OBJECTIVE

To investigate the association between parity and exophytic bladder cancer growth in the UPII-SV40T transgenic mouse model of bladder cancer.

METHODS

The 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.

RESULTS

Multiparous 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.

CONCLUSIONS

These 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.