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Author (up) Blask, D.E.; Brainard, G.C.; Dauchy, R.T.; Hanifin, J.P.; Davidson, L.K.; Krause, J.A.; Sauer, L.A.; Rivera-Bermudez, M.A.; Dubocovich, M.L.; Jasser, S.A.; Lynch, D.T.; Rollag, M.D.; Zalatan, F.
Title Melatonin-depleted blood from premenopausal women exposed to light at night stimulates growth of human breast cancer xenografts in nude rats Type Journal Article
Year 2005 Publication Cancer Research Abbreviated Journal Cancer Res
Volume 65 Issue 23 Pages 11174-11184
Keywords Human Health; Animals; Breast Neoplasms/*blood/genetics/pathology; Cell Growth Processes/physiology; Circadian Rhythm/*physiology; Female; Humans; Light; Liver Neoplasms, Experimental/metabolism; Male; Melatonin/blood/*deficiency; Premenopause/blood; RNA, Messenger/biosynthesis/genetics; Rats; Rats, Nude; Receptors, Melatonin/biosynthesis/genetics; Transplantation, Heterologous
Abstract The increased breast cancer risk in female night shift workers has been postulated to result from the suppression of pineal melatonin production by exposure to light at night. Exposure of rats bearing rat hepatomas or human breast cancer xenografts to increasing intensities of white fluorescent light during each 12-hour dark phase (0-345 microW/cm2) resulted in a dose-dependent suppression of nocturnal melatonin blood levels and a stimulation of tumor growth and linoleic acid uptake/metabolism to the mitogenic molecule 13-hydroxyoctadecadienoic acid. Venous blood samples were collected from healthy, premenopausal female volunteers during either the daytime, nighttime, or nighttime following 90 minutes of ocular bright, white fluorescent light exposure at 580 microW/cm2 (i.e., 2,800 lx). Compared with tumors perfused with daytime-collected melatonin-deficient blood, human breast cancer xenografts and rat hepatomas perfused in situ, with nocturnal, physiologically melatonin-rich blood collected during the night, exhibited markedly suppressed proliferative activity and linoleic acid uptake/metabolism. Tumors perfused with melatonin-deficient blood collected following ocular exposure to light at night exhibited the daytime pattern of high tumor proliferative activity. These results are the first to show that the tumor growth response to exposure to light during darkness is intensity dependent and that the human nocturnal, circadian melatonin signal not only inhibits human breast cancer growth but that this effect is extinguished by short-term ocular exposure to bright, white light at night. These mechanistic studies are the first to provide a rational biological explanation for the increased breast cancer risk in female night shift workers.
Address Laboratory of Chrono-Neuroendocrine Oncology, Bassett Research Institute, The Mary Imogene Bassett Hospital, Cooperstown, New York 13326, USA. david.blask@bassett.org
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Series Editor Series Title Abbreviated Series Title
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ISSN 0008-5472 ISBN Medium
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Notes PMID:16322268 Approved no
Call Number LoNNe @ kagoburian @ Serial 721
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Author (up) 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
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Language English Summary Language Original Title
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Series Volume Series Issue Edition
ISSN 0008-5472 ISBN Medium
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Notes PMID:25062775; PMCID:PMC4119539 Approved no
Call Number IDA @ john @ Serial 355
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Author (up) Leung, L.; Grundy, A.; Siemiatycki, J.; Arseneau, J.; Gilbert, L.; Gotlieb, W.H.; Provencher, D.M.; Aronson, K.J.; Koushik, A.
Title Shift Work Patterns, Chronotype, and Epithelial Ovarian Cancer Risk Type Journal Article
Year 2019 Publication Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology Abbreviated Journal Cancer Epidemiol Biomarkers Prev
Volume in press Issue Pages 1055-9965.EPI-18-1112
Keywords Human Health; chronotype; Cancer; epithelial ovarian cancer; Ovarian cancer
Abstract BACKGROUND: Shift work causing circadian disruption is classified as a 'probable carcinogen' and may contribute to the pathogenesis of hormone-sensitive cancers. This study investigated shift work exposure in relation to epithelial ovarian cancer (EOC) risk. METHODS: In a population-based case-control study with 496 EOC cases and 906 controls, lifetime occupational histories were collected and used to calculate cumulative years of shift work exposure, average number of night shifts per month, and average number of consecutive night shifts per month. Odds ratios (ORs) and 95% confidence intervals (CIs) for associations with EOC risk were estimated using logistic regression. Associations were also examined according to chronotype and menopausal status. RESULTS: Over half of the cases (53.4%) and controls (51.7%) worked evening and/or night shifts. There was no clear pattern of increasing EOC risk with increasing years of shift work; the adjusted OR (95%CI) of EOC comparing the highest shift work category vs. never working shift work was 1.20 (0.89-1.63). This association was more pronounced among those self-identified as having a “morning” chronotype (OR=1.64, 95%CI: 1.01-2.65). Associations did not greatly differ by menopausal status. CONCLUSION: These results do not strongly demonstrate a relationship between shift work and EOC risk. IMPACT: This study collected detailed shift work information and examined shift work patterns according to shift times and schedules. The findings highlight that chronotype should be considered in studies of shift work as an exposure.
