Cited by 2,871Epigenetics and DNA MethylationChromatin Remodeling and CancerGenomics and Chromatin Dynamics

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

Open access
Baylin, Stephen B., Jones, Peter A.·2011·Nature Reviews Cancer

Abstract

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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Crossref · 10.1038/nrc3130

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163 of 163 references verified0 citation errors · 0 not checkable

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  • 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 malignancies.

    “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]

    In “Promoter CpG island DNA hypermethylation” (page unavailable), the paper describes methylation of an H19 insulator, loss of CTCF binding, and IGF2 activation in pre-neoplastic kidneys, with a link to colon cancer progression. In “Genetics meets epigenetics” (page unavailable), it discusses methylator phenotypes in gliomas and increased DNA hypermethylation in leukaemia. It does not link disrupted chromosomal topology or oncogene insulation to methylator phenotypes across the named cancers, and its kidney example concerns Wilms’ tumour rather than renal cell carcinoma. (LLM, conf=0.84)

    Experimental — accuracy not yet measured
  • Enhanced histone acetylation induced by HDACi allows overexpression of genes involved in cell cycle arrest, such as cyclin-dependent kinase inhibitors or the GADD45 gene family.

    “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]

    In ‘The potential for epigenetic therapy for cancer’ (page unavailable), the review says HDAC inhibitors inhibit histone deacetylation and can augment gene reactivation when combined with DNA methyltransferase inhibitors. It does not say that HDAC inhibitors cause overexpression of cell-cycle-arrest genes, or identify cyclin-dependent kinase inhibitors or GADD45 as examples. (LLM, conf=0.82)

    Experimental — accuracy not yet measured
  • Insulator dysfunction may also be accompanied by promoter silencing events and by alterations to other pathways affected by 2-HG.

    “Insulator dysfunction may also be accompanied by promoter silencing events28,29, and by alterations to other pathways affected by 2-HG7,30.”
  • Novel selective benzamide-based HDAC1/2 inhibitors have been described that exhibit greater than 100-fold selectivity relative to other HDACs.

    “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]

    The section 'The potential for epigenetic therapy for cancer' discusses HDAC inhibitors generally, but does not describe benzamide-based HDAC1/2 inhibitors or their selectivity. Searches for benzamide, HDAC1/2, and 100-fold selectivity found no passage addressing those details; page numbers are unavailable in our copy. (LLM, conf=0.73)

    Experimental — accuracy not yet measured
  • HDAC inhibitors such as SAHA and MS-275 promote cell cycle arrest and apoptosis.

    “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]

    In “The potential for epigenetic therapy for cancer” (page not available), the review discusses HDAC inhibitors and vorinostat, identified as SAHA in the References. It does not say that SAHA or MS-275 promotes cell-cycle arrest or apoptosis; searches for those effects and MS-275 found no supporting passage. (LLM, conf=0.74)

    Experimental — accuracy not yet measured

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Cites

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3 of the 166 references couldn’t be matched to a known paper.

Research works printed but not linked: 2

  1. [2]Allis C Jenuwein T Reinberg D Caparros M Epigenetics Cold Spring Harbor Laboratory Press 2007
  2. [29]Allis CD Jenuwein T Reinberg D Overview and concepts Cold Spring Harbor Laboratory Press New York 2007

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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
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
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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