SMARCA4 vulnerability in H3K27M midline glioma: A silver bullet for a lethal disease

Carol C L Chen; Augusto Faria Andrade; Nada Jabado

doi:10.1016/j.molcel.2022.12.028

SMARCA4 vulnerability in H3K27M midline glioma: A silver bullet for a lethal disease

Mol Cell. 2023 Jan 19;83(2):163-164. doi: 10.1016/j.molcel.2022.12.028.

Authors

Carol C L Chen¹, Augusto Faria Andrade¹, Nada Jabado²

Affiliations

¹ Department of Human Genetics, McGill University, Montreal, QC H3A 0C7, Canada.
² Department of Human Genetics, McGill University, Montreal, QC H3A 0C7, Canada; Division of Experimental Medicine, Department of Medicine, McGill University, Montreal, QC H4A 3J1, Canada; Department of Pediatrics, McGill University, and The Research Institute of the McGill University Health Centre, Montreal, QC H4A 3J1, Canada. Electronic address: nada.jabado@mcgill.ca.

PMID: 36669477
DOI: 10.1016/j.molcel.2022.12.028

Abstract

To investigate epigenetic dependencies and identify therapeutic vulnerabilities, Mo et al.¹ and Panditharatna et al.² performed CRISPR screens and show that deadly H3K27M gliomas are dependent on mammalian BAF (SWI/SNF) chromatin remodeling complex.

MeSH terms

Animals
DNA Helicases / genetics
Glioma* / genetics
Humans
Mammals
Nuclear Proteins
Transcription Factors

Substances

SMARCA4 protein, human
DNA Helicases
Nuclear Proteins
Transcription Factors