Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3903196 | Urology | 2008 | 4 Pages |
ObjectivesTo investigate the association between parity and exophytic bladder cancer growth in the UPII-SV40T transgenic mouse model of bladder cancer.MethodsThe UPII-SV40T transgenic mice express the simian virus 40 large T antigen specifically in the urothelium (driven by uroplakin II promoter) and reliably develop bladder cancer. UPII-SV40T transgenic female mice were either never bred (nulliparous; n = 6) or placed in breeding pairs and allowed full-term pregnancies and lactation. Multiparous animals (n = 5) had between 2 and 4 litters. UPII-SV40T transgenic male mice were sham-operated (intact; n = 9) or castrated (n = 8) at 24 weeks of age. Noninvasive, contrast-enhanced, flat panel detector-based, cone beam computed tomographic imaging of animals at 32 weeks of age permitted quantification of bladder cancer volumes.ResultsMultiparous animals had significantly smaller bladder cancers than their nulliparous female (P < .001) and intact male (P = .007) counterparts but not different from castrated males. Bladder cancer volume in nulliparous females was significantly larger than castrated males (P < .001) but not different from intact males.ConclusionsThese results suggest that pregnancy, parity, lactation, or a combination of these may play a protective role in bladder cancer by inhibiting tumor growth. This could be an important model system for studying the effects of pregnancy/lactation hormones on bladder cancer, which could lead to identification of additional risk factors of bladder cancer.