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Lulu Mao

Researcher at Tulane University

Publications -  31
Citations -  1837

Lulu Mao is an academic researcher from Tulane University. The author has contributed to research in topics: Melatonin & Circadian rhythm. The author has an hindex of 22, co-authored 31 publications receiving 1599 citations.

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Melatonin: an inhibitor of breast cancer

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.
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Molecular Mechanisms of Melatonin Anticancer Effects

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.
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Circadian regulation of molecular, dietary, and metabolic signaling mechanisms of human breast cancer growth by the nocturnal melatonin signal and the consequences of its disruption by light at night.

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).
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Inhibition of breast cancer cell invasion by melatonin is mediated through regulation of the p38 mitogen-activated protein kinase signaling pathway

TL;DR: Melatonin exerts an inhibitory effect on breast cancer cell invasion through down-regulation of the p38 pathway, and inhibition of M MP-2 and MMP-9 expression and activity.
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Circadian and melatonin disruption by exposure to light at night drives intrinsic resistance to tamoxifen therapy in breast cancer.

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.