Vitamin A, retinoids and breast cancer.

Both epidemiologic and experimental evidence are highly suggestive of an inverse relationship between vitamin A status and cancer induction. However, protection by vitamin A and retinoids has not been a universal finding, nor are the compounds equally effective in inhibiting cancer induction at all organ sites. Although the experimental evidence for a protective effect of retinoids is especially strong for mammary cancer, the epidemiologic evidence is less convincing. Chronic pharmacologic administration of retinoids may be limited by their potential toxicity; such potential toxicity is particularly important in light of the expectation that, in order to achieve effective anticarcinogenesis in a clinical setting, administration of retinoids may be required at relatively high doses for extended periods. Clinical trials to determine the efficacy of several retinoids as cancer preventive agents are only in the early stages. Meanwhile, experimentation to develop synthetic vitamin A analogs with increased activity, increased target organ specificity, and reduced toxicity must continue. The question of increasing anticarcinogenic activity by increasing vitamin A intake in populations whose vitamin A status is normal is more difficult to assess. The vast majority of epidemiologic studies indicate that groups with a relatively high intake of carotenoids are at a reduced risk for cancer in several target tissues. However, in populations whose vitamin A status is not deficient, increases in vitamin A and carotene intake are not well correlated with increases in serum vitamin A.(ABSTRACT TRUNCATED AT 250 WORDS)