Latest Cancer News
In the new study, rats with human breast cancer tumors were exposed to 12 hours of normal light followed by 12 hours of dim light, simulating dim light in a nighttime environment.
Half of the rodents were also given melatonin supplements during the dim light period.
Tumor growth in rats that did not receive melatonin was nearly triple that of those that did receive melatonin, the researchers reported. The researchers also found that tumors in rats that did not receive melatonin became completely resistant to doxorubicin, while tumors in rats that received melatonin remained sensitive to the chemotherapy drug and regressed rapidly.
The study was to be presented Monday at a meeting of the American Association for Cancer Research (AACR) in New Orleans. Experts note that findings in animals often fail to be replicated in humans, and studies presented at medical meetings are also considered preliminary until published in a peer-reviewed journal.
Still, the study's authors believe two enzymes may play a role in a resistance to doxorubicin that's tied to dim light at night.
"When we analyzed tumors from rats that did not receive nighttime melatonin supplementation, we detected substantially increased levels of two enzymes that break down doxorubicin to a less active form," Steven Hill, chair for breast cancer research at Tulane University School of Medicine in New Orleans, explained in an AACR news release.
He believes that an increase in the levels of these enzymes might speed the transport of doxorubicin away from cancer cells, "compared with tumors from rats receiving nighttime melatonin supplementation."
"Tumors from rats receiving nighttime melatonin supplementation had lower levels of these enzymes," Hill said. "So we think that melatonin helps maintain high levels of active doxorubicin in the cancer cells, whereas suppression of circadian melatonin production by exposure to light at night has the opposite effect."
-- Robert Preidt
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SOURCE: American Association for Cancer Research, news release, Sept. 29, 2014