2021
DOI: 10.1016/j.jmb.2021.167094
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Epigenetic “Drivers” of Cancer

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Cited by 15 publications
(9 citation statements)
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“…2 e). Remarkably, the binding of p63 and Srebp appeared to largely overlap in the same genomic regions, that importantly appeared to be also enriched for permissive histone posttranslational modifications [ 81 ], such as acetylation of lysine 27 of histone 3 (H3K27ac), trimethylation of lysine 4 of histone 3 (H3K4me3) and acetylation of histone 4 (H4ac) (Fig. 2 e).…”
Section: Resultsmentioning
confidence: 99%
“…2 e). Remarkably, the binding of p63 and Srebp appeared to largely overlap in the same genomic regions, that importantly appeared to be also enriched for permissive histone posttranslational modifications [ 81 ], such as acetylation of lysine 27 of histone 3 (H3K27ac), trimethylation of lysine 4 of histone 3 (H3K4me3) and acetylation of histone 4 (H4ac) (Fig. 2 e).…”
Section: Resultsmentioning
confidence: 99%
“…We recently showed that in PDAC-derived mouse cells p53 controls metabolic pathways by transcriptionally regulating a gene expression programme impinging on aminoacid metabolism [30]. Within this, regulation of methionine uptake appeared to affect the biosynthesis of S-adenosyl-methionine, a major methyl donor, altering the ability of the cell to cope with perturbation of DNA methylation and triggering genomic instability [6,17,30]. Thus, a link between epigenetic regulation of chromatin and metabolism emerged as underlying control mechanism of p53-mediated genomic integrity [27,49].…”
Section: Resultsmentioning
confidence: 99%
“…Cancer has been historically seen as a genetic disease [ 24 ]. Epigenetic modifications are more frequent than genetic changes, and occur early in carcinogenesis rendering them possible therapeutic targets [ 25 ].…”
Section: Discussionmentioning
confidence: 99%