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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. url  doi
openurl 
  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 (up) *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  
Permanent link to this record
 

 
Author Kantermann, T.; Roenneberg, T. url  doi
openurl 
  Title Is light-at-night a health risk factor or a health risk predictor? Type Journal Article
  Year 2009 Publication Chronobiology International Abbreviated Journal Chronobiol Int  
  Volume 26 Issue 6 Pages 1069-1074  
  Keywords (up) *Chronobiology Disorders; Circadian Rhythm; Environmental Exposure; Humans; *Light; Neoplasms; Risk Factors  
  Abstract In 2007, the IARC (WHO) has classified “shift-work that involves circadian disruption” as potentially carcinogenic. Ample evidence leaves no doubt that shift-work is detrimental for health, but the mechanisms behind this effect are not well understood. The hormone melatonin is often considered to be a causal link between night shift and tumor development. The underlying “light-at-night” (LAN) hypothesis is based on the following chain of arguments: melatonin is a hormone produced under the control of the circadian clock at night, and its synthesis can be suppressed by light; as an indolamine, it potentially acts as a scavenger of oxygen radicals, which in turn can damage DNA, which in turn can cause cancer. Although there is no experimental evidence that LAN is at the basis of increased cancer rates in shiftworkers, the scenario “light at night can cause cancer” influences research, medicine, the lighting industry and (via the media) also the general public, well beyond shiftwork. It is even suggested that baby-lights, TVs, computers, streetlights, moonlight, emergency lights, or any so-called “light pollution” by urban developments cause cancer via the mechanisms proposed by the LAN hypothesis. Our commentary addresses the growing concern surrounding light pollution. We revisit the arguments of the LAN theory and put them into perspective regarding circadian physiology, physical likelihood (e.g., what intensities reach the retina), and potential risks, specifically in non-shiftworkers.  
  Address Institute for Medical Psychology, University of Munich LMU, Munich, Germany  
  Corporate Author Thesis  
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  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:19731106 Approved no  
  Call Number IDA @ john @ Serial 134  
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Author Vetter, C.; Juda, M.; Lang, D.; Wojtysiak, A.; Roenneberg, T. url  openurl
  Title Blue-enriched office light competes with natural light as a zeitgeber Type Journal Article
  Year 2011 Publication Scandinavian Journal of Work, Environment & Health Abbreviated Journal Scand J Work Environ Health  
  Volume 37 Issue 5 Pages 437-445  
  Keywords (up) *Circadian Rhythm; *Color; Humans; *Lighting; *Occupational Health; Sleep; Wakefulness; blue light; circadian disruption; Circadian rhythm; sleep  
  Abstract OBJECTIVES: Circadian regulation of human physiology and behavior (eg, body temperature or sleep-timing), depends on the “zeitgeber” light that synchronizes them to the 24-hour day. This study investigated the effect of changing light temperature at the workplace from 4000 Kelvin (K) to 8000 K on sleep-wake and activity-rest behavior. METHODS: An experimental group (N=27) that experienced the light change was compared with a non-intervention group (N=27) that remained in the 4000 K environment throughout the 5-week study period (14 January to 17 February). Sleep logs and actimetry continuously assessed sleep-wake behavior and activity patterns. RESULTS: Over the study period, the timing of sleep and activity on free days steadily advanced parallel to the seasonal progression of sunrise in the non-intervention group. In contrast, the temporal pattern of sleep and activity in the experimental group remained associated with the constant onset of work. CONCLUSION: The results suggest that artificial blue-enriched light competes with natural light as a zeitgeber. While subjects working under the warmer light (4000 K) appear to entrain (or synchronize) to natural dawn, the subjects who were exposed to blue-enriched (8000 K) light appear to entrain to office hours. The results confirm that light is the dominant zeitgeber for the human clock and that its efficacy depends on spectral composition. The results also indicate that blue-enriched artificial light is a potent zeitgeber that has to be used with diligence.  
  Address Institute for Medical Psychology, Centre of Chronobiology, Ludwig-Maximilians-Universitat, Munich, Germany  
  Corporate Author Thesis  
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  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0355-3140 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:21246176 Approved no  
  Call Number IDA @ john @ Serial 350  
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Author Reiter, R.J.; Tan, D.X.; Erren, T.C.; Fuentes-Broto, L.; Paredes, S.D. url  doi
openurl 
  Title Light-mediated perturbations of circadian timing and cancer risk: a mechanistic analysis Type Journal Article
  Year 2009 Publication Integrative Cancer Therapies Abbreviated Journal Integr Cancer Ther  
  Volume 8 Issue 4 Pages 354-360  
  Keywords (up) *Circadian Rhythm; Humans; Light/*adverse effects; Melatonin/antagonists & inhibitors; Neoplasms/*etiology/physiopathology; Risk Factors; Sleep Deprivation/complications; oncogenesis  
  Abstract In industrialized countries, certain types of cancer, most notably, breast and prostate, are more frequent than in poorly developed nations. This high cancer frequency is not explained by any of the conventional causes. Within the past decade, numerous reports have appeared that link light at night with an elevated cancer risk. The three major consequences of light at night are sleep deprivation, chronodisruption, and melatonin suppression. Each of these individually or in combination may contribute to the reported rise in certain types of cancer. In this article, the potential mechanisms underlying the basis of the elevated cancer risk are briefly discussed. Finally, if cancer is a consequence of excessive nighttime light, it is likely that other diseases/conditions may also be exaggerated by the widespread use of light after darkness onset.  
  Address Department of Cellular and Structural Biology, University of Texas Health Science Center, San Antonio, TX 78229, USA. reiter@uthscsa.edu  
  Corporate Author Thesis  
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  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1534-7354 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:20042411 Approved no  
  Call Number IDA @ john @ Serial 290  
Permanent link to this record
 

 
Author Landgraf, D.; McCarthy, M.J.; Welsh, D.K. url  doi
openurl 
  Title The role of the circadian clock in animal models of mood disorders Type Journal Article
  Year 2014 Publication Behavioral Neuroscience Abbreviated Journal Behav Neurosci  
  Volume 128 Issue 3 Pages 344-359  
  Keywords (up) *Circadian Rhythm; mood; mood disorders; circadian disruption  
  Abstract An association between circadian clock function and mood regulation is well established and has been proposed as a factor in the development of mood disorders. Patients with depression or mania suffer disturbed sleep-wake cycles and altered rhythms in daily activities. Environmentally disrupted circadian rhythms increase the risk of mood disorders in the general population. However, proof that a disturbance of circadian rhythms is causally involved in the development of psychiatric disorders remains elusive. Using clock gene mutants, manipulations of sleep-wake and light-dark cycles, and brain lesions affecting clock function, animal models have been developed to investigate whether circadian rhythm disruptions alter mood. In this review, selected animal models are examined to address the issue of causality between circadian rhythms and affective behavior.  
  Address Research Service, Veterans Affairs San Diego Healthcare System  
  Corporate Author Thesis  
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  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0735-7044 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:24660657 Approved no  
  Call Number IDA @ john @ Serial 316  
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