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Author Anbalagan, M.; Dauchy, R.; Xiang, S.; Robling, A.; Blask, D.; Rowan, B.; Hill, S.
Title SAT-337 Disruption Of The Circadian Melatonin Signal By Dim Light At Night Promotes Bone-lytic Breast Cancer Metastases Type Journal Article
Year 2019 Publication Journal of the Endocrine Society Abbreviated Journal
Volume 3 Issue Supplement_1 Pages
Keywords Human Health; Cancer; Breast cancer; melatonin; shift work; mouse models
Abstract Breast cancer metastasis to bone is a major source of morbidity and mortality in women with advanced metastatic breast cancer. Morbidity from metastasis to bone is compounded by the fact that they cannot be surgically removed and can only be treated with chemotherapy and/or radiation therapy. Thus, there is critical need to develop new treatment strategies that kill bone metastatic tumors and reduce osteolytic lesions to improve patient quality of life and extend patient survival. Circadian rhythms are daily cycles of ~24 h that control many if not most physiologic processes and their disruption by exposure to light at night (LAN) or jet lag has been shown to be strongly associated with the development of cancer, particularly breast cancer. We have found that disruption of the anti-cancer circadian hormone melatonin (MLT) by light at night can significantly enhance the metastatic potential in breast cancer cells. Our work supports the report of the International Agency for Research on Cancer that shift work is a “probable human carcinogen” and highlights the association between exposure to light at night and invasive breast cancer. We recently reported that human breast tumor xenografts grown in athymic nude female rats housed in a photoperiod of 12h light at day: 12h dim light at night (dLAN, 0.2 lux – blocks the nighttime circadian MLT signal), display resistance to doxorubicin (Dox). More importantly, tumor growth and drug resistance could be blocked by the administration of Dox in circadian alignment with nocturnal MLT during dLAN. Our recent preliminary studies show that poorly invasive ERα positive MCF-7 breast cancer cells, when injected into the tibia (to mimic bone metastatic disease) of Foxn1nu athymic nude mice (which produce a strong circadian nighttime melatonin signal) housed in a dLAN photoperiod (suppressed nocturnal MLT production) developed full blown breast cancer tumors in bone (P<0.05) that are highly osteolytic (P<0.05). Moreover, patients with metastatic breast cancer are routinely treated with doxorubicin, which itself can promote bone damage. Our studies demonstrate that MLT slows the growth of metastatic breast cancer in bone but that the chrono-therapeutic use of doxorubicin in circadian alignment with melatonin in Foxn1nu mice with tibial breast tumors, reduced tumor growth in bone, reduced bone erosion, and promoted the formation of new bone. Successful use of this chronotherapeutic use of Dox and MLT in clinical trials increasing efficacy in preventing or suppressing breast cancer metastasis to bone while decreasing toxic side effects of doxorubicin would provide a revolutionary advancement in the treatment of bone metastatic breast cancer and decrease the morbidity and mortality associated with breast cancer metastasis to bone.
Address Tulane University School of Medicine, New Orleans, LA, United States
Corporate Author Thesis
Publisher Oxford Academic Place of Publication Editor
Language English Summary Language English Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 2472-1972 ISBN Medium
Area Expedition Conference
Notes Approved no
Call Number GFZ @ kyba @ Serial 2433
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Author Anisimov, V.N.; Vinogradova, I.A.; Panchenko, A.V.; Popovich, I.G.; Zabezhinskii, M.A.
