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Could visible light contribute to the development of leukaemia and other cancers in children?

Med Hypotheses 64(4):8 (2005) PMID 15694708

This paper suggests to rigorously test the hypothesis that there are causal links between visible light and the development of leukaemia and other cancers in children. Light can be considered as a candidate risk factor because it suppresses melatonin biosynthesis which may play a role in a series of anticancer defences. Indeed, melatonin may offer some protection against all ''hallmarks of cancer'' [i.e., self-sufficiency in growth signals; insensitivity to growth-inhibitory signals; evasion of programmed cell death (apoptosis); limitless replicative potential; sustained angiogenesis; tissue invasion and metastasis] recently suggested by Hanahan and Weinberg. Already ongoing investigations into the possible nexus of light, endocrine systems and the development of cancers will be further fueled by recent insights into photoreception and - transduction, including the discovery of ''novel'' photoreceptors in the eye. Among a variety of different photosensory tasks, these receptors constitute crucial gates for light information from the environment which is employed for the temporal organization of our physiology and it has been proposed that chronodisruption, i.e., a significant disturbance of the coordination and thus order of biological rhythms, could contribute to the development of cancers.With regard to public health, the pervasive exposures to light - at work and in homes - imply that visible radiation could be a strong risk factor defined epidemiologically as a causal contributor to disease in a large proportion of cases. Importantly, if light were to be corroborated as a contributor to cancers in children, it would be amenable to manipulations with the perspective of reducing inherent risks significantly. In fact, it could be much easier - and much more effective - to reevaluate and modify lighting systems than to manipulate other possible determinants of the chronic processes of cancer such as genetic, nutritional or lifestyle factors.

Copyright © 2005 Elsevier Ltd. All rights reserved.

DOI: 10.1016/j.mehy.2004.09.021
Version: za2963e q8zaf q8zb5 q8zcf q8zdd q8zed q8zfe q8zg1

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