Abstract
Retinoids are well established chemopreventive agents for experimental carcinogenesis of many target organs including mammary gland, urinary bladder, lung, skin, liver, pancreas, colon and esophagus. Modification of the basic retinoid structure has produced analogs with enhanced target organ specificity, increased inhibitory activity and reduced toxicity. N-(4-hydroxyphenyl) retinamide (4-HPR) currently appears to be the most efficaceous retinoid against carcinogen-induced breast, urinary bladder, and lung cancer in rodents. Retinoids are most effective when administered shortly after the carcinogen treatment; however, the treatment can be delayed significantly while maintaining its chemopreventive effect. Under various experimental conditions, combining retinoid treatment with other modifiers of growth enhances its chemopreventive activity; for example, retinoid plus hormonal modulation can provide better protection against mammary cancer than either treatment alone. The role of carotenoids in cancer chemoprevention is less well defined. Studies have been complicated by the poor absorption and low tissue levels of carotenoids in the rodent models used for such studies. Aside from experimental skin carcinogenesis, little information is available relative to the effect of carotenoids on the chemoprevention of cancer at other organ sites.