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Issue 3, 2009
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Epigenetics in metal carcinogenesis: nickel, arsenic, chromium and cadmium

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Abstract

Although carcinogenic metals have been known to disrupt a wide range of cellular processes the precise mechanism by which they exert their carcinogenic effects is not known. Over the last decade or two, studies in the field of metal carcinogenesis suggest that epigenetic mechanisms may play a role in metal-induced carcinogenesis. In this review we summarize the evidence demonstrating that exposure to carcinogenic metals such as nickel, arsenic, chromium, and cadmium can perturb DNA methylation levels as well as global and gene specific histone tail posttranslational modification marks. We also wish to emphasize the importance of understanding that gene expression can be regulated by both genetic and epigenetic mechanisms and both these must be considered when studying the mechanism underlying the toxicity and cell transforming ability of carcinogenic metals and other toxicants, as well as aberrant changes in gene expression that occur during disease states such as cancer.

Graphical abstract: Epigenetics in metal carcinogenesis: nickel, arsenic, chromium and cadmium

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Publication details

The article was received on 13 Feb 2009, accepted on 24 Mar 2009 and first published on 09 Apr 2009


Article type: Tutorial Review
DOI: 10.1039/B903049B
Citation: Metallomics, 2009,1, 222-228
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    Epigenetics in metal carcinogenesis: nickel, arsenic, chromium and cadmium

    A. Arita and M. Costa, Metallomics, 2009, 1, 222
    DOI: 10.1039/B903049B

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