REVIEW article

Front. Oncol.

Sec. Pediatric Oncology

Volume 15 - 2025 | doi: 10.3389/fonc.2025.1587157

This article is part of the Research TopicRecent Biological Insights into Pediatric Brain TumorsView all 10 articles

Aberrant Histone modifications in pediatric brain tumors

Provisionally accepted
Erin T HamanishiErin T Hamanishi1,2,3,4Derek DangDerek Dang1,2,5Sriram VennetiSriram Venneti1,2,5,6*
  • 1Laboratory of Brain Tumor Metabolism and Epigenetics, Department of Pathology, University of Michigan Medical School, Ann Arbor, United States
  • 2Chad Carr Pediatric Brain Tumor Center, University of Michigan, Ann Arbor, United States
  • 3Division of Pediatric Hematology-Oncology and Pediatric Bone Marrow Transplant, Department of Pediatrics, University of Michigan Medical School, Ann Arbor, United States
  • 4Department of Pediatrics, University of Michigan Medical School, Ann Arbor, United States
  • 5Department of Pathology, University of Michigan Medical School, Ann Arbor, Indiana, United States
  • 6Department of Pediatrics, School of Medicine, Michigan Medicine, University of Michigan, Ann Arbor, Michigan, United States

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Epigenetic modifications, particularly histone post-translational modifications (PTMs), are central to pediatric brain tumor pathogenesis, impacting chromatin structure, gene expression, and genomic stability. Disruptions in histone PTMs, especially lysine methylation and acetylation, arising due to histone mutations or aberrant enzyme modulation are critical drivers of oncogenesis. Lysine methylation, catalyzed by histone methyltransferases (KMTs), modulates chromatin interactions and gene expression through activation or repression, depending on the methylation state and the specific histone residue. Key enzymes, including histone methyltransferases and demethylases, and associated proteins exemplify the functions of writers, readers, and erasers in maintaining histone modification balance. Similarly, histone acetylation, a dynamic process regulated by histone acetyltransferases (HATs) and histone deacetylases (HDACs), plays a crucial role in pediatric brain tumors. Alterations in these components lead to aberrant gene expression and tumorigenesis.Understanding these disrupted processes offers potential for targeted therapies to rewire oncogenic chromatin states and potentially improve patient outcomes.

Keywords: epigenetics, Histone Modifications, Histone Methylation, histone acetylation, pediatric

Received: 04 Mar 2025; Accepted: 21 May 2025.

Copyright: © 2025 Hamanishi, Dang and Venneti. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Sriram Venneti, Department of Pediatrics, School of Medicine, Michigan Medicine, University of Michigan, Ann Arbor, 48109, Michigan, United States

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

Supplementary Material