Quasi in contemporanea al convegno di Venezia, si è svolto anche un altrointeressantissimo simposio.Light, Endocrine Systems and Cancer
2-3 May 2002, Cologne

La conclusione di una delle comunicazioni, il cui riassunto trovate alla
fine di questo email, è: "To date, these studies provide the most definitive
experimental evidence that light exposure during darkness increases the risk
of cancer progression via elimination of the nocturnal melatonin signal"

Traduzione:Questi studi forniscono la più definitiva evidenza che
l'esposizione notturna alla luce aumenta il rischio di cancro a causa della
eliminazione del segnale notturno della melatonina

Trovate informazioni nel sito:
http://www.uni-koeln.de/symposium2002/index2.html

Vale assolutamente la pena di dare un'occhiata ai numerosi abstract che trovate nel sito:
http://www.nel.edu/Press/Light-Endocrine-Cancer.htm#SUPPL2
da cui potete anche ordinare gli atti.


Ecco due dei piu' interessanti riassunti:

Light during darkness, melatonin suppression and cancer progression
Over the past few years, we have shown that the surge of melatonin in the
circulation during darkness represents a potent oncostatic signal to
tissue-isolated rat hepatoma 7288CTC, which is an ER+ adenocarcinoma of the
liver. This oncostatic effect occurs via a melatonin receptor-mediated
suppression of tumor cAMP production that leads to a suppression of the
tumor uptake of linoleic acid (LA), an essential fatty acid with substantial
oncogenic properties. The ability of LA to promote cancer progression is
accomplished by its intracellular metabolism to 13-hydroxyoctadecadienoic
acid (13-HODE) which amplifies the activity of the epidermal growth factor
receptor/mitogen-activated protein kinase pathway leading to cell
proliferation. By blocking tumor LA uptake, melatonin effectively blocks the
production of 13-HODE and thus, markedly attenuates tumor growth. A similar
effect of melatonin is observed in tissue-isolated, ER+ MCF-7 human breast
cancer xenografts and nitrosomethylurea (NMU)-induced rat mammary cancers.
When male rats bearing tissue-isolated hepatomas are exposed either to
constant bright light (300 lux) or dim light (0.25 lux) during the dark
phase of a 12L:12D photoperiod, the latency to onset was significantly
reduced while the growth of tumors was markedly increased over a 4 wk period
as compared with control tumors in 12L:12D-exposed rats. In constant light-
and dim light during darkness-exposed rats, melatonin levels were completely
suppressed while tumor growth, LA uptake and 13-HODE production were
markedly increased. Similar results were obtained in constant bright
light-exposed female rats bearing tissue-isolated NMU-induced mammary
cancers or MCF-7 human breast cancer xenografts. To date, these studies
provide the most definitive experimental evidence that light exposure during
darkness increases the risk of cancer progression via elimination of the
nocturnal melatonin signal and its suppression of tumor LA uptake and
metabolism to 13-HODE.



Ocular Input for Human Melatonin Regulation: Relevance to Breast Cancer
The impact of breast cancer on women across the world has been extensive and
severe. As prevalence of breast cancer is greatest in industrialized
regions, exposure to light at night has been proposed as a potential risk
factor. This theory is supported by the epidemiological observations of
decreased breast cancer in blind women and increased breast cancer in women
who do shift-work. In addition, human, animal and in vitro studies which
have investigated the melatonin-cancer dynamic indicate an apparent
relationship between light, melatonin and cancer, albeit complex. Recent
developments in understanding melatonin regulation by light in humans are
examined, with particular attention to factors that contribute to the
sensitivity of the light-induced melatonin suppression response.
Specifically, the role of spectral characteristics of light is addressed,
and recent relevant action spectrum studies in humans and other mammalian
species are discussed. Across five action spectra for circadian and other
non-visual responses, a peak sensitivity between 446–484 nm was identified.
Under highly controlled exposure circumstances, less than 1 lux of
monochromatic light elicited a significant suppression of nocturnal
melatonin. In view of the possible link between light exposure, melatonin
suppression and cancer risk, it is important to continue to identify the
basic related ocular physiology. Visual performance, rather than circadian
function, has been the primary focus of architectural lighting systems. It
is now necessary to reevaluate lighting strategies, with consideration of
circadian influences, in an effort to maximize physiological homeostasis and
health.