A stem cell–like chromatin pattern may predispose tumor suppressor genes to DNA hypermethylation and heritable silencing

By Joyce Ohm, Kelly M. McGarvey, Xiaobing Yu, Linzhao Cheng, Kornel E. Schuebel, Leslie M. Cope, Helai P. Mohammad, Wei Chen, V. C. Daniel, Wayne Yu and 7 more. Nature Genetics, 2007

1,146 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/e300cd2e82eccf19455e409853edad42a8073cec

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Citations in the corpus

Linking DNA methylation and histone modification: patterns and paradigms (2009, background): “Indeed, several studies now show that a significant proportion of de novo methylated CpG islands are target sites for Polycomb protein bindin”
Cancer epigenetics: from mechanism to therapy. (2012, background): “regulators have raised intriguing correlations between cancerassociated DNA hypermethylation and genes marked with ‘‘bivalent’’ histone modifications in multipotent cells (Easwaran et al., 2012; Ohm et al., 2007).”
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).”
Polycomb group proteins: multi-faceted regulators of somatic stem cells and cancer. (2010, positive): “In fact, the PcG target genes identified in ESCs are 12 times more likely to be hypermethylated in cancers than non-PcG targets (Ohm et al., 2007; Widschwendter et al., 2007).”
Polycomb group proteins: navigators of lineage pathways led astray in cancer (2009, neutral): “Fusion of the nucleoporin gene NUP98 to HOXA9 by the chromosome translocation t(7;11)(p15;p15) in human myeloid leukaemia.”
DNA methylation and cancer. (2010, background): “It was postulated that first the target genes are marked by H3K27 methylation and then de novo DNA methylation of sequences of concern takes place (Ohm et al., 2007; Widschwendter et al., 2007).”
CpG islands and the regulation of transcription. (2011, positive): “…the pattern of polycomb-dependent gene silencing established in ES cells, DNA methylation may hypothetically facilitate maintenance of a ‘‘pseudo-pluripotent state,’’ thereby favoring unrestrained proliferation of cancer cells (Keshet et al. 2006; Ohm et al. 2007; Schlesinger 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].”
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”
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”
Regions of focal DNA hypermethylation and long-range hypomethylation in colorectal cancer coincide with nuclear lamina–associated domains (2011, background): “Although earlier work has shown enrichment of polycomb sites at methylation-prone promoter”