Here's a plot that I made from data taken from the PATCH estrogen patch therapy study. It plots the % reduction in PSA from baseline (100%) at time = 0 as a function of testosterone levels over a period of 4 weeks.
As you know, estrogen effectively castrates men, causing a drop in testosterone over time to castrate levels (< 50 ng/dL). My question was: is this a linear relationship? The answer is "Yes", and one can extrapolate the trend a short distance down to zero PSA at zero testosterone level.
It's exciting to discover linear relationships from complex data sets!
Bob
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janebob99
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1. I've been on Lupron for 5+ years. If I switch to TDE, will it simply step into Lupron's footprints and carry on like nothing happened (as far as treatment of the cancer itself)?
2. Does one eventually reach castrate resistance on TDE, as with ADT? I don't recall anyone on this forum actually reporting that.
Here's what I understand. Since TDE and ADT have the exact same mechanism of action (suppression of FSH and LH hormones), and both of them effectively castrate men (T< 50 ng/dL), it follows that you can substitute one for the other at any point in a treatment cycle.
Estrogen has been used to castrate men for over 70 years (since 1950), in various forms of delivery. The modern delivery method, transdermal, eliminates the old problem of blood clots from oral estrogen (DES).
Someone posted recently that his T had dropped to 3 ng/dL (which is sub-castrate) while on estrogen patches. I forget who said that...
You could also consider adding TDE to Lupron (combo therapy), which your MO might be more likely to do. Just a thought...
The goal of castration should be to reduce T-levels to less than 10 ng/dL in order to maximize survival outcomes. TDE can do this, as well as combinations of other drugs.
Yes, once cancer cells become castrate resistant, then ADT or TDE will probably not work anymore. That's when doing BAT therapy really shines.
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