Abstract
Approximately 45% of the human genome is composed of transposable elements (TEs). Expression of these elements is tightly regulated during normal development. TEs may be expressed at high levels in embryonic stem cells but are epigenetically silenced in terminally differentiated cells. As part of the global 'epigenetic dysregulation' that cells undergo during transformation from normal to cancer, TEs can lose epigenetic silencing and become transcribed, and, in some cases, active. Here, we summarize recent advances detailing the consequences of TE activation in cancer and describe how these understudied residents of our genome can both aid tumorigenesis and potentially be harnessed for anticancer therapies.
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