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Cancer is a complex disorder characterized by intricate genetic and epigenetic events. Elucidating the mechanism behind these events may help design appropriate therapeutic strategies. We propose a model where activated oncogenes compromise the replication process, triggering the DNA damage response (DDR) pathway, fueling genomic instability. Based on our findings genomic instability is now considered as an enabling hallmark of cancer. Moreover we present a novel pathway linking DDR with the alternative reading frame (ARF), a major tumor suppressor. We propose how this interlink can be therapeutically exploited. Finally, we discuss the role of deregulated replication-licensing within the oncogene-damage induced model.

Cell movement is driven by a spatially extended, self-organized, mechanochemical machine consisting of numerous actin polymers, accessory proteins and molecular motors. This impressive assembly self-organizes over several orders of magnitude in space and time, from the fast dynamics of individual molecular-sized building blocks to the persistent motion of whole cells over minutes and hours. We focus on the mechanisms underlying this remarkable self-organization using the simplest available model systems. We combine quantitative analysis of cell morphology and spatio-temporal dynamics at the molecular level with biophysical measurements, toward the goal of understanding how global cell shape and movement are determined. Our results feed into and direct the development of theoretical models of moving cells.