Fgfr3 mutation is not the sole driver of tumorigenesis in the bladder.

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Fgfr3 mutation is not the sole driver of tumorigenesis in the bladder. Fgfr3mutation is not the sole driver of tumorigenesis in the bladder. The samples are from 12-month-old wild-type (A–D), UroIICre+Fgfr3+/K644E (E–H), UroIICre+Fgfr3+/K644M (I–L), UroIICre+Fgfr3+/K644EK-RasG12D/+ (M–P) and UroIICre+Fgfr3+/K644Eβ-cateninexon3/+ (Q–T) mice. Hematoxylin and eosin (H&E) staining showed no apparent lesions in the urothelium in all Fgfr3 mutants (A,E,I,M) except for the compound model with β-cateninexon3/+ (Q), in which hyperplasia was observed (red arrowhead; also in S,T). No significant cell proliferation was observed (B,F,J,N) except for the area of hyperplastic lesion in UroIICre+Fgfr3+/K644Eβ-cateninexon3/+ mice (black arrowhead) (R). Upregulation of pERK1/2 (G,K,O,S) and Sprouty2 (H,L,P,T) was observed in Fgfr3 mutant mice, compared with wild type (C,D, respectively). Scale bar: 200 μm. Imran Ahmad et al. Dis. Model. Mech. 2011;4:548-555 © 2011. Published by The Company of Biologists Ltd