediatric high-grade glioma
diffuse midline glioma
oncohistone
H3K27M
Online Access:https://www.mdpi.com/1422-0067/21/19/7193
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spelling doaj-22034c5a313443ac9bd8421c2b9ee6822020-11-25T02:49:01ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672020-09-01217193719310.3390/ijms21197193Histone-Mutant Glioma: Molecular Mechanisms, Preclinical Models, and Implications for TherapyMaya S. Graham0Ingo K. Mellinghoff1Department of Neurology, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USADepartment of Neurology, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USAPediatric high-grade glioma (pHGG) is the leading cause of cancer death in children. Despite histologic similarities, it has recently become apparent that this disease is molecularly distinct from its adult counterpart. Specific hallmark oncogenic histone mutations within pediatric malignant gliomas divide these tumors into subgroups with different neuroanatomic and chronologic predilections. In this review, we will summarize the characteristic molecular alterations of pediatric high-grade gliomas, with a focus on how preclinical models of these alterations have furthered our understanding of their oncogenicity as well as their potential impact on developing targeted therapies for this devastating disease.https://www.mdpi.com/1422-0067/21/19/7193pediatric high-grade gliomadiffuse midline gliomaoncohistoneH3K27M
collection DOAJ
language English
format Article
sources DOAJ
author Maya S. Graham
Ingo K. Mellinghoff
spellingShingle Maya S. Graham
Ingo K. Mellinghoff
Histone-Mutant Glioma: Molecular Mechanisms, Preclinical Models, and Implications for Therapy
International Journal of Molecular Sciences
pediatric high-grade glioma
diffuse midline glioma
oncohistone
H3K27M
author_facet Maya S. Graham
Ingo K. Mellinghoff
author_sort Maya S. Graham
title Histone-Mutant Glioma: Molecular Mechanisms, Preclinical Models, and Implications for Therapy
title_short Histone-Mutant Glioma: Molecular Mechanisms, Preclinical Models, and Implications for Therapy
title_full Histone-Mutant Glioma: Molecular Mechanisms, Preclinical Models, and Implications for Therapy
title_fullStr Histone-Mutant Glioma: Molecular Mechanisms, Preclinical Models, and Implications for Therapy
title_full_unstemmed Histone-Mutant Glioma: Molecular Mechanisms, Preclinical Models, and Implications for Therapy
title_sort histone-mutant glioma: molecular mechanisms, preclinical models, and implications for therapy
publisher MDPI AG
series International Journal of Molecular Sciences
issn 1661-6596
1422-0067
publishDate 2020-09-01
description Pediatric high-grade glioma (pHGG) is the leading cause of cancer death in children. Despite histologic similarities, it has recently become apparent that this disease is molecularly distinct from its adult counterpart. Specific hallmark oncogenic histone mutations within pediatric malignant gliomas divide these tumors into subgroups with different neuroanatomic and chronologic predilections. In this review, we will summarize the characteristic molecular alterations of pediatric high-grade gliomas, with a focus on how preclinical models of these alterations have furthered our understanding of their oncogenicity as well as their potential impact on developing targeted therapies for this devastating disease.
topic pediatric high-grade glioma
diffuse midline glioma
oncohistone
H3K27M
url https://www.mdpi.com/1422-0067/21/19/7193
work_keys_str_mv AT mayasgraham histonemutantgliomamolecularmechanismspreclinicalmodelsandimplicationsfortherapy
AT ingokmellinghoff histonemutantgliomamolecularmechanismspreclinicalmodelsandimplicationsfortherapy
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