Accepted_test
Over half of the human genome consists of interspersed repeats that result from copy-and-paste events carried out by retrotransposons. These elements are typically kept in check through epigenetic silencing to prevent genome instability. In cancer, changes in the epigenetic landscape can lead to abnormal expression of these genetic elements, which can act as internal mutagens and contribute to clonal evolution and cancer development. Our specific goal is to uncover new regulatory mechanisms, networks, and potentially genomic elements that control the transcriptional activity of retroelements in both cancer and normal cells. By conducting a thorough analysis of high-throughput transcriptional datasets and developing new computational frameworks, we hope to identify potential regulatory mechanisms that control retrotransposon expression in both normal and cancer cells, bridging the gap between seemingly unrelated observations of epigenetic target inhibition and retrotransposon expression.