Epigenetic mechanisms in commonly occurring cancers

Abstract

Cancer is a collection of very complex diseases that share many traits while differing in many ways as well. This makes a universal cure difficult to attain, and it highlights the importance of understanding each type of cancer at a molecular level. Although many strides have been made in identifying the genetic causes for some cancers, we now understand that simple changes in the primary DNA sequence cannot explain the many steps that are necessary to turn a normal cell into a rouge cancer cell. In recent years, some research has shifted to focusing on detailing epigenetic contributions to the development and progression of cancer. These changes occur apart from primary genomic sequences and include DNA methylation, histone modifications, and miRNA expression. Since these epigenetic modifications are reversible, drugs targeting epigenetic changes are becoming more common in clinical settings. Daily discoveries elucidating these complex epigenetic processes are leading to advances in the field of cancer research. These advances, however, come at a rapid and often overwhelming pace. This review specifically summarizes the main epigenetic mechanisms currently documented in solid tumors common in the United States and Europe.

FIG. 1.

DNA methylation, histone modification, and micro RNA (miRNA) expression work together to control the complex environment of epigenetics in cancer. Promoter hypomethylation is linked to the expression of genes, including miRNA, DNA methyltransferases (DNMTs), and histone modifiers (1). DNMTs can, in turn, hypermethylate promoters and turn off these same genes (2). Histone-modifying enzymes can affect gene expression by adding or removing certain marks (3). miRNAs are processed and targeted to mRNA, leading to a decrease in the protein expression of certain enzymes (4).