Abstract
Abstract All of the studies on the global and selective gene promoter changes in epigenetic marks induced by carcinogenic Nickel compounds have been mostly done in tissue culture model systems. Here we report the results of the first study to evaluate the global changes in epigenetic marks and changes in gene expression that occur in the peripheral blood lymphocytes of a human population occupationally exposed to Nickel compounds. Nickel (II) is a toxic nonessential transition metal used in modern industry with other metals to form alloys to produce coins, jewelry, stainless steel, Ni-Cd batteries, and carbon nanoparticles. Nickel is of great environmental concern because occupational exposure to Ni compounds has been associated with an increased risk for lung and nasal cancers. Using an ELISA method, a decrease in both H3K4me3 and H3K9me2 histone marks were found with increasing levels of Nickel in the urine of subjects recruited to the study from a nickel refinery in Jinchang, China. Changes in global levels of other epigenetic marks are also being measured in the samples of subjects recruited to the study. Inter- and intra-individual variability of H3K4me3 and H3K9me2 and other epigenetic marks will also be evaluated in primary lymphocytes of this particular Chinese population. Additionally, changes in gene expression patterns between individuals with low exposure to Ni and those with higher exposure will be compared in order to identify a possible biomarker of Ni exposure. Studies on the effect of Ni compounds to human health are very important since Nickel is a classified human carcinogen. Here we are studying for the first time the mechanisms of nickel-associated changes in gene regulation and global histone epigenetic marks found in the primary lymphocytes of a human population occupationally exposed to Nickel compounds. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2012. doi:10.1158/1538-7445.AM2011-2012
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