This review summarizes current findings with respect to melatonin and breast and endometrial cancer. Melatonin appears to have a role in cancer prevention. Laboratory studies indicate that the mechanism of action of melatonin against breast cancer is multi-faceted, including antioxidant, antimitotic, and antiangiogenic activity, as well as effects in the immune system and fat metabolism. Melatonin might be involved in the regulation of tumor growth. Melatonin appears to block estrogen receptor alpha (ERα) and affect aromatase. Epidemiologic studies have found a relationship between night shift work and melatonin production. Both case-control and prospective population studies have linked night shift work with higher breast cancer risk and, more recently, endometrial cancer (also highly sensitive to estrogen). The support for an association between sleep duration and risk of breast cancer is less convincing. The authors comment that additional studies are needed to further delineate the potential of melatonin in cancer prevention.

This review describes the properties of melatonin as it involves epigenetic mechanisms of breast cancer. Epigenetic changes are alterations in gene expression not caused by changes in the underlying DNA. Five types of evidence suggest that melatonin works via epigenetic processes. Melatonin has been shown to (1) influence transcriptional activity of nuclear receptors (ERα, GR and RAR) participating in the regulation of breast cancer cell growth; (2) downregulate the expression of genes responsible for the local synthesis or activation of estrogens, including aromatase (possibly mediated by methylation of the CYP19 gene or deacetylation of CYP19 histones); (3) inhibit telomerase activity and expression induced by natural estrogens and synthetic compounds with estrogenic properties; (4) influence the cell cycle through the inhibition of cyclin D1 expression; (5) influence circadian rhythm disturbances caused by light at night and similar alterations of the light/dark cycle, with the subsequent deregulation of PER2, which functions as a tumor suppressor gene.

Using six different measures, the study evaluated the antioxidant potency of the following juices and drinks: apple juice, açaí juice, black cherry juice, blueberry juice, cranberry juice, Concord grape juice, orange juice, red wines, iced tea beverages, and pomegranate juice. All of the juices were commercial brands available in the U.S. market. Pomegranate juice was found to have antioxidant potency that was more than 20 percent greater than any of the other beverages tested. The antioxidant capacity of the beverages were ranked in the following order: pomegranate juice > red wine > Concord grape juice > blueberry juice > black cherry juice, açaí juice, cranberry juice > orange juice, iced tea, apple juice.

The present study investigated the effects of extracts of blueberries, black currant, black chokeberries, apple, sea buckthorn, plum, lingonberries, cherries, and raspberries on proliferation of hormone receptor positive breast cancer cells. The extracts decreased the proliferation of breast cancer cells and the effect was proportional to concentration. There were great variations in the antioxidants, cartenoids, flavonols, hydroxycinnamic acids, anthocyanins, phenolics and Vitamin C in the extracts. The antiproliferative effects correlated with levels of some carotenoids and with vitamin C levels. The same inhibition of cell proliferation could not be found using Vitamin C alone, suggesting a possible synergistic effect of Vitamin C and other substances.

In this study, the antioxidant melatonin was quantified in two kinds of tart cherries (Montmorency and Balaton). Both cherries contain high levels of melatonin compared to the typical melatonin concentrations in the blood of mammals. Montmorency cherries are a much richer source of melatonin than Balaton cherries, containing six times the amount. The authors conclude that cherries could be an important source of melatonin since it is readily absorbed when ingested.