Epithelial cells of PtenPEΔ/Δ prostates developed hyperplasia, subsequently forming prostate adenocarcinoma and rapidly progressing upon additional deletion of Jun. The aggressive phenotype observed in JunPEΔ/Δ; PtenPEΔ/Δ prostates resulted in decreased survival of mice and increased prostate weight and size. This evidence concerns the gene JUN and prostate adenocarcinoma.