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Epigenetics of breast cancer

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In breast cancer there is a global 40% loss of methylated cytosine, but DNA hypermethylation indicates which genes are turned off in tumors and tumor cell lines. Every tumor type has its own pattern of hypermethylation. Genes important in familial breast cancer are also epigenetically silenced. In sporatic tumors, BRCA1 expression was wiped out by a combination of loss of heterozygosity (gene deletion) and epigenetic silencing (hypermethylation). In familial BRCA1 tumors, hypermethylation occasionally serves as an alternate mechanism for the 'second hit', when there was not loss of heterozygosity. Other known cancer genes are hypermethylated in breast cancers, such as those that affect cell cycle (p16 INK4a), and hormone receptors (ER, PR). New epigenomic approaches revealed the novel importance of potential tumor suppressor genes, such as the prolactin receptor and WRN, the Werner syndrome gene associated with premature aging and increased cancer risk, which is silenced in a subset of breast cancers. In addition to direct DNA hypermethylation, modification of histones is another epigenetic mechanism with implications in breast cancer. Overall, there is global loss of monomethylation and trimethylation of histone H4 in cancer. New epigenetic drugs targeting DNA methylation and histone deacetylation are in development for the treatment of breast cancer.

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Keywords

  • Breast Cancer
  • Prolactin
  • Familial Breast Cancer
  • Increase Cancer Risk
  • Histone Deacetylation