[1]杨 帆 张剑宁.儿童弥漫内生型桥脑胶质瘤H3K27M突变的研究进展[J].中国临床神经外科杂志,2021,26(02):131-132.[doi:10.13798/j.issn.1009-153X.2021.02.024]
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儿童弥漫内生型桥脑胶质瘤H3K27M突变的研究进展()
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《中国临床神经外科杂志》[ISSN:1009-153X/CN:42-1603/TN]

卷:
26
期数:
2021年02期
页码:
131-132
栏目:
综述
出版日期:
2021-02-25

文章信息/Info

文章编号:
1009-153X(2021)02-0131-02
作者:
杨 帆 张剑宁
100048 北京,解放军总医院第一医学中心神经外科医学部(杨 帆、张剑宁)
关键词:
弥漫内生型桥脑胶质瘤儿童H3K27M突变靶向治疗
分类号:
R 739.41
DOI:
10.13798/j.issn.1009-153X.2021.02.024
文献标志码:
A

参考文献/References:

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[3] Schwartzentruber J, Korshunov A, Liu XY, et al. Driver mutations in histone H3.3 and chromatin remodelling genes in paediatric glioblastoma [J]. Nature, 2012, 482(7384): 226-231.
[4] Wu G, Broniscer A, McEachron TA, et al. Somatic histone H3 alterations in pediatric diffuse intrinsic pontine gliomas and non-brainstem glioblastomas [J]. Nat Genet, 2012, 44(3): 251-253.
[5] Castel D, Philippe C, Calmon R, et al. Histone H3F3A and HIST1H3B K27M mutations define two subgroups of diffuseintrinsic pontine gliomas with different prognosis and phe-notypes [J]. Acta Neuropathol, 2015, 130(6): 815-827.
[6] Fontebasso AM, Papillon-Cavanagh S, Schwartzentruber J, et al. Recurrent somatic mutations in ACVR1 in pediatric midline high-grade astrocytoma [J]. Nat Genet, 2014, 46(5): 462-466.
[7] Mackay A, Burford A, Carvalho D, et al. Integrated molecu-lar meta-analysis of 1, 000 pediatric high-grade and diffuseintrinsic pontine glioma [J]. Cancer Cell, 2017, 32(4): 520-537.
[8] Taylor KR, Mackay A, Truffaux N, et al. Recurrent activa-ting ACVR1 mutations in diffuse intrinsic pontine glioma [J]. Nat Genet, 2014, 46(5): 457-461.
[9] Wu G, Diaz AK, Paugh BS, et al. The genomic landscape of diffuse intrinsic pontine glioma and pediatric non-brain-stem high-grade glioma [J]. Nat Genet, 2014, 46: 444-450.
[10] Cao R, Zhang Y. The functions of E(Z)/EZH2-mediated methylation of lysine 27 in histone H3 [J]. Curr Opin Genet Dev, 2004, 14(2): 155-164.(下转第136页)(上接第132页)
[11] Tie F, Banerjee R, Stratton CA, et al. CBP-mediated acety-lation of histone H3 lysine 27 antagonizes Drosophila Polycomb silencing [J]. Development, 2009, 136(18): 3131-3141.
[12] Sturm D, Witt H, Hovestadt V, et al. Hotspot mutations in H3F3A and IDH1 define distinct epigenetic and biological subgroups of glioblastoma [J]. Cancer Cell, 2012, 22(4): 425-437.
[13] Lewis PW, Müller MM, Koletsky MS, et al. Inhibition of PRC2 activity by a gain-of-function H3 mutation found in pediatric glioblastoma [J]. Science, 2013, 340(6134): 857-861.
[14] Chan KM, Han J, Fang D, et al. A lesson learned from the H3.3K27M mutation found in pediatric glioma: a new approach to the study of the function of histone modifica-tions in vivo [J]. Cell Cycle, 2013, 12(16): 2546-2552.
[15] Piunti A, Hashizume R, Morgan MA, et al. Therapeutic targeting of polycomb and BET bromodomain proteins in diffuse intrinsic pontine gliomas [J]. Nat Med, 2017, 23(4): 493-500.
[16] Chan KM, Fang D, Gan H, et al. The histone H3.3K27M mutation in pediatric glioma reprograms H3K27 methylationand gene expression [J]. Genes Dev, 2013, 27(9): 985-990.
[17] Bender S, Tang Y, Lindroth AM, et al. Reduced H3K27me3 and DNA hypomethylation are major drivers of gene expre-ssion in K27M mutant pediatric high-grade gliomas [J]. Cancer Cell, 2013, 24(5): 660-672.
[18] Zarghooni M, Bartels U, Lee E, et al. Whole-genome profi-ling of pediatric diffuse intrinsic pontine gliomas highlights platelet-derived growth factor receptor alpha and poly (ADP-ribose) polymerase as potential therapeutic targets [J]. J Clin Oncol, 2010, 28(8): 1337-1344.
[19] Mohammad F, Weissmann S, Leblanc B, et al. EZH2 is a potential therapeutic target for H3K27M-mutant pediatric gliomas [J]. Nat Med, 2017, 23(4): 483-492.
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备注/Memo

备注/Memo:
通讯作者:张剑宁,E-mail:jnzhang@yahoo.com
更新日期/Last Update: 2021-02-25