Address Department of Social and Preventive Medicine, Universite de Montreal; Department of Social and Preventive Medicine
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ISSN 1055-9965 ISBN Medium
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Notes PMID:30842128 Approved no
Call Number GFZ @ kyba @ Serial 2261
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Author (up) Mark A. Suckow, William R. Wolter and Giles E. Duffield
Title The Impact of Environmental Light Intensity on Experimental Tumor Growth Type Journal Article
Year 2017 Publication Anticancer Research Abbreviated Journal
Volume 37 Issue 9 Pages 4967-4971
Keywords Animals
Abstract Background/Aim: Cancer research requires for consistent models that minimize environmental variables. Within the typical laboratory animal housing facility, animals may be exposed to varying intensities of light as a result of cage type, cage position, light source, and other factors; however, studies evaluating the differential effect of light intensity during the light phase on tumor growth are lacking. Materials and Methods: The effect of cage face light intensity, as determined by cage rack position was evaluated with two tumor models using the C57Bl/6NHsd mouse and transplantable B16F10 melanoma cells or Lewis lung carcinoma (LLC) cells. Animals were housed in individually-ventilated cages placed at the top, middle, or bottom of the rack in a diagonal pattern so that the top cage was closest to the ceiling light source, and cage face light intensity was measured. Following a two-week acclimation period at the assigned cage position, animals were subcutaneously administered either 1.3×106 B16F10 melanoma cells or 2.5×105 Lewis lung carcinoma cells. Weights of excised tumors were measured following euthanasia 18 days (melanoma) or 21 days (LCC) after tumor cell administration. Results: Cage face light intensity was significantly different depending on the location of the cage, with cages closest to the light source have the greatest intensity. Mean tumor weights were significantly less (p<0.001 for melanoma; p&#8804;0.01 for LCC) in middle light intensity mice compared to high and low light intensity mice. Conclusion: The environmental light intensity to which experimental animals are exposed may vary markedly with cage location and can significantly influence experimental tumor growth, thus supporting the idea that light intensity should be controlled as an experimental variable for animals used in cancer research.
Address
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Notes Approved no
Call Number LoNNe @ kyba @ Serial 1749
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Author (up) Papantoniou, K.; Pozo, O.J.; Espinosa, A.; Marcos, J.; Castano-Vinyals, G.; Basagana, X.; Ribas, F.C.; Mirabent, J.; Martin, J.; Carenys, G.; Martin, C.R.; Middleton, B.; Skene, D.J.; Kogevinas, M.
Title Circadian variation of melatonin, light exposure, and diurnal preference in day and night shift workers of both sexes Type Journal Article
Year 2014 Publication Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology Abbreviated Journal Cancer Epidemiol Biomarkers Prev
Volume 23 Issue 7 Pages 1176-1186
Keywords Human Health, physiology
Abstract BACKGROUND: Light-at-night has been shown in experimental studies to disrupt melatonin production but this has only partly been confirmed in studies of night shift workers. In this cross-sectional study, we examined the circadian variation of melatonin in relation to shift status, individual levels of light-at-night exposure, and diurnal preference, an attribute reflecting personal preference for activity in the morning or evening. METHODS: One hundred and seventeen workers (75 night and 42 day) of both sexes, ages 22 to 64 years, were recruited from four companies. Participants collected urine samples from all voids over 24 hours and wore a data logger continuously recording their light exposure. Sociodemographic, occupational, lifestyle, and diurnal preference information were collected by interview. Concentrations of urinary 6-sulfatoxymelatonin (aMT6s), the main melatonin metabolite, were measured. RESULTS: Mean aMT6s levels were lower in night [10.9 ng/mg creatinine/hour; 95% confidence interval (CI), 9.5-12.6] compared with day workers (15.4; 95% CI, 12.3-19.3). The lowest aMT6s levels were observed in night workers with morning preference (6.4; 95% CI, 3.0-13.6). Peak time of aMT6s production occurred 3 hours later in night (08:42 hour, 95% CI, 07:48-09:42) compared with day workers (05:36 hour, 95% CI, 05:06-06:12). Phase delay was stronger among subjects with higher light-at-night exposure and number of nights worked. CONCLUSIONS: Night shift workers had lower levels and a delay in peak time of aMT6s production over a 24-hour period. Differences were modified by diurnal preference and intensity of light-at-night exposure. IMPACT: Night shift work affects levels and timing of melatonin production and both parameters may relate to future cancer risk.
Address Authors' Affiliations: Centre for Research in Environmental Epidemiology (CREAL); IMIM (Hospital del Mar Medical Research Institute); Universitat Pompeu Fabra, Barcelona (UPF); CIBER Epidemiologia y Salud Publica (CIBERESP), Madrid, Spain; National School of Public Health, Athens, Greece
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 1055-9965 ISBN Medium
Area Expedition Conference
Notes PMID:24812038 Approved no
Call Number LoNNe @ christopher.kyba @ Serial 1111
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