We have intrinsic properties of components of human centromeres, finding them to be surprisingly elastic. These elastic components become rigidified when incorporated into active kinetochores, and suppress centromeric accessibility, thereby suppressing transcription. These data have massive consequences for translocations in cancer cells where we have mapped centromere-like domains in euchromatin, which are sites of fragility. The current focus is to establish whether centromere-like domains in fragile sites can alter the structural stability of those sites.