Mouse Genome Informatics
cn
    Ptentm2Mak/Ptentm2Mak
Tg(Fabp1-cre)1Jig/0

involves: 129P2/OlaHsd * C57BL/6 * FVB/N
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
       
tumorigenesis
• mutants exhibit increased susceptibility to N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN)-induced bladder cancer, with 50% developing transitional cell carcinomas (TCC) and 25% developing carcinoma in situ (CIS) and dysplasia compared to 8% of wild-type mice developing TCC and 8% developing CIS and dysplasia at 16 weeks after BBN administration
• mutants develop spontaneous superficial papillary transitional cell carcinomas, with an incidence of 10% in 40-80 week old mutants

renal/urinary system
• two mutants exhibit hydronephrosis due to presence of large cancers in the bladder or renal pelvis
• thickening of the urothelial layer by 8 weeks of age due to increases in cell number and cell size
• urothelial hyperplasia is due to increased proliferation of bladder epithelial cells
• absolute numbers of bladder epithelial cells are increased 1.6-fold over wild-type levels at 8 weeks of age and 2.6-fold at 48 weeks of age
• size of individual bladder epithelial cells is greater than control cells; increase in size is not due to polyploidy as both diploid and tetraploid cell fractions are increased

homeostasis/metabolism
• mutants exhibit increased susceptibility to N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN)-induced bladder cancer, with 50% developing transitional cell carcinomas (TCC) and 25% developing carcinoma in situ (CIS) and dysplasia compared to 8% of wild-type mice developing TCC and 8% developing CIS and dysplasia at 16 weeks after BBN administration

Mouse Models of Human Disease
OMIM IDRef(s)
Bladder Cancer 109800 J:113388