Abstract
Advances in sequencing technologies and the bioinformatic analysis of big data facilitate the study of jumping genes' activity in the human genome in cancer from a broad perspective. Retrotransposons, which move from one genomic site to another by a copy-and-paste mechanism, are regulated by various molecular pathways that may be disrupted during tumorigenesis. Active retrotransposons can stimulate type I IFN responses. Although accumulated evidence suggests that retrotransposons can induce inflammation, the research investigating the exact mechanism of triggering these responses is ongoing. Understanding these mechanisms could improve the therapeutic management of cancer through the use of retrotransposon-induced inflammation as a tool to instigate immune responses to tumors.