A key regulator of cell morphology is the actin cytoskeleton and it has long been appreciated that the cytoskeleton is characteristically altered in cancer. Actin is organized into polymeric structures with distinct dynamics which in turn participate in a wide variety of cell processes including adhesion, migration, cell division and apoptosis. Despite displaying an altered actin cytoskeleton, transformed cells retain--and in many cases increase--their ability to adhere, move, divide and respond to apoptotic stimuli. Thus cancer cells maintain responsive actin cytoskeletons. Actin dynamics are regulated by numerous actin-binding proteins and chief among these are the tropomyosins which are core components of the microfilament. Recent advances in genomic and proteomic profiling confirm that Tm expression profiles are profoundly changed in transformed cells. It is therefore timely to review the role of Tms in the regulation of actin dynamics that pertain to crucial phenotypic changes in cancer. In this review we discuss how actin filaments containing different Tm isoforms respond to the activation of cell signalling pathways and consider the implications of this for cancer progression and therapy.