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Purpose: To study the FGF signaling axis in prostate homeostasis and tumorigenesis, to evaluate dietary factors in modulating FGF signals in the prostate. Scope: To develop mouse models resembling human prostate tumor progressions for screening therapeutic strategies for prostate cancers and evaluating dietary factors in prostate cancer prevention. Major Finding: Ectopic expression of the constitutively-active FGFRI (caFGFRI) in the prostate induces high-grade prostatic intraepithelial neoplasia (PIN) in transgenic mice in an expression level-dependent manner. Repression of the resident FGFR2 in the prostate also disturbs homeostasis in the prostate as well as potentiated the PIN lesions induced by the ectopic caFGFRI. Up-to-date Progress: Establishing mouse colonies with prostate-specific disruption of Fgfr2 loci and expression of the ectopic caFGFRI in dependent of androgen for further characterizations of the FGF signaling and dietary factors in prostate lesions. Generation of a conditional expression vector for expressing FGFRI in the prostate. Characterization of the prostate of FGFR2 conditional null mice. Significance: Together with previous data from the Dunning prostate tumor model, the findings demonstrate that aberrant FGF signals in the prostate strongly disrupt tissue homeostasis, and promote prostate tumor development and progression. The model provides a useful tool for evaluating other tumor initiating factors, including those that cause genetic instability and other oncogenic lesions in prostate tumorigenesis.