Meta-Biol

• Pathways

FGFR3 fusions promote cellular proliferation and tumorigenesis that can be inhibited by tyrosine kinase inhibitors, suggesting that signaling is dependent on autophosphorylation of tyrosine residues in the intracellular region as is the case for WT FGFR3 (Singh et al, 2012; Parker et al, 2013; Williams et al, 2013; Wu et al, 2013; Yuan et al, 2014). FGFR3 fusions are reported to activate the ERK , STAT and AKT pathways, but not the PLC gamma pathway as the fusions generally lack the tyrosine residue required for PLC gamma recruitment (Parker et al, 2013; Williams et al, 2013; Wu et al, 2013; reviewed in Parker et al, 2014; Carter et al, 2015).