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Deregulation of H3K27 methylation in cancer

Nature Genetics volume 42, pages 100–101 (2010)Cite this article

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A new study now reports recurrent somatic mutation of EZH2, a histone methyltransferase that modifies H3K27, in diffuse large B-cell lymphoma (DLBCL). There is now evidence for both increased and decreased activity of enzymes controlling H3K27 methylation in cancer, suggesting that a precise balance of this methylation is critical for normal cell growth.

Powerful high-throughput sequencing technologies are now facilitating the identification of somatic mutations in cancer. On page 181 of this issue, Marco Marra and colleagues1 report next-generation sequencing of genomic and tumor DNA from an individual with diffuse large B-cell lymphoma (DLBCL) and discovery of a somatic mutation of the EZH2 gene, located within an exon encoding the catalytic SET domain of the protein. This mutation was found in 22% DLBCL-derived samples and ∼10% of follicular lymphoma–derived samples but not in mantle cell or T-cell lymphoma. EZH2 is a polycomb-group protein that mediates repression of gene transcription through its histone 3 lysine 27 (H3K27) methyltransferase activity. This suggests a role for aberrant regulation of H3K27 methylation in cancer.

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Figure 1: Deregulation of H3K27 methylation in cancer.

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  1. Eva Martinez-Garcia and Jonathan D. Licht are in the Division of Hematology-Oncology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.,

    Eva Martinez-Garcia & Jonathan D Licht

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  1. Eva Martinez-Garcia
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  2. Jonathan D Licht
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Correspondence to Jonathan D Licht.

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Martinez-Garcia, E., Licht, J. Deregulation of H3K27 methylation in cancer. Nat Genet 42, 100–101 (2010). https://doi.org/10.1038/ng0210-100

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