Epigenetic stem cell signature in cancer

By M. Widschwendter, H. Fiegl, D. Egle, E. Mueller-Holzner, G. Spizzo, C. Marth, D. Weisenberger, Mihaela Campan, Joanne Young, I. Jacobs and 1 more. Nature Genetics, 2007

1,133 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/96d7bb5b6561e0e0ce53e1c88f0750585869b61f

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Citations in the corpus

Cancer epigenetics: Tumor Heterogeneity, Plasticity of Stem-like States, and Drug Resistance (2014, background): “…proportion of genes with this cancer specific change are those with a history of a specific pattern of chromatin regulation in embryonic stem cells (Schlesinger et al., 2007; Widschwendter et al., 2007; Ohm et al., 2007) and that we have also traced back to adult stem cells (Easwaran et al., 2012).”
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).”
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).”
Epigenetic Modifications as Therapeutic Targets (2010, background): “Notably, recent evidence has shown that genes targeted by the PRC in embryonic stem cells are more likely than others to become methylated in cance”
CpG islands and the regulation of transcription. (2011, positive): “Acquisition of CGI methylation in cancer has been found to occur preferentially at genes marked by H3K27me3 in ES cells (Ohm et al. 2007; Widschwendter et al. 2007; Illingworth et al. 2010).”
Bmi1 is essential in Twist1-induced epithelial–mesenchymal transition (2010, background): “Bmi1 is a member of the polycomb-repressive complex 1 (PRC1) that has an essential role in maintaining chromatin silencin”
Dynamic DNA methylation across diverse human cell lines and tissues (2013, neutral): “Genome Research 559 www.genome.org”
Gene Body Methylation can alter Gene Expression and is a Therapeutic Target in Cancer (2014, background): “This may also be due to transcription factor occupancy of reactivated genes and epigenetic switching for silenced genes, since most of de novo methylated promoter regions are targets of the polycomb repressive complex (Gal-Yam et al., 2008; Widschwendter et al., 2007).”
DNA methylation: superior or subordinate in the epigenetic hierarchy? (2011, background): “reported that PcG targets in ESCs were 12-fold more likely to become methylated in cancer.(69) Nearly 49% of genes methylated in colon cancer were PcG targets in ESCs in another study.”
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”
Epigenetics and Colorectal Cancer (2011, background): “It has also been proposed that the aberrant methylation of genes might lock stem cells in an undifferentiated state, predisposing them to malignant transformation”
eFORGE: A Tool for Identifying Cell Type-Specific Signal in Epigenomic Data (2016, result): “This is consistent with previous findings that DNAm changes in cancer tissue aid the emergence of a possible stem cell phenotype (Widschwendter 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.”
Polycomb group proteins: multi-faceted regulators of somatic stem cells and cancer. (2010, positive): “In support of this model, cancer cells frequently exhibit stem cell-like gene expression and chromatin structure signatures (Ben-Porath et al., 2008; Widschwendter et al., 2007).”