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The de Bruin lab's mission is to establish fundamental principles of听cell cycle control involved in the听maintenance of genome stability and cancer initiation听and development. The lab has used a wide range of听model organisms and approaches听with a final goal of finding ways to identify and exploit therapeutic听opportunities听for cancer鈥檚 addiction to growth and proliferation.听Our group has established the molecular mechanism by which G1/S听transcription is inactivated during S听phase and how it is maintained in听response to replication stress. Our work indicates that G1/S transcription听plays an essential role in the tolerance to replication stress. Since听replication stress is a major cause of听genomic听instability in cancer, this represents a crucial new area for cancer studies in听the lab.

听We recently established that cellular听growth has a central role in determining CDK inhibitor sensitivity. This听work听suggests that听independent of increased CDK activity, when cell division is inhibited, but听cell growth听continues, cells simply get too big to maintain a proliferative听state or maintain genome stability. Since听enhanced growth signalling is common听in cancers, this helps explain the anti-cancer efficacy of CDK听inhibitors. This听new insight is now being used to ask more specific questions to understand the听mechanisms听that determine a cell鈥檚 sensitivity to CDK inhibitors.