A decade of exploring the cancer epigenome — biological and translational implications

By S. Baylin, Peter A. Jones. Nature Reviews. Cancer, 2011

2,776 citations recorded by the source corpus.

The past decade has highlighted the central role of epigenetic processes in cancer causation, progression and treatment. Next-generation sequencing is providing a window for visualizing the human epigenome and how it is altered in cancer. This view provides many surprises, including linking epigenetic abnormalities to mutations in genes that control DNA methylation, the packaging and the function of DNA in chromatin, and metabolism. Epigenetic alterations are leading candidates for the development of specific markers for cancer detection, diagnosis and prognosis. The enzymatic processes that control the epigenome present new opportunities for deriving therapeutic strategies designed to reverse transcriptional abnormalities that are inherent to the cancer epigenome.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/3e4a500d60aba8bc4b3b4946a9466878c20baaad

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Citations in the corpus

Large-Scale Discovery of Disease-Disease and Disease-Gene Associations (2016, background): “…to better understand the severity of patients symptoms 17 , to anticipate onset and path of disease progressions (particularly important for cancer patients in later stages 18 ), or to better understand disease processes on a molecular level enabling the development of better treatments 19 .”
Cancer epigenetics: from mechanism to therapy. (2012, background): “More recently, high-resolution genome-wide mapping of this modification in pluripotent and differentiated cells has also confirmed the dynamic nature of DNAmethylation, evidently signifying the existence of an enzymatic activity within mammalian cells that either erases or alters this chromatin modi”
Occupying chromatin: Polycomb mechanisms for getting to genomic targets, stopping transcriptional traffic, and staying put (2013, neutral): “The importance of dissecting PcG mechanisms is heightened by an expanding body of literature that implicates PcG machinery in gene regulatory networks gone awry in cancer cells (reviewed in Baylin and Jones, 2011; Bracken and Helin, 2009; Mills, 2010; Simon and Lange, 2008).”
Evolution of the cancer stem cell model. (2014, background): “Epigenetic modiﬁcations of DNA, histones, and nucleosomes as well as noncoding RNAs, including miRNA, allow for modiﬁcation of gene expression (Baylin and Jones, 2011; Iorio and Croce, 2012).”
Inhibiting DNA methylation causes an interferon response in cancer via dsRNA including endogenous retroviruses (2015, neutral): “Mechanisms can include reversal of abnormal promoter DNA methylation, re-expression of silenced genes including tumor suppressors (Baylin and Jones, 2011), and changes to cancer signaling pathways including apoptosis, cell-cycle activity, and stem cell functions (Tsai et al.”
High-resolution genome-wide DNA methylation maps of mouse primary female dermal fibroblasts and keratinocytes (2014, neutral): “The present understanding of CG methylation suggests a diverse role in genome regulation including in the determination of cell type specificity, cellular differentiation, suppression of transposable elements, X-chromosome inactivation, genomic imprinting, DNA-protein interaction and tumerogenesis [”