Kamis, 28 Februari 2008

[cancercured] Caffeine

Dr. Martin of Kurosawa Group researched caffeine and wrote in his blog
that caffeine is an anti cancer agent.See the below article.I am
wondering about coffee enemas. Did dr. Gerson use coffee enemas for
detoxification or for direct anti cancer effect especially in bowel
cancer?
carla



Caffeine inhibits adenosine-induced accumulation of hypoxia-inducible
factor-1alpha, vascular endothelial growth factor, and interleukin-8
expression in hypoxic human colon cancer cells.

Merighi S, Benini A, Mirandola P, Gessi S, Varani K, Simioni C, Leung
E, Maclennan S, Baraldi PG, Borea PA.

Department of Clinical and Experimental Medicine, Pharmacology Unit,
University of Ferrara, Ferrara, Italy.

Frequent coffee consumption has been associated with a reduced risk
of colorectal cancer in a number of case-control studies. Coffee is a
leading source of methylxanthines, such as caffeine. The induction of
vascular endothelial growth factor (VEGF) and interleukin-8 (IL-8) is
an essential feature of tumor angiogenesis, and the hypoxia-inducible
factor-1 (HIF-1) transcription factor is known to be a key regulator
of this process. In this study, we investigated the effects of
caffeine on HIF-1 protein accumulation and on VEGF and IL-8
expression in the human colon cancer cell line HT29 under hypoxic
conditions. Our results show that caffeine significantly inhibits
adenosine-induced HIF-1alpha protein accumulation in cancer cells. We
show that HIF-1alpha and VEGF are increased through A3 adenosine
receptor stimulation, whereas the effects on IL-8 are mediated via
the A2B subtype. Pretreatment of cells with caffeine significantly
reduces adenosine-induced VEGF promoter activity and VEGF and IL-8
expression. The mechanism of caffeine seems to involve the inhibition
of the extracellular signal-regulated kinase 1/2 (ERK1/2), p38, and
Akt, leading to a marked decrease in adenosine-induced HIF-1alpha
accumulation, VEGF transcriptional activation, and VEGF and IL-8
protein accumulation. From a functional perspective, we observe that
caffeine also significantly inhibits the A3 receptor-stimulated cell
migration of colon cancer cells. Conditioned media prepared from
colon cells treated with an adenosine analog increased human
umbilical vein endothelial cell migration. These data provide
evidence that adenosine could modulate the migration of colon cancer
cells by an HIF-1alpha/VEGF/IL-8-dependent mechanism and that
caffeine has the potential to inhibit colon cancer cell growth.


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