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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

Nat Med

Publication Date

12/2014

Volume

20

Pages

1394 - 1396

Keywords

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