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. Author manuscript; available in PMC: 2015 Oct 21.
Published in final edited form as: J Pathol. 2014 Mar 31;233(2):148–158. doi: 10.1002/path.4334

Table 1. Summary of mouse cohorts and bladder phenotype.

Genotype Cohort
size (n)		 Age
at time of
analysis		 Non-bladder
related deaths
(n)		 Increased
urothelial
thickness (n)		 Cellular
abnormalities
(n)
Control 11 10-18 months None None None
UroIICre
Fgfr3+/K644E 		25 5-15 months 2 (8%) None None
UroIICre
Ptenflox/flox 		20 9-18 months 4 (20%) 12 (60%) mild None
UroIICre
Fgfr3+/K644E
Ptenflox/flox 		24 11-18 months 4 (17%) 4 (17%) mild,
19 (79%) severe,
23 (96%) total		 20 (83%)
UroIICre
Fgfr3K644E/K644E 		12 7-13 month 10 (83%)* 11 (92%) mild None
UroIICre
Fgfr3K644E/K644E
Ptenflox/flox 		3 10-12 months None 2 (66%) severe 2 (66%)

The mouse cohorts analysed in this study are summarised. Cellular abnormalities observed include vacuolisation, enlarged cells, and loss of cell orientation within the urothelium. Causes of non-bladder related deaths include infection and lymphoma, and termination due to skin rash on the back owing to Cre-lox recombination occurred in the epidermis [18].

*

UroIICreFgfr3K644E/K644E mice were sacrificed at the time when kyphosis became prevalent. This phenotype is due to a low-level of Fgfr3 expression in the presence of homozygous Fgfr3K644Eneo allele [11].