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Epigenetic Changes of DNA Repair Genes in Cancer


Epigenetic Changes of DNA Repair Genes in Cancer

Christoph Lahtz et al. J Mol Cell Biol.


'Every Hour Hurts, The Last One Kills'. That is an old saying about getting old. Every day, thousands of DNA damaging events take place in each cell of our body, but efficient DNA repair systems have evolved to prevent that. However, our DNA repair system and that of most other organisms are not as perfect as that of Deinococcus radiodurans, for example, which is able to repair massive amounts of DNA damage at one time. In many instances, accumulation of DNA damage has been linked to cancer, and genetic deficiencies in specific DNA repair genes are associated with tumor-prone phenotypes. In addition to mutations, which can be either inherited or somatically acquired, epigenetic silencing of DNA repair genes may promote tumorigenesis. This review will summarize current knowledge of the epigenetic inactivation of different DNA repair components in human cancer.


Figure 1
Figure 1
Epigenetic inactivation of a DNA repair gene promoter. Promoters are often embedded within CpG islands. These CpG-rich sequences are usually unmethylated in normal tissues and are associated with the active histone mark H3K4me3. H3K4me3 prevents DNA methylation. During tumorigenesis, the CpG island becomes methylated, is associated with inactive chromatin marks (e.g. H3K9me3), and the gene becomes silenced.

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