Shulin Xiang

TL;DR: Research in animal and human models has indicated that LEN-induced disruption of the circadian nocturnal melatonin signal promotes the growth, metabolism, and signaling of human breast cancer and drives breast tumors to endocrine and chemotherapeutic resistance.

TL;DR: The results demonstrate that the MT1 receptor is a major transducer of melatonin’s actions in the breast, suppressing mammary gland development and mediating the anticancer actions ofmelatonin through multiple pathways.

TL;DR: A review article as mentioned in this paper discusses recent work on the melatonin-mediated circadian regulation and integration of molecular, dietary, and metabolic signaling mechanisms involved in human breast cancer growth and the consequences of circadian disruption by exposure to light at night (LAN).

TL;DR: Together, the findings show how dLEN-mediated disturbances in nocturnal melatonin production can render tumors insensitive to tamoxifen, and showed that melatonin acted both as a tumor metabolic inhibitor and a circadian-regulated kinase inhibitor to reestablish the sensitivity of breast tumors to tamxifen and tumor regression.

TL;DR: Light-at-night (LAN) induced circadian disruption of the nocturnal melatonin signal activates human breast cancer growth, metabolism, and signaling, providing the strongest mechanistic support, thus far, for epidemiological studies demonstrating the elevated breast cancer risk in night shift workers and other individuals increasingly exposed to LAN.