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Artificial Light Stimulates Breast Cancer Growth In Mice: Study

Researchers at the Bassett Research Institute of the Mary Imogene Bassett Hospital in Cooperstown, New York and The Thomas Jefferson University in Philadelphia, Pa have found that the growth of breast cancer in laboratory mice was // stimulated by the nighttime exposure to artificial light. The study, which was funded by the National Cancer Institute and the National Institute of Environmental Health Sciences, also found that the tumors were stimulated by the suppression of a hormone called as melatonin. The development of breast tumors was slowed down by nighttime darkness.

This study could offer an explanation as to why the rate of breast cancer is high in female workers who work night shifts. The complete details of the study are published in the December 1, 2005 issue of the journal Cancer Research. "This is the first experimental evidence that artificial light plays an integral role in the growth of human breast cancer," said David A. Schwartz, M.D, NIEHS Director "This finding will enable scientists to develop new strategies for evaluating the effects of light and other environmental factors on cancer growth." Previous research had already highlighted the role of melatonin in the sleep and waking cycles. Now this research shows that melatonin has a role to play in the growth of cancer as well. "Melatonin interferes with the tumor's ability to use linoleic acid as a growth signal, which causes tumor metabolism and growth activity to shut down," says David Blask, M.D., Ph.D., a neuroendocrinologist with the Bassett Research Institute and lead author on the study. The researchers first injected human breast cancer cells into laboratory mice and then after tumors developed, they injected tumor-free, melatonin-rich blood into these mice. It was found that melatonin slowed the growth of these tumors. "We observed rapid growth comparable to that seen with administration of daytime blood samples, when tumor activity is particularly high," Blask said."Comp
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