Title Light-at-Night-Induced Circadian Disruption, Cancer and Aging Type Journal Article
Year 2012 Publication Current Aging Science Abbreviated Journal
Volume 5 Issue 3 Pages 170-177
Keywords Animals; Light-at-night; aging; cancer; cardiovascular diseases; circadian; circadian rhythm; diabetes; disruption; melatonin; shift-work
Abstract Light-at-night has become an increasing and essential part of the modern lifestyle and leads to a number of health problems, including excessive body mass index, cardiovascular diseases, diabetes, and cancer. The International Agency for Research on Cancer (IARC) Working Group concluded that “shift-work that involves circadian disruption is probably carcinogenic to humans” (Group 2A) [1]. According to the circadian disruption hypothesis, light-at-night might disrupt the endogenous circadian rhythm and specifically suppress nocturnal production of the pineal hormone melatonin and its secretion into the blood. We evaluated the effect of various light/dark regimens on the survival, life span, and spontaneous and chemical carcinogenesis in rodents. Exposure to constant illumination was followed by accelerated aging and enhanced spontaneous tumorigenesis in female CBA and transgenic HER-2/neu mice. In male and female rats maintained at various light/dark regimens (standard 12:12 light/dark [LD], the natural light [NL] of northwestern Russia, constant light [LL], and constant darkness [DD]) from the age of 25 days until natural death, it was found that exposure to NL and LL regimens accelerated age-related switch-off of the estrous function (in females), induced development of metabolic syndrome and spontaneous tumorigenesis, and shortened life span both in male and females rats compared to the standard LD regimen. Melatonin given in nocturnal drinking water prevented the adverse effect of the constant illumination (LL) and natural light (NL) regimens on the homeostasis, life span, and tumor development both in mice and rats. The exposure to the LL regimen accelerated colon carcinogenesis induced by 1,2-dimethylhydrazine (DMH) in rats, whereas the treatment with melatonin alleviated the effects of LL. The maintenance of rats at the DD regimen inhibited DMH-induced carcinogenesis. The LL regimen accelerated, whereas the DD regimen inhibited both mammary carcinogenesis induced by N-nitrosomethylurea and transplacental carcinogenesis induced by N-nitrosoethylurea in rats. Treatment with melatonin prevented premature aging and tumorigenesis in rodents. The data found in the literature and our observations suggest that the use of melatonin would be effective for cancer prevention in humans at risk as a result of light pollution.
Address
Corporate Author Thesis
Publisher Place of Publication Editor
Language Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
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ISSN ISBN Medium
Area Expedition Conference
Notes Approved no
Call Number LoNNe @ christopher.kyba @ Serial 377
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Author Cherrie, J.W.
Title Shedding Light on the Association between Night Work and Breast Cancer Type Journal Article
Year 2019 Publication Annals of Work Exposures and Health Abbreviated Journal Ann Work Expo Health
Volume 63 Issue 6 Pages 608–611
Keywords Commentary; Human Health; Cancer; Breast cancer; shift work
Abstract Shift work that involves circadian disruption has been classified as probably carcinogenic to humans by the International Agency for Research on Cancer, although more recent epidemiological evidence is not consistent. Several mechanisms have been postulated to explain an association between night work and female breast cancer, but the most likely is suppression of the hormone melatonin by light exposure at night. Three articles recently published in this journal describe aspects of exposure to light during night work. These articles and other evidence suggest that nighttime light levels may not always be sufficient to affect melatonin production, which could in part explain the inconsistencies in the epidemiological data. There is need to improve the specificity and reliability of exposure assessments in future epidemiological studies of night shift workers.
Address Institute of Occupational Medicine, Research Avenue North, Edinburgh, UK
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 2398-7308 ISBN Medium
Area Expedition Conference
Notes PMID:31175355 Approved no
Call Number GFZ @ kyba @ Serial 2530
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Author Cho, Y.M.; Ryu, S.-H.; Lee, B.R.; Kim, K.H.; Lee, E.; Choi, J.
Title Effects of artificial light at night on human health: A literature review of observational and experimental studies applied to exposure assessment Type Journal Article
Year 2015 Publication Chronobiology International Abbreviated Journal Chronobiol. Int.
