Epigenetic processes converge on chromatin in order to direct a cell's gene expression profile. This includes both maintaining a stable cell identity, but also priming the cell for specific controlled transitions, such as differentiation or response to stimuli. In cancer, this normally tight control is often disrupted, leading to a wide scale hyper-plasticity of the epigenome and allowing stochastic gene activation and silencing, cell state transition, and potentiation of the effects of genetic lesions. Many of these epigenetic disruptions will confer a proliferative advantage to cells, allowing for a selection process to occur and leading to tumorigenesis even in the case of reversible or unstable epigenetic states. This review seeks to highlight how the fundamental epigenetic shifts in cancer contribute to tumorigenesis, and how understanding an integrated view of cancer genetics and epigenetics may more effectively guide research and treatment.
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Review Article| August 14 2020
Epigenetic plasticity, selection, and tumorigenesis
William A. Flavahan
Department of Pathology and Center for Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, U.S.A.
Correspondence: William A. Flavahan (firstname.lastname@example.org)
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William A. Flavahan; Epigenetic plasticity, selection, and tumorigenesis. Biochem Soc Trans 28 August 2020; 48 (4): 1609–1621. doi: https://doi.org/10.1042/BST20191215
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