Since many years, researchers in the field of cell cycle and cell death are aware of the fact that both signaling pathways are ultimately connected, as defects in cell cycle control can trigger cell death. Both events are intimately linked to allow normal development, maintain tissue homeostasis and to prevent pathology, most importantly here, cancer.

The latter is also reflected by the fact that numerous anticancer agents trigger either DNA-damage or interfere with microtubule dynamics that affect cell cycle progression at different stages by activating different checkpoints. If these checkpoints cannot be satisfied, cell usually undergo senescence or, more frequently, cell death that can occur along different molecular routes. However, how checkpoint failure ultimately triggers cell death is still poorly investigated and key-molecules connecting both pathways are ill-defined.

Understanding this crosstalk at the molecular level will ultimately deepen our understanding of cancer pathogenesis in general and facilitate optimization of current and experimental cancer therapy regimens.
Given the relevance of both mechanisms in the control of cancer pathogenesis, their broad therapeutic drug-targeting potential but the rather limited communication between researchers working in the different fields, the main objectives of this workshop are:

  • Fill the gap of knowledge between the groups on basic molecular mechanisms of cell cycle, the DNA-damage response and cell death control
  • Pinpoint nodes of intersection, linking both signaling pathways
  • Define key-molecules at these intersections and discuss mechanisms controlling their function
  • Share information on possible consequences of deregulating these key-molecules from the level of single cell resolution (live-cell imaging) to the whole organism (e.g. mouse genetics)
  • Explore suitability of candidates as possible drug-targets, e.g. in preclinical models of malignant disease
  • Discuss translational aspects for human disease

Exchange of knowledge between researchers in both fields appears suboptimal, possibly also due to the historic view that both molecular mechanisms, i.e. cell cycle and cell death are evolutionary conserved, yet largely separate events. Both events are usually linked by DNA-damage response (DDR) pathways, which on their own are also highly complex.

Studying key-aspects of all these events appeared feasible only to few. However, most anticancer agents currently used to treat patients interfere with cell cycle control, ultimately triggering cancer cell death. Despite the obvious clinical importance of interfering with one pathway to activate the other, elements connecting cell cycle, DDR and cell death are still poorly defined. Nonetheless, our expanding knowledge on cell cycle and cell death control, driven also by the shortcomings of currently used anticancer agents, has helped to identify additional molecular targets in the cell cycle machinery that can be inhibited to trigger tumor cell death, e.g. microtubule-motor proteins or APC/C components.

Yet, again, molecular mechanisms triggering subsequent cell death remain largely unexplored but a better understanding of this crosstalk will help to explain the limited efficacy of some approaches. We believe that such a workshop will help to bridge the gap between researchers working in both fields either on basic molecular mechanisms, as well as those interested in basic as well as translational cancer research.





Universitätszentrum Obergurgl

Gaisbergweg 5

6456 Obergurgl


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