Abstract
The circadian clock controls a large array of behavioral and physiological systems of fundamental importance to most organisms. Consequently, abnormal functioning of the clock results in severe dysfunctions and pathologies. Although epidemiological studies show a clear correlation between disruption of circadian rhythms and incidence of breast cancer, a molecular interpretation of how clock-related mechanisms may link to tumor development remains elusive. Here we speculate on the molecular pathways that may couple the circadian machinery to breast cancer.
MeSH terms
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ARNTL Transcription Factors
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Acetylation
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Animals
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Basic Helix-Loop-Helix Transcription Factors / physiology
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Breast Neoplasms / epidemiology
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Breast Neoplasms / etiology*
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Breast Neoplasms / genetics
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Breast Neoplasms / physiopathology
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CLOCK Proteins
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Cell Transformation, Neoplastic / genetics*
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Chromatin / metabolism
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Circadian Rhythm / genetics
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Circadian Rhythm / physiology*
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Cyclin D1 / physiology
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Developed Countries
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Disease Susceptibility
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Estrogen Receptor alpha / physiology
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Estrogens
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Female
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Gene Expression Regulation
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Genes, Tumor Suppressor
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Histone Acetyltransferases / physiology*
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Histones / metabolism
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Humans
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Mammals / physiology
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Mammary Neoplasms, Experimental / etiology
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Mammary Neoplasms, Experimental / genetics
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Mammary Neoplasms, Experimental / physiopathology
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Melatonin / physiology
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Mice
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Models, Biological
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Neoplasms, Hormone-Dependent / etiology
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Neoplasms, Hormone-Dependent / genetics
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Neoplasms, Hormone-Dependent / physiopathology
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Nuclear Proteins / physiology
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Protein Processing, Post-Translational / physiology
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Risk
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Trans-Activators / physiology*
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Transcription Factors / physiology
Substances
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ARNTL Transcription Factors
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BMAL1 protein, human
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Bmal1 protein, mouse
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Basic Helix-Loop-Helix Transcription Factors
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Chromatin
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Estrogen Receptor alpha
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Estrogens
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Histones
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Nuclear Proteins
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Trans-Activators
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Transcription Factors
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Cyclin D1
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CLOCK Proteins
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CLOCK protein, human
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Clock protein, mouse
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Histone Acetyltransferases
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Melatonin