Polycomb-mediated methylation on Lys27 of histone H3 pre-marks genes for de novo methylation in cancer

By Yeshayahu Schlesinger, R. Straussman, I. Keshet, S. Farkash, M. Hecht, J. Zimmerman, Eran Eden, Zohar Yakhini, E. Ben-Shushan, B. Reubinoff and 3 more. Nature Genetics, 2007

1,230 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/3ec6d25f49edc64a5619e2ed0fe5a090c76f4882

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

Citations in the corpus

A double take on bivalent promoters. (2013, background): “Loci bivalent in ES cells are often found to be DNA-hypermethylated in adult cancers, and it was speculated that bivalency or the presence of PcG proteins might predispose those genes for later DNA hypermethylation (Ohm et al. 2007; Schlesinger et al. 2007; Widschwendter et al. 2007).”
Gene silencing in cancer by histone H3 lysine 27 trimethylation independent of promoter DNA methylation (2008, background): “Several groups have reported that genes marked by PcG in embryonic stem cells are more susceptible to DNA methylation in cance”
Distinct Epigenomic Landscapes of Pluripotent and Lineage-committed Human Cells (2010, background): “Previous studies have suggested that H3K27me3-marked promoters are linked to DNA hypermethylation in cancer cells (Ohm et al., 2007; Schlesinger et al., 2007; Viré et al., 2006; Widschwendter et al., 2007).”
A Novel CpG Island Set Identifies Tissue-Specific Methylation at Developmental Gene Loci (2008, background): “that are marked by association with polycomb group proteins in embryonic stem cells [47–49].”
Polycomb group proteins: navigators of lineage pathways led astray in cancer (2009, neutral): “A previously unidentified alternatively spliced isoform of t(8;21) transcript promotes leukemogenesis.”
Epigenetics and Colorectal Cancer (2011, background): “Furthermore, polycomb mediated pre-marks, indicated by histone H3K27 methylation, have been shown to recruit DNMTs, and could, therefore, have a role in the misdirection of methyltransferases in cancer”
CpG islands and the regulation of transcription. (2011, neutral): “Early studies suggested that CGI promoters may often lack TATA boxes and display heterogeneous TSSs (Reynolds et al. 1984).”
Phosphorylation of EZH2 activates STAT3 signaling via STAT3 methylation and promotes tumorigenicity of glioblastoma stem-like cells (2013, background): “…a significant subset of PRC2 target genes is repressed in various tumors, some of which are further silenced by promoter hypermethylation, implying crucial roles of the Polycomb pathway in cancer initiation and progression (Schlesinger et al., 2007; Viré et al., 2006; Widschwendter et al., 2007).”
Repression of E-cadherin by the polycomb group protein EZH2 in cancer (2008, background): “Cancer cells that contain DNA-methylated genes are specifically packaged in nuclesomes with the histone H3K27 trimethylation (Schlesinger et al., 2007).”
Epigenetic gene silencing in cancer: the DNA hypermethylome. (2007, methodology): “The use of epigenomic technologies for different acetylation and methylation modifications of histones (71,72) and methylated DNA (51,52) in embryonic stem cells provides a chromatin signature of pluripotent cell lines.”