Thursday, 6-Apr-2006
A newly-discovered mode of action of testosterone is showing great
promise in the fight against prostate cancer, with tests showing a 60%
reduction in tumor size in mice.
Testosterone has been associated with a higher rate of certain cancers.
Classically, testosterone passes through the cell membrane to act inside
the cell. However recent work has indicated that testosterone may also
act at the cell surface, through receptors called Ambs (androgen
membrane binding sites).
Now a team led by Professor Christos Stournaras (University of
Heraklion, Greece) has discovered that activating these cell-surface
testosterone binding sites can significantly reduce the size of prostate
cancer tumours.
When testosterone is bound to another protein such as BSA, it does not
enter the cell, and so can only be expressed at the cell membrane.
Professor Stournaras's team treated mice which had been given prostate
cancer through inoculation with LNCaP cancer cells. They found that
after one month of treatment with testosterone bound to the protein BSA
(Bovine Serum Albumin) there was a 60% reduction in tumour size, with no
apparent side-effects.
Professor Stournaras said: "This work strongly supports the concept that
drugs which activate membrane androgen receptors may represent a new
class of anti-tumour agents in prostate cancer.
This is new, and we need to make sure that these results can be
transferred to humans in a satisfactory way. But if we can develop drugs
which act safely on these Ambs (androgen membrane binding sites) then we
will have a completely new therapeutic option for prostate cancer".
http://www.endocrinology.org
knowledge is power - growing old is mandatory - growing wise is optional
"Many more men die with prostate cancer than of it. Growing old is
invariably fatal. Prostate cancer is only sometimes so."
http://community.webtv.net/PALMER_ENT/doc
Ed Friedman - 07 Apr 2006 18:50 GMT
> Thursday, 6-Apr-2006
>
> A newly-discovered mode of action of testosterone is showing great
> promise in the fight against prostate cancer, with tests showing a 60%
> reduction in tumor size in mice.
This is actually old news. I've been telling people on this newsgroup
about this for over a year now.
The original paper about this can be seen at:
http://jcem.endojournals.org/cgi/content/abstract/90/2/893
My own biomedical model, which is largely based on this paper can be
seen at:
http://www.tbiomed.com/content/2/1/10
Basically, when both mAR and iAR are present and functional, then
maximum stimulation of mAR coupled with minimum stimulation of iAR leads
to apoptosis.
This principle has also been used to design an experiment which showed
that hormonal blockaded followed by testosterone plus finasteride was ~5
times more effective than continual blockade using mice with LNCaP.
This paper can be seen at:
http://www3.interscience.wiley.com/cgi-bin/abstract/112221624/ABSTRACT
However, according to my model, care should be taken by any prostate
cancer patients tempted to try any of these treatments. If you have a
mutation that removes mAR so that it is absent or non-functional, then
T-BSA will be worthless, whereas T will be quite effective. Also, if
you have a mutation that interferes with the ability of the mAR to
produce apoptotic proteins, then both T-BSA and T will be harmful.
Obviously, the more prostate cancer cells that exist before treatment is
started, the more likely that such a harmful mutation might be present.
Ed Friedman