Tagamet, is a potentially powerful anti-cancer drug, especially if
combined with other compounds.
If you conduct a PubMed search on cimetidine and cancer you will
find over 1000 references.
The epidermal growth factor receptor (EGFR) is over expressed on
carcinoma cells. These epithelial cells comprise over 80% of all
cancers. Blocking the activity of these receptors is the subject of
many research projects.
This study shows that common, inexpensive, non-toxic cimetidine
blocks the activation of EGFR. When EGF, epidermal growth factor,
binds EGFR it initiates an autophosphorylation reaction which
activates the receptor and its tyrosine kinase activity. Cimetidine
blocks this response, thereby blocking EGFRs ability to promote
cancer cell growth and the inhibition of apoptosis.
The authors found that cimetidine decreased the level of cyclic AMP
in the cancer cells. The lack of cyclic AMP impaired the
autophosphorylation of the EGFR and inhibited its activity. This is
an observation of monumental significance. Other histamine H2
receptor inhibitors, such as ranitidine and famotidine, do not
decrease the level of cyclic AMP in cells.
I have written extensively about the prostaglandin PGE2 and its
ability to suppress the immune response in general and its ability
to promote angiogenesis and the growth of cancer cells. PGE2
promotes the synthesis of cyclic AMP. I have also written about the
role stress hormones, such as norepinephrine and epinephrine, play
in inhibiting the immune response and promoting cancer cell growth
and development. These hormones also activate cyclic AMP synthesis.
Cimetidine could decrease cyclic AMP levels in cells by blocking
membrane adenylate cyclase, the enzyme that actually makes cyclic
AMP, or by increasing the activity of cyclic AMP phosphodiesterase,
the enzyme that degrades cyclic AMP. To date, no one knows how
cimetidine influences cyclic AMP levels in cells.
Cimetidine, probably via decreased cyclic AMP levels, decreases the
development of regulatory T cells. These cells, referred to as TREG,
suppress immune functioning. These cells are activated by the immune
hormones IL-10 and TGF-beta, hormones that cimetidine downregulates.
In addition, cimetidine activates the synthesis of IL-12, the major
enhancer of cell mediated immunity.
There are two major forms of TREG immune inhibitor cells. These
cells inhibit a vigorous immune response against cancer, leukemia,
bacterial and viral infections, such as HIV.
The IL-10/TGFbeta hormones responsible for the activation of this
subset of TREG cells is inhibited by cimetidine due to its ability
to reduce cyclic AMP levels in cells.
The second subset, FOXP3 TREG cells, is also activated by cyclic
AMP. This implies that cimetidine can inhibit this population of
TREG cells as well.
The implications of this line of research are enormous. Cimetidine,
by lowering cyclic AMP levels in cells, can reactivate the immune
response against cancer, HIV and other diseases while inhibiting
angiogenesis and the growth of cancer cells.
The daily dose is 800 mgs a day, 200 mgs four times a day. And you
don't need a prescription.
Stay tuned...
Grouppe Kurosawa, Medicine in the Public Interest
This essay is republished from our subscription blog in the public
interest.
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