Epigenetics in Cancer

English Version

Classic genetics alone cannot explain the diversity of phenotypes within a population. Nor does classic genetics explain how, despite their identical DNA sequences, monozygotic twins or cloned animals can have different phenotypes and different susceptibilities to a disease. The concept of epigenetics offers a partial explanation of these phenomena. First introduced by C.H. Waddington in 1939 to name “the causal interactions between genes and their products, which bring the phenotype into being,” epigenetics was later defined as heritable changes in gene expression that are not due to any alteration in the DNA sequence.

The best-known epigenetic marker is DNA methylation. The initial finding of global hypomethylation of DNA in human tumors was soon followed by the identification of hypermethylated tumor suppressor genes, and then, more recently, the discovery of inactivation of microRNA (miRNA) genes by DNA methylation. These and other demonstrations of how epigenetic changes can modify gene expression have led to human epigenome projects and epigenetic therapies. Moreover, we now know that DNA methylation occurs in a complex chromatin network and is inf luenced by the modifications in histone structure that are commonly disrupted in cancer cells.

Epigenetic research uses powerful techniques for the study of DNA methylation, such as sodium bisulfite modification associated with polymerasechain-reaction procedures. Terms used in epigenetic research are defined in the Glossary. Comprehensive epigenomic techniques have yielded preliminary descriptions of the epigenomes of human cancer cells. This review summarizes new developments concerning hypermethylation of the promoter regions of tumor-suppressor genes and describes possible applications of epigenetics to the treatment of patients with cancer.

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