In:
Science, American Association for the Advancement of Science (AAAS), Vol. 346, No. 6216 ( 2014-12-19), p. 1458-1459
Abstract:
Diffuse intrinsic pontine glioma (DIPG) is an incurable pediatric brain tumor. About 80% of these tumors contain mutations in genes that encode histones (H3.3 or H3.1) ( 1 , 2 ), proteins that package DNA into chromatin. These mutations, which change lysine 27 to methionine (K27M), are believed to sequester Polycomb repressive complex 2 (PRC2), which normally represses gene expression through histone methylation (see the figure). In the absence of PRC2, genes that should be silent are expressed, which is thought to drive cell transformation ( 3 – 5 ). However, the precise role of histone mutations in tumorigenesis is unclear, and strategies to target the mutations remain elusive. As reported by Funato et al. on page 1529 of this issue ( 6 ), as well as by Hashizume et al. ( 7 ), models of K27M-mutant DIPG can be used to elucidate the mechanisms of transformation and to identify new approaches to therapy.
Type of Medium:
Online Resource
ISSN:
0036-8075
,
1095-9203
DOI:
10.1126/science.aaa3814
Language:
English
Publisher:
American Association for the Advancement of Science (AAAS)
Publication Date:
2014
detail.hit.zdb_id:
128410-1
detail.hit.zdb_id:
2066996-3
detail.hit.zdb_id:
2060783-0
SSG:
11
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