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Pharmacologic inhibition of histone demethylation as a therapy for pediatric brainstem glioma.

Nature medicine (2014-11-18)
Rintaro Hashizume, Noemi Andor, Yuichiro Ihara, Robin Lerner, Haiyun Gan, Xiaoyue Chen, Dong Fang, Xi Huang, Maxwell W Tom, Vy Ngo, David Solomon, Sabine Mueller, Pamela L Paris, Zhiguo Zhang, Claudia Petritsch, Nalin Gupta, Todd A Waldman, C David James
RÉSUMÉ

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.

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Description du produit

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Kit de détection in situ de mort cellulaire avec peroxydase ApopTag, The ApopTag Peroxidase In Situ Apoptosis Detection Kit detects apoptotic cells in situ by labeling & detecting DNA strand breaks by the TUNEL method.
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Anticorps anti-histone H3.3 (mutant K27M), from rabbit, purified by affinity chromatography
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SF7761 Human DIPG H3.3-K27M Cell Line, SF7761 pediatric diffuse intrinsic pontine glioma (DIPG) cell line harbors the histone H3.3 Lys 27-to-methionine (K27M) mutation and can support research and drug development efforts targeting DIPG.
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MISSION® esiRNA, targeting human KDM6A (1)