Coordinated activities of wild-type plus mutant EZH2 drive tumor-associated hypertrimethylation of lysine 27 on histone H3 (H3K27) in human B-cell lymphomas

By C. Sneeringer, M. Scott, K. Kuntz, S. Knutson, R. Pollock, V. Richon, R. Copeland. Proceedings of the National Academy of Sciences of the United States of America, 2010

682 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/ef3ca560f431cc8c3c4d5f72629830c8f43e499d

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Citations in the corpus

Cancer epigenetics: from mechanism to therapy. (2012, background): “Functional characterization of this mutation demonstrated that it conferred increased catalytic activity and a preference for converting H3K27me1 to H3K27me2/3, again supporting the contention that EZH2 is an oncogene (Sneeringer et al., 2010).”
Epigenetic plasticity and the hallmarks of cancer (2017, background): “The gain-of-function mutations create a hyperactive methyltransferase enzyme (32, 33).”
Oncogenic histone methyltransferase EZH2: A novel prognostic marker with therapeutic potential in endometrial cancer (2017, neutral): “Additional findings to support an oncogenic role for EZH2 have recently emerged; recurrent mutations of the tyrosine 641 (Y641) and alanine 677 (A677) residues of EZH2 have been reported in B-cell lymphomas [23, 24].”
The role of mutations in epigenetic regulators in myeloid malignancies (2012, background): “Somatic heterozygous activating mutations in EZH2 at the Y641 reside were recently identified in germinal diffuse large B-cell lymphomas (69), and these mutations were shown to increase dimethylation and trimethylation of H3K27 in biochemical studies (70, 71).”
Selective Killing of Mixed Lineage Leukemia Cells by a Potent Small-Molecule DOT1L Inhibitor (2011, neutral): “Incorporation of radioactivity into nucleosome substrate was measured in a flashplate similar to previously described studies (Sneeringer et al., 2010).”
Transcriptional regulation by Polycomb group proteins (2013, background): “; and from the Novo Nordisk Foundation, the Danish Cancer Society and the Danish Council for Strategic Research (12-110503) to K.”
EZH2 is required for germinal center formation and somatic EZH2 mutations promote lymphoid transformation (2013, background): “DLBCL cell lines harboring EZH2 point mutations display aberrant accumulation of H3K27me3 compared to wild type (WT)-EZH2 cells (McCabe et al., 2012a; Sneeringer et al., 2010).”
EZH2 inhibition as a therapeutic strategy for lymphoma with EZH2-activating mutations (2012, background): “A new human B-cell non-Hodgkin’s lymphoma cell line (Karpas 422) exhibiting both t(14;18) and t(4;11) chromosomal translocations.”