Light at Night Co‐distributes with Incident Breast but not Lung Cancer in the Female Population of Israel

Kloog, Itai; Haim, Abraham; Stevens, Richard G.; Barchana, Micha; Portnov, Boris A.

doi:10.1080/07420520801921572

Cited by 194 publications

(143 citation statements)

References 48 publications

Supporting

Mentioning

131

Contrasting

Unclassified

Order By: Relevance

“…Epidemiological studies have shown that melatonin decreases the risk of developing breast and other kinds of cancer (Kliukiene et al, 2001;Kloog et al, 2008;Schernhammer et al, 2008Schernhammer et al, , 2009Schernhammer et al, , 2009Schernhammer et al, , 2010Alpert et al, 2009). However, very little is known about the molecular mechanisms by which melatonin accomplishes its anticancer effects.…”

Section: Discussionmentioning

confidence: 99%

Melatonin triggers p53Ser phosphorylation and prevents DNA damage accumulation

Santoro¹,

Marani²,

Blandino³

et al. 2011

Oncogene

View full text Add to dashboard Cite

Several epidemiological studies have shown that high levels of melatonin, an indolic hormone secreted mainly by the pineal gland, reduce the risks of developing cancer, thus suggesting that melatonin triggers the activation of tumor-suppressor pathways that lead to the prevention of malignant transformation. This paper illustrates that melatonin induces phosphorylation of p53 at Ser-15 inhibiting cell proliferation and preventing DNA damage accumulation of both normal and transformed cells. This activity requires p53 and promyelocytic leukemia (PML) expression and efficient phosphorylation of p53 at Ser-15 residue. Melatonin-induced p53 phosphorylation at Ser-15 residue does not require ataxia telangiectasiamutated activity, whereas it is severely impaired upon chemical inhibition of p38 mitogen-activated protein kinase activity. By and large, these findings imply that the activation of the p53 tumor-suppressor pathway is a critical mediator of melatonin and its anticancer effects. Therefore, it provides molecular insights into increasing observational evidence for the role that melatonin has in cancer prevention.

show abstract

Section: Discussionmentioning

confidence: 99%

Melatonin triggers p53Ser phosphorylation and prevents DNA damage accumulation

Santoro¹,

Marani²,

Blandino³

et al. 2011

Oncogene

View full text Add to dashboard Cite

show abstract

“…Additionally, covering night shift work for 20 years or more has been shown to be notably associated with increased risk of ER-α-related breast cancer [148]. Positive correlation between ALAN intensity (using satellite images) with breast cancer incidences has been clearly demonstrated among Israeli women across 147 communities [149] and also worldwide with approximately 70% and 50% higher risk, respectively, of breast cancer incidences at the highest ALAN intensity compared with the lowest exposure [150]. Furthermore, several observational studies have demonstrated a plausible association between bedroom chronic exposure to moderate levels of ALAN and increased breast cancer prevalence [151][152][153].…”

Section: Circadian Disruption and Breast Cancermentioning

confidence: 95%

Artificial light-at-night – a novel lifestyle risk factor for metabolic disorder and cancer morbidity

Zubidat

Haim

2017

Journal of Basic and Clinical Physiology and Pharmacology

Self Cite

View full text Add to dashboard Cite

Both obesity and breast cancer are already recognized worldwide as the most common syndromes in our modern society. Currently, there is accumulating evidence from epidemiological and experimental studies suggesting that these syndromes are closely associated with circadian disruption. It has been suggested that melatonin (MLT) and the circadian clock genes both play an important role in the development of these syndromes. However, we still poorly understand the molecular mechanism underlying the association between circadian disruption and the modern health syndromes. One promising candidate is epigenetic modifications of various genes, including clock genes, circadian-related genes, oncogenes, and metabolic genes. DNA methylation is the most prominent epigenetic signaling tool for gene expression regulation induced by environmental exposures, such as artificial light-at-night (ALAN). In this review, we first provide an overview on the molecular feedback loops that generate the circadian regulation and how circadian disruption by ALAN can impose adverse impacts on public health, particularly metabolic disorders and breast cancer development. We then focus on the relation between ALAN-induced circadian disruption and both global DNA methylation and specific loci methylation in relation to obesity and breast cancer morbidities. DNA hypo-methylation and DNA hyper-methylation, are suggested as the most studied epigenetic tools for the activation and silencing of genes that regulate metabolic and monostatic responses. Finally, we discuss the potential clinical and therapeutic roles of MLT suppression and DNA methylation patterns as novel biomarkers for the early detection of metabolic disorders and breast cancer development.

show abstract

“…B 370: 20140120 night accounts for any sizeable proportion of the breast cancer burden in society, then ambient light level as measured by satellite at night should be correlated with breast cancer risk across communities [33]. This has been tested and confirmed within Israel [34], and among 164 countries of the world [35].…”

Section: Diseases Of Modern Lifementioning

confidence: 96%

Electric light, particularly at night, disrupts human circadian rhythmicity: is that a problem?

Stevens

Zhu

2015

Phil. Trans. R. Soc. B

Self Cite

138

View full text Add to dashboard Cite

Over the past 3 billion years, an endogenous circadian rhythmicity has developed in almost all life forms in which daily oscillations in physiology occur. This allows for anticipation of sunrise and sunset. This physiological rhythmicity is kept at precisely 24 h by the daily cycle of sunlight and dark. However, since the introduction of electric lighting, there has been inadequate light during the day inside buildings for a robust resetting of the human endogenous circadian rhythmicity, and too much light at night for a true dark to be detected; this results in circadian disruption and alters sleep/wake cycle, core body temperature, hormone regulation and release, and patterns of gene expression throughout the body. The question is the extent to which circadian disruption compromises human health, and can account for a portion of the modern pandemics of breast and prostate cancers, obesity, diabetes and depression. As societies modernize (i.e. electrify) these conditions increase in prevalence. There are a number of promising leads on putative mechanisms, and epidemiological findings supporting an aetiologic role for electric lighting in disease causation. These include melatonin suppression, circadian gene expression, and connection of circadian rhythmicity to metabolism in part affected by haem iron intake and distribution.

show abstract

Light at Night Co‐distributes with Incident Breast but not Lung Cancer in the Female Population of Israel

Cited by 194 publications

References 48 publications

Melatonin triggers p53Ser phosphorylation and prevents DNA damage accumulation

Melatonin triggers p53Ser phosphorylation and prevents DNA damage accumulation

Artificial light-at-night – a novel lifestyle risk factor for metabolic disorder and cancer morbidity

Electric light, particularly at night, disrupts human circadian rhythmicity: is that a problem?

Contact Info

Product

Resources

About