Cover image

Although human L1 elements are actively mobilized in many cancers, a role for somatic L1 retrotransposition in tumor initiation has not been conclusively demonstrated. In this issue, a new study shows that L1 can initiate colorectal cancer by evading somatic repression and then mutating the gatekeeper APC tumor suppressor gene in normal colon cells. The illustration depicts an L1 source element (labeled “L1”) generating a new somatic L1 insertion that disrupts the APC gene (arrow depicting mobilization). The highly active “hot” L1 source element that generated the insertion is found only in specific human populations, suggesting that some L1s can create a novel form of ancestry-specific cancer risk. (Cover illustration by Jennifer Fairman, © Fairman Studios, LLC, 2016. [For details, see Scott et al., pp. 745–755.])