Diffuse intrinsic pontine gliomas (DIPG) are highly aggressive and difficult to treat tumors arising in the ventral pons of the brain stem. Despite therapeutic advances, DIPG is incurable and most patients, primarily children, die within 2 years of diagnosis. DIPG is one of the leading causes of death in children with brain tumors (1).A somatic mutation of histone H3.3 resulting in a lysine 27 to methionine substitution (H3.3K27M) occurs in 60% of DIPG (2). In H3.3K27M DIPG patient samples, levels of H3K27 dimethylation (H3K27me2) and trimethylation (H3K27me3) are reduced globally. These epigenetic changes are thought to be important factors driving DIPG oncogenesis (2,3,4). Expression of H3.3K27M was also recently shown to be associated with increased levels of H3K27 acetylation (H3K27ac) and recruitment of bromodomain proteins at sites of active transcription (5). Treatment of H3.3K27M DIPG cells with a bromodomain and extra-terminal domain (BET) inhibitor was found to inhibit proliferation and induced differentiation. BET inhibitors are thus a promising therapeutic approach for the treatment of DIPG.1. Schroeder KM et al. (2014) Pediatr. Res. 75(1-2): 205–209.2. Lewis PW et al. (2013) Science 340(6134): 857–861.3. Chan K-M et al. (2013) Genes & Development 27: 985-990.4. Hashizume R et al. (2014) Nat Med. 20(12):1394-6. 5. Piunti A et al. (2017) Nat. Med. 23(4): 493-500.6. Mueller S et al. (2014) Neuro Oncol. 16(3): 352-360.，官网链接：https://www.sigmaaldrich.cn/product/mm/scc127m 默克 科研、开发、生产。 作为生命科学行业的全球领先供应商，我们致力于为科研、生物技术开发和生产，以及制药药物疗法开发和生产提供各类解决方案和服务。

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