Human epidemiology suggests a protective effect of tomatoes or tomato
phytochemicals, such as
lycopene, on
prostate cancer risk. However, human epidemiology alone cannot reveal causal relations. Laboratory animal models of
prostate cancer provide opportunities to investigate hypotheses regarding dietary components in precisely controlled, experimental systems, contributing to our understanding of diet and
cancer risk relations. We review the published studies evaluating the impact of tomatoes and/or
lycopene in preclinical models of prostate
carcinogenesis and
tumorigenesis. The feeding of tomatoes or tomato components demonstrates anti-
prostate cancer activity in both transplantable xenograft models of
tumorigenesis and models of chemically- and genetically-driven
carcinogenesis. Feeding pure
lycopene shows anticancer activity in most studies, although outcomes vary by model system, suggesting that the impact of pure
lycopene can depend on dose, duration, and specific carcinogenic processes represented in different models. Nonetheless, studies with the transgenic
adenocarcinoma of the mouse prostate (TRAMP) model of
carcinogenesis typically demonstrate similar bioactivity to that of tomato feeding. In general, interventions that commence earlier in
carcinogenesis and are sustained tend to be more efficacious. Accumulated data suggest that
lycopene is one, but perhaps not the only, anticancer bioactive compound in tomatoes. Although it is clear that tomatoes and
lycopene have anti-
prostate cancer activity in rodent models, major knowledge gaps remain in understanding dose-response relations and molecular mechanisms of action. Published and future findings from rodent studies can provide guidance for translational scientists to design and execute informative human clinical trials of
prostate cancer prevention or in support of
therapy.