Im going to revive this since it still seems unanswered