Chaetocin-mediated SUV39H1 inhibition targets stemness and oncogenic networks of diffuse midline gliomas and synergizes with ONC201.

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Abstract

Diffuse intrinsic pontine gliomas (DIPG/DMG) are devastating pediatric brain tumors with extraordinarily limited treatment options and uniformly fatal prognosis. Histone H3K27M mutation is a common recurrent alteration in DIPG and disrupts epigenetic regulation. We hypothesize that genome-wide H3K27M-induced epigenetic dysregulation makes tumors vulnerable to epigenetic targeting.

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Author and article information

Journal

Journal ID (iso-abbrev): Neuro Oncol

Title: Neuro-oncology

Publisher: Oxford University Press (OUP)

ISSN (Electronic): 1523-5866

ISSN (Print): 1522-8517

Publication date (Electronic): Apr 05 2024

Volume: 26

Issue: 4

Affiliations

[1 ] Brain Tumor Center, Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.

[2 ] Department of Neurology and Rehabilitation Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.

[3 ] Department of Pediatrics, University of Cincinnati and Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.

[4 ] Department of Pediatrics, Division of Pediatric Hematology-Oncology, University of Michigan School of Medicine, Ann Arbor, Michigan, USA.

Article

Publisher Item ID: 7452742

DOI: 10.1093/neuonc/noad222

PMC ID: 10995509

PubMed ID: 38011799

SO-VID: 94637761-6089-44c5-8973-cbfd00c95f17

History

Keywords: D2 dopamine receptor (DRD2) signaling,H3K9 methyltransferase SUV39H1,chaetocin,diffuse intrinsic pontine glioma (DIPG/DMG),small-molecule epigenetic compound screen,stemness and oncogenic networks

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