CONCLUSION

In summary, we have demonstrated that changes in the DNA content as seen in human prostate cancer cells is also seen in our transgenic model. Furthermore, introducing an oncogene that is known to interact with proteins involved in growth factor-activated MAPK module of the signal transduction pathway caused prostatic pathology. In addition, the malignancies seen in the prostates of our transgenic mice are of epithelial origin as seen in human patients and therefore a relevant model system. Finally, pPEV has been designed to function as a universal, androgen-regulated expression system, and as such, it will be an extremely useful vector for rapidly cloning and targeting transgene expression to the prostate gland.