**9. Conclusions**

The FP sarcomas presented here are characterized by chromosomal rearrangements that generate pathognomonic fusion transcripts and oncoproteins. It is certainly desirable to primarily block or destroy the translocation products of the sarcomas themselves with targeted therapeutic approaches. However, this has not yet been possible for the fusion transcription factors EWSR1-ETS, PAX3/7-FOXO1, and the SS18-SSX fusion oncogene. But it seems promising to prevent important binding partners of these fusion oncogenes, which are essential for mediating the oncogenic processes, from successfully binding to these fusion oncogenes. An example of this is the observed blockade of the interaction of EWSR1-FLI1 with RNA helicase A by YK-4-279, and the results of initial therapeutic interventions are of great interest here.

Currently, the greatest progress seems to be promised by approaches that address mediators of the fusion-positive interactome. Essential here seems the pathological takeover of the transcriptional machinery by these fusion oncogenes and the manifestation of their epigenetic state by histone deacetylases. Approaches that block epigenetic reader proteins such as BRD4 or transcription-specific cyclin kinases such as CDK 9 and 12 indicate promising results. The remarkable efficacy of HDAC inhibitors is highly interesting. Also, the use of these inhibitors seems to significantly reduce the stability of fusion oncogenes. On the other hand, particularly high therapeutic effects were achieved experimentally where these inhibitors were used in combination. It can therefore be assumed that targeted therapeutic approaches will be particularly successful in the future where they specifically address pathological processes of the fusion oncogenes and block several identified processes simultaneously. In doing so, the existing plasticity of the tumor must be kept in mind or synergistic processes must be identified by combining the drugs, which will probably make it possible to reduce their concentration and thus toxicity of individual doses.
