--- "susanmchallen"
wrote:
Cimetidine, the generic version of the popular anti-ulcer drug
Tagamet, is a potentially powerful anti-cancer drug, especially if
combined with other compounds.
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.
http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?
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.
http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?
db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=18502198&itool=pubmed_
docsum
>
> 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.
>
> http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?
>
db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=18613849&itool=pubmed_
> docsum
>
> 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.
>
> http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?
>
db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=16785520&itool=pubmed_
> docsum
>
> 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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