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Lakshmikuttyamma A et al. – Reexpression of hypermethylated p15INK4B and E–cadherin required histone H3K9 demethylation that was achieved directly by inhibiting SUV39H1 expression or activity, or indirectly by decreasing the amount of SUV39H1 associated with the p15INK4B and E–cadherin promoters using 5–aza–2'–deoxycytidine. The results from this study highlight the potential of H3K9 methyltransferases as therapeutic targets for reactivating expression of hypermethylated genes.

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