In breast cancer cells transfected with MT1 exposed to 1.2 microT of the 50 Hz EMF, the expression of p53 and c-myc increased significantly after melatonin treatment.

Single nucleotide polymorphisms within the genes of clock, clock-controlled, and melatonin pathways have been found to confer excess cancer risk or protection from cancer.

The combined treatment with metformin + melatoni (2 mg/L in drinking water during the night time) significantly suppressed Ehrlich tumor growth.

Melatonin's anticancer effects in vivo involves inhibition of linoleic acid(LA)uptake and its metabolism to mitogenically active 13-hydroxyoctadecadienoic acid (13-HODE).

The three major consequences of light at night are sleep deprivation, chronodisruption, and melatonin suppression.

The multilevel endocrine changes caused by circadian disruption with melatonin suppression (LAN) lead to the oncogenic targeting of the endocrine-responsive breast in women and possibly the prostate.

MT1 receptor is a major transducer of melatonin's actions in the breast, suppressing mammary gland development and mediating the anticancer actions of melatonin.

Breast cancer is consistently diagnosed more often in spring. Its mechanism may depend upon seasonal sunlight mediation of vitamin D and seasonal mediation of nocturnal melatonin peak level and duration.

Positive association between 6-sulphatoxymelatonin (aMT6s) and risk of breast cancer.

Light-at-night exposure can induce deleterious epi-genetic changes in Per3 (5-VNTR)-(4-VNTR) genes.