Milea Timbergen

71 mutation present in DTF, it is clear that Wnt/β-catenin signalling is activated which plays an essential role in carcinogenesis. Inhibition of this pathway may provide a vulnerability in DTF that can therapeutically be exploited. However, drugs should operate at the level of β-catenin, interacting with transcription co-factors or target specific key downstream factors to avoid serious adverse effects 43, 44 . Additionally, other signalling pathways like Notch1 and Hedgehog have also been implicated to play a role in DTF development and may be therapeutically targeted by small molecules 45, 46 . Future studies are needed to gain more insight into the role of these additional signalling pathways, the cross-talks between each pathway and their contribution to the DTF tumorigenesis. Conclusions Our study demonstrated no difference between either WT, S45F or T41A mutated DTF tumours regarding the investigated Wnt target gene expression levels. Apparently a differential Wnt/β-catenin signalling activity does not determine the observed differences in clinical behaviour between S45F and T41A DTF mutants. 3