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A decade of exploring the cancer epigenome—biological and translational implications
Open accessAbstract
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.
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“Conversely, disruption of chromosomal topology and oncogene insulation may be more generally relevant to methylator phenotypes observed in colorectal and renal cell carcinomas, leukemia and other malignancies28.”
From Insulator dysfunction and oncogene activation in IDH mutant gliomas (2016) · cites this paper as [28]
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“Previous studies showed that enhanced histone acetylation induced by HDACi allowed the overexpression of genes involved in cell cycle arrest such as cyclin-dependent kinase inhibitors or the growth arrest and DNA damage-inducible protein GADD45 gene family (11, 28, 40, 45-49).”
From Histone Deacetylase (HDAC) Inhibitor Kinetic Rate Constants Correlate with Cellular Histone Acetylation but Not Transcription and Cell Viability (2013) · cites this paper as [11]
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“Insulator dysfunction may also be accompanied by promoter silencing events28,29, and by alterations to other pathways affected by 2-HG7,30.”
From Insulator dysfunction and oncogene activation in IDH mutant gliomas (2016) · cites this paper as [28]
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“Among them, novel selective benzamide-based HDAC1/2 inhibitors have been described that exhibit greater than 100-fold selectivity relative to other HDACs (11, 28).”
From Histone Deacetylase (HDAC) Inhibitor Kinetic Rate Constants Correlate with Cellular Histone Acetylation but Not Transcription and Cell Viability (2013) · cites this paper as [11]
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“It has previously been shown that HDAC inhibitors such as SAHA and MS-275 promote cell cycle arrest and apoptosis”
From Histone Deacetylase (HDAC) Inhibitor Kinetic Rate Constants Correlate with Cellular Histone Acetylation but Not Transcription and Cell Viability (2013) · cites this paper as [11]
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“Among activated genes that subside with pulsed HDACi administration are genes known to be powerful effectors of cell cycle arrest in multiple cell types and may promote apoptosis (11, 50).”
From Histone Deacetylase (HDAC) Inhibitor Kinetic Rate Constants Correlate with Cellular Histone Acetylation but Not Transcription and Cell Viability (2013) · cites this paper as [11]
Experimental — accuracy not yet measuredIn the citing paper
“Three general processes have major effects on cancer initiation and progression. First, discrete somatic mutations lead to tumor suppressor loss-of-function and oncoprotein gain-of-function [1]; second, epigenetic alterations change patterns of gene expression [2]; and third, alterations in the tumor microenvironment also lead to broad changes in gene expression [3].”
From The hypoxic tumor microenvironment: A driving force for breast cancer progression (2016) · cites this paper as [2]
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3 of the 166 references couldn’t be matched to a known paper.
Research works printed but not linked: 3
- Allis, C., Jenuwein, T. & Reinberg, D. Epigenetics (ed. Caparros, M.) (Cold Spring Harbor Laboratory Press, 2007).
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Metadata
- Authors
- Baylin, S. B., & Jones, P. A.
- Affiliations
- Johns Hopkins University (US)
- University of Southern California (US)
- Corresponding author
- Baylin, Stephen B.
- Jones, Peter A.
- Venue
- Nature Reviews Cancer
- Published
- 2011-09-23
- Volume
- 11
- Issue
- 10
- Pages
- 726-734
- ISSN
- 1474-175X (ISSN-L)
- 1474-1768
- PMC
- PMC3307543
- OpenAlex
- W2041686632
- Cited by
- 2,871
- References
- 166
- Citations by year
- 2026: 105 · 2025: 107 · 2024: 130 · 2023: 148 · 2022: 179 · 2021: 207 · 2020: 175 · 2019: 209 · 2018: 192 · 2017: 233 · 2016: 241 · 2015: 248 · 2014: 288 · 2013: 231 · 2012: 171
- FWCI
- 20.15
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature reviews. Cancer (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Entertainment Industry Foundation
- National Institutes of Health
- National Cancer Institute (R01CA043318, R37CA082422)
- National Institute of Environmental Health Sciences
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- cancer epigenome, DNA methylation, chromatin, epigenetic therapy, tumor markers, cancer diagnosis and prognosis, tumor progression, DNA packaging, epigenetic enzymes, cancer metabolism, epigenetic mutations
- MeSH terms
- Animals, Humans, Neoplasms, Genome, Epigenesis, Genetic, History, 20th Century, History, 21st Century, Translational Research, Biomedical, Epigenomics
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