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Pediatric brainstem gliomas often harbor oncogenic K27M mutation of histone H3.3. Here we show that GSKJ4 pharmacologic inhibition of K27 demethylase JMJD3 increases cellular H3K27 methylation in K27M tumor cells and demonstrate potent antitumor activity both in vitro against K27M cells and in vivo against K27M xenografts. Our results demonstrate that increasing H3K27 methylation by inhibiting K27 demethylase is a valid therapeutic strategy for treating K27M-expressing brainstem glioma.

Original publication

DOI

10.1038/nm.3716

Type

Journal article

Journal

Nature medicine

Publication Date

12/2014

Volume

20

Pages

1394 - 1396

Addresses

Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.

Keywords

Cell Line, Tumor, Animals, Humans, Mice, Glioma, Brain Stem Neoplasms, Pyrimidines, Benzazepines, Histones, Xenograft Model Antitumor Assays, Apoptosis, Cell Proliferation, Gene Expression Regulation, Neoplastic, Methylation, Child, Jumonji Domain-Containing Histone Demethylases