TAILIEUCHUNG - Tissue of origin determines cancer-associated CpG island promoter hypermethylation patterns

Antioxidant molecules have been shown to counteract oxidative stress in laboratory experiments (for example, in cells or animal studies). However, there is debate as to whether consuming large amounts of antioxidants in supplement form actually benefits health. There is also some concern that consuming antioxidant supplements in excessive doses may be harmful. Vegetables and fruits are healthy foods and rich sources of antioxidants. Official . Government policy urges people to eat more vegetables and fruits. Concerns have not been raised about the safety of any amounts of antioxidants in food. For more information on antioxidants in foods, visit the | Sproul et al. Genome Biology 2012 13 R84 http 2012 13 10 R84 Genome Biology RESEARCH Open Access Tissue of origin determines cancer-associated CpG island promoter hypermethylation patterns 13 1 1 14 Duncan Sproul Robert R Kitchen Colm E Nestor J Michael Dixon Andrew H Sims David J Harrison Bernard H Ramsahoye1 5 and Richard R Meehan1 2 Abstract Background Aberrant CpG island promoter DNA hypermethylation is frequently observed in cancer and is believed to contribute to tumor progression by silencing the expression of tumor suppressor genes. Previously we observed that promoter hypermethylation in breast cancer reflects cell lineage rather than tumor progression and occurs at genes that are already repressed in a lineage-specific manner. To investigate the generality of our observation we analyzed the methylation profiles of 1 154 cancers from 7 different tissue types. Results We find that 1 009 genes are prone to hypermethylation in these 7 types of cancer. Nearly half of these genes varied in their susceptibility to hypermethylation between different cancer types. We show that the expression status of hypermethylation prone genes in the originator tissue determines their propensity to become hypermethylated in cancer specifically genes that are normally repressed in a tissue are prone to hypermethylation in cancers derived from that tissue. We also show that the promoter regions of hypermethylation-prone genes are depleted of repetitive elements and that DNA sequence around the same promoters is evolutionarily conserved. We propose that these two characteristics reflect tissue-specific gene promoter architecture regulating the expression of these hypermethylation prone genes in normal tissues. Conclusions As aberrantly hypermethylated genes are already repressed in pre-cancerous tissue we suggest that their hypermethylation does not directly contribute to cancer development via silencing. Instead aberrant hypermethylation reflects .

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