It is now hoped that the present Symposium, dealing with another inexpensive and readily available food, tomatoes, will enhance interest in and funding for additional research, to underwrite future recommendations for possibly enhanced production and use of tomato-derived nutritional elements, with the goal of application to the prevention of major chronic diseases, the treatment of which is costly and often ineffective. Intervention trials designed to show a reduction of cancer incidence in the general population are logistically and practically impossible for most types of cancer, including cancer of the oral cavity. Thus evidence for chemoprevention must be indirect, using laboratory and animal models, epidemiologic surveys, and trials showing reversal of premalignant lesions or cancer prevention in high-risk groups. In several animal models, beta-carotene and other antioxidant nutrients inhibit oral carcinogenesis. Epidemiologic studies consistently relate low intake of these nutrients with high cancer risk.
Smokers have lower beta-carotene levels in plasma and oral mucosal cells than nonsmokers.
Eight clinical trials have now shown that beta-carotene and vitamin E produce regression of oral leukoplakia, but chemoprevention studies in oral leukoplakia have limitations, which we review. All available evidence supports a significant role for antioxidant nutrients in preventing oral cancer. Evidence supports the potential role of beta-carotene in cancer prevention. Although observational epidemiologic studies are not entirely consistent, many show an inverse association between dietary intake or blood levels of beta-carotene and subsequent cancer risk. However, because of the long latency period for cancer, which may be a decade or more, the six-year duration of treatment in this trial may have been inadequate to detect an anticancer effect.