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The epigenome and cancer prevention: A complex story of dietary supplementation.
- Source :
-
Cancer letters [Cancer Lett] 2014 Jan 28; Vol. 342 (2), pp. 275-84. Date of Electronic Publication: 2012 Jan 20. - Publication Year :
- 2014
-
Abstract
- Epigenetic changes have been implicated in virtually all types of human malignancies. In contrast to genetic changes, epigenetic changes occur in a gradual manner during the tumorigenic process and they are potentially reversible. Because epigenetic changes have frequently been detected in high-risk populations, they are attractive targets to prevent the initiation of premalignant lesions or their advance to a malignant stage. A wide range of chemical entities has been found capable of altering the epigenome in animal models and humans. Epidemiological and laboratory-based studies suggested that these agents may have an anti-neoplastic effect against different cancer types. Several of these agents have been tested as dietary supplements, often with conflicting results. In this review, we discuss recent developments in our understanding of agents capable of modulating the epigenome and their potential to prevent human cancer when administered as dietary supplements.<br /> (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)
- Subjects :
- Animals
Biomarkers, Tumor metabolism
Cell Transformation, Neoplastic drug effects
Cell Transformation, Neoplastic genetics
DNA Methylation drug effects
Gene Expression Regulation, Neoplastic drug effects
Histones metabolism
Humans
MicroRNAs metabolism
Neoplasms epidemiology
Neoplasms genetics
Neoplasms metabolism
Neoplasms pathology
Risk Factors
Anticarcinogenic Agents therapeutic use
Biomarkers, Tumor genetics
Dietary Supplements
Epigenesis, Genetic drug effects
Neoplasms prevention & control
Subjects
Details
- Language :
- English
- ISSN :
- 1872-7980
- Volume :
- 342
- Issue :
- 2
- Database :
- MEDLINE
- Journal :
- Cancer letters
- Publication Type :
- Academic Journal
- Accession number :
- 22266189
- Full Text :
- https://doi.org/10.1016/j.canlet.2012.01.021