It looked like Provenge and SBRT last October had lowered and stabilized my rapidly rising PSA to around 1.8 for three months. Then three weeks ago it mysteriously doubled in a month to 3.1
A new PSMA scan showed four new scattered bone mets appearing since last PSMA scan 3 months prior. Micro mets maturing? I started Xtandi mono therapy ten days ago- but to avoid breast development also added 20 mg Tamoxifen. Ten days later PSA dropped from 3.190 to .910 but hemoglobin also dropped from 11.8 down to 10.3 So although news is both good and bad we are curious as to what happened.
The plan was to use Xtandi mono therapy in order to maintain testosterone so hopefully hemoglobin would rise and PSA would decline. While free of all drugs (Orgovyx, & LU-177) since August, testosterone had slowly rose to 152 then declined then a month later to 135, then 129 and a few days ago dropped to 39.5
Assumption was made that Xtandi blocked cancer receptors but did not lower testosterone. What say the brilliant brethren?
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"Assumption was made that Xtandi blocked cancer receptors but did not lower testosterone." Xtandi usually raises T initially because it blocks T receptors and the T has nowhere to go, and accumulates in the serum. The excess T is eventually metabolized into DHT and estrogen, so balding and gynecomastia are common side effects of monotherapy . If T gets too high, T production will shut down.
But notice I wrote T receptors (androgen receptors -ARs) and not cancer receptors. IDK if there are ARs in the bone marrow or if T activates blood cell production through some other mechanism. Let us know if it works!
Xtandi monotherapy was suggested by Dr. Dorf at COH which provided some optimism. One other factor was that the blood work was performed 18 hours after a 3- hour endoscopic spine surgery to trim off some bulging disk that was hitting a nerve. Could that have muddied the waters?
so T_A , do you believe that Testosterone is indeed the gasoline on the fire of PCa as has been taught in Med School forever or do you think newer, better, bigger studies might have now refuted this idea ?
Of course,T activates androgen receptors on cancer cells. There are no studies that refute that. In fact, Morgentaler's saturation hypothesis depends upon the fact that all receptors are activated at very low T levels.
The question I have is if XTANDI does not lower testosterone, why is my testosterone plunging? It was actually going down on its own prior to XTANDI and then it suddenly dropped.
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