About the Project
Results so far showed that 70% of the patients harbour events in genes that can be hit by clinically available or investigated drugs. However, drug effects in some cases do not cover all oncogenic functions associated with the aberrated gene (e.g. EZH2) or, alternatively, can be circumvented by allosteric effects of other proteins (e.g. CDK4). In addition, there are still numerous driver events in paediatric cancer for which no drug is available (e.g. transcription factor fusion genes). The current project aims to target incompletely drugged or undruggable cancer drivers identified in high-risk paediatric cancer patients by developing tailored proteolysis-targeting chimeras (PROTACs). Instead of target inhibition, bifunctional PROTACs cause ubiquitination-mediated proteasomal degradation by recruiting E3 ligases to the targets of interest. PROTACs are associated with more potent and longer lasting effects compared to conventionally studied small-molecule drugs and open new avenues for improved paediatric cancer treatment.
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