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Glioblastoma

Histone mutations take the MYCN

Nature Reviews Cancer volume 13, pages 382–383 (2013)Cite this article

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the gene expression signatures from GBMs with G34 and K27 mutations are significantly different

Jones and colleagues used two independent data sets to verify their initial observation that the gene expression signatures from GBMs with G34 and K27 mutations are significantly different. The authors then made use of the KNS42 cell line, which was established from a 16-year-old patient with GBM and which has a G34V mutation in H3F3A (which encodes one of the H3.3 proteins). Global levels of H3K36me3 were unchanged in these cells, unlike a previously published single GBM sample with a G34R H3F3A mutation in which H3K36me3 levels were increased. The authors used chromatin immunoprecipitation linked with next-generation whole-genome sequencing (ChIP–seq) to look at the binding of an H3K36me3-specific antibody in KNS42 cells compared with GBM cells that had wild-type H3F3A. There were 156 genes found to be differentially bound, and, consistent with the fact that H3K36me3 is associated with active chromatin, RNA polymerase II was also bound to many of these genes in KNS42 cells. Moreover, these differentially bound and expressed genes were present in the gene signatures associated with G34-mutant GBMs.

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References

ORIGINAL RESEARCH PAPER

  1. Bjerke, L. et al. Histone H3.3 mutations drive pediatric glioblastoma through upregulation of MYCN. Cancer Discov. 28 Mar 2013 (doi:10.1158/2159-8290.CD-12-0426)

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FUTHER READING

  1. Lewis, P. W. et al. Inhibition of PRC2 activity by a gain-of-function H3 mutation found in pediatric glioblastoma. Science 28 Mar 2013 (doi:10.1026/science.1232245)

  2. McCarthy, N. The histones have it. Nature Rev. Cancer 8 Apr 2013 (doi:10.1038/nrc3517)

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Authors
  1. Nicola McCarthy
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McCarthy, N. Histone mutations take the MYCN. Nat Rev Cancer 13, 382–383 (2013). https://doi.org/10.1038/nrc3527

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