The DOI matches its Crossref record; 191 of the 191 references it cites were found in a registry or an index.
Cancer as a dysregulated epigenome allowing cellular growth advantage at the expense of the host
Abstract
Although at the genetic level cancer is caused by diverse mutations, epigenetic modifications are characteristic of all cancers, from apparently normal precursor tissue to advanced metastatic disease, and these epigenetic modifications drive tumour cell heterogeneity. We propose a unifying model of cancer in which epigenetic dysregulation allows rapid selection for tumour cell survival at the expense of the host. Mechanisms involve both genetic mutations and epigenetic modifications that disrupt the function of genes that regulate the epigenome itself. Several exciting recent discoveries also point to a genome-scale disruption of the epigenome that involves large blocks of DNA hypomethylation, mutations of epigenetic modifier genes and alterations of heterochromatin in cancer (including large organized chromatin lysine modifications (LOCKs) and lamin-associated domains (LADs)), all of which increase epigenetic and gene expression plasticity. Our model suggests a new approach to cancer diagnosis and therapy that focuses on epigenetic dysregulation and has great potential for risk detection and chemoprevention.
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Cites
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Cited by
Epigenetic plasticity and the hallmarks of cancer
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“However, pervasive alterations in chromatin state, methylation, and gene expression suggest that the contributions of epigenetic alterations must also be carefully considered (3, 92).”
BackgroundEpigenetic Determinants of Cancer
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Epigenetic silencing of TH1-type chemokines shapes tumour immunity and immunotherapy
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Epigenetic modulators, modifiers and mediators in cancer aetiology and progression
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Self-citationThe Key Role of Epigenetics in Human Disease Prevention and Mitigation
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Self-citation
Metadata
- Authors
- Timp, W., & Feinberg, A. P.
- Venue
- Nature Reviews Cancer
- Published
- 2013-06-13
- Volume
- 13
- Issue
- 7
- Pages
- 497-510
- ISSN
- 1474-175X (ISSN-L)
- 1474-1768
- OpenAlex
- W1990711772
- Cited by
- 586
- References
- 191
- FWCI
- 4.61
- Type
- journal article
- Language
- en
- Open access
- closed
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