Abstract
The adenomatous polyposis coli gene (APC) is frequently mutated in sporadic colon cancer and has been described as a „gatekeeper“ for colon tumorigenesis. A recent paper published in the Journal of Cell Biology by Caldwell et al. reports that clinically relevant mutations in APC induce defective cytokinesis and aneuploidy, independent of Wnt signaling. This insight adds to evidence that mutations in APC may play a causative role in tumor formation in part by mediating genomic instability.