Modeling the Landscape of Histone-Mutant Pediatric High-Grade Gliomas: A Study in Partner Alterations-Reference-Cited by-同舟云学术

Modeling the Landscape of Histone-Mutant Pediatric High-Grade Gliomas: A Study in Partner Alterations

Published:2023-07-07 Issue:7 Volume:13 Page:1516-1517
ISSN:2159-8274
Container-title:Cancer Discovery
language:en
Short-container-title:

Author:

Lubanszky Evan¹²^ORCID,Hawkins Cynthia¹²³^ORCID

Affiliation:

1. 1Arthur and Sonia Labatt Brain Tumour Research Centre, The Hospital for Sick Children, Toronto, Ontario, Canada.

2. 2Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.

3. 3Division of Pathology, The Hospital for Sick Children, Toronto, Ontario, Canada.

Abstract

Summary:Pediatric high-grade gliomas represent a group of deadly, heterogeneous tumors, often driven by histone mutations and the accumulation of clonal mutations, correlating with different tumor types, locations, and age of onset. In this study, McNicholas and colleagues present 16 in vivo models of histone-driven gliomas to investigate subtype-specific tumor biology and treatment options.See related article by McNicholas et al., p. 1592 (7).

Publisher

American Association for Cancer Research (AACR)

Subject

Oncology

Link

https://aacrjournals.org/cancerdiscovery/article-pdf/13/7/1516/3345618/1516.pdf

Reference7 articles.

1. Integrated molecular meta-analysis of 1,000 pediatric high-grade and diffuse intrinsic pontine glioma;Mackay;Cancer Cell,2017

2. Driver mutations in histone H3.3 and chromatin remodelling genes in paediatric glioblastoma;Schwartzentruber;Nature,2012

3. Patient-derived orthotopic xenograft models of pediatric brain tumors: in a mature phase or still in its infancy?;Hermans;Front Oncol,2019

4. A novel mouse model of diffuse midline glioma initiated in neonatal oligodendrocyte progenitor cells highlights cell-of-origin dependent effects of H3K27M;Tomita;Glia,2022

5. Histone H3.3 K27M accelerates spontaneous brainstem glioma and drives restricted changes in bivalent gene expression;Larson;Cancer Cell,2019