Volume 32 Issue 9 Pages 1294-1310
Keywords Artificial light at night; breast cancer; circadian rhythm; light exposure; light pollution
Abstract It has frequently been reported that exposure to artificial light at night (ALAN) may cause negative health effects, such as breast cancer, circadian phase disruption and sleep disorders. Here, we reviewed the literature assessing the effects of human exposure to ALAN in order to list the health effects of various aspects of ALAN. Several electronic databases were searched for articles, published through August 2014, related to assessing the effects of exposure to ALAN on human health; these also included the details of experiments on such exposure. A total of 85 articles were included in the review. Several observational studies showed that outdoor ALAN levels are a risk factor for breast cancer and reported that indoor light intensity and individual lighting habits were relevant to this risk. Exposure to artificial bright light during the nighttime suppresses melatonin secretion, increases sleep onset latency (SOL) and increases alertness. Circadian misalignment caused by chronic ALAN exposure may have negative effects on the psychological, cardiovascular and/or metabolic functions. ALAN also causes circadian phase disruption, which increases with longer duration of exposure and with exposure later in the evening. It has also been reported that shorter wavelengths of light preferentially disturb melatonin secretion and cause circadian phase shifts, even if the light is not bright. This literature review may be helpful to understand the health effects of ALAN exposure and suggests that it is necessary to consider various characteristics of artificial light, beyond mere intensity.
Address b Department of Preventive Medicine , College of Medicine, Korea University , Seoul , Republic of Korea
Corporate Author Thesis
Publisher Taylor & Francis Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0742-0528 ISBN Medium
Area Expedition Conference
Notes PMID:26375320 Approved no
Call Number IDA @ john @ Serial 1269
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Author Dauchy, R.T.; Xiang, S.; Mao, L.; Brimer, S.; Wren, M.A.; Yuan, L.; Anbalagan, M.; Hauch, A.; Frasch, T.; Rowan, B.G.; Blask, D.E.; Hill, S.M.
Title Circadian and melatonin disruption by exposure to light at night drives intrinsic resistance to tamoxifen therapy in breast cancer Type Journal Article
Year 2014 Publication Cancer Research Abbreviated Journal Cancer Res
Volume 74 Issue 15 Pages 4099-4110
Keywords *Cancer; breast cancer; melatonin; endocrinology; tamoxifen; *Circadian Rhythm; circadian disruption; human health; epidemiology
Abstract Resistance to endocrine therapy is a major impediment to successful treatment of breast cancer. Preclinical and clinical evidence links resistance to antiestrogen drugs in breast cancer cells with the overexpression and/or activation of various pro-oncogenic tyrosine kinases. Disruption of circadian rhythms by night shift work or disturbed sleep-wake cycles may lead to an increased risk of breast cancer and other diseases. Moreover, light exposure at night (LEN) suppresses the nocturnal production of melatonin that inhibits breast cancer growth. In this study, we used a rat model of estrogen receptor (ERalpha(+)) MCF-7 tumor xenografts to demonstrate how altering light/dark cycles with dim LEN (dLEN) speed the development of breast tumors, increasing their metabolism and growth and conferring an intrinsic resistance to tamoxifen therapy. These characteristics were not observed in animals in which the circadian melatonin rhythm was not disrupted, or in animals subjected to dLEN if they received nocturnal melatonin replacement. Strikingly, our results also showed that melatonin acted both as a tumor metabolic inhibitor and a circadian-regulated kinase inhibitor to reestablish the sensitivity of breast tumors to tamoxifen and tumor regression. Together, our findings show how dLEN-mediated disturbances in nocturnal melatonin production can render tumors insensitive to tamoxifen. Cancer Res; 74(15); 4099-110. (c)2014 AACR.
Address Departments of Structural and Cellular Biology and Tulane Cancer Center and Louisiana Cancer Research Consortium; Tulane Circadian Cancer Biology Group; and
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0008-5472 ISBN Medium
Area Expedition Conference
Notes PMID:25062775; PMCID:PMC4119539 Approved no
Call Number IDA @ john @ Serial 355
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