Oncogenic Mechanisms of Histone H3 Mutations.

Publication Type Review
Authors Weinberg D, Allis C, Lu C
Journal Cold Spring Harb Perspect Med
Volume 7
Issue 1
Date Published 01/03/2017
ISSN 2157-1422
Keywords Chromatin, Glioma, Histone-Lysine N-Methyltransferase, Histones, Mutation, Missense
Abstract Recurrent missense mutations in histone H3 were recently reported in pediatric gliomas and soft tissue tumors. Strikingly, these mutations only affected a minority of the total cellular H3 proteins and occurred at or near lysine residues at positions 27 and 36 on the amino-terminal tail of H3 that are subject to well-characterized posttranslational modifications. Here we review recent progress in elucidating the mechanisms by which these mutations perturb the chromatin landscape in cells through their effects on chromatin-modifying machinery, particularly through inhibition of specific histone lysine methyltransferases. One common feature of histone mutations is their ability to arrest cells in a primitive state refractory to differentiation induction, highlighting the importance of studying these mutations in their proper developmental context.
DOI 10.1101/cshperspect.a026443
PubMed ID 27864305
PubMed Central ID PMC5204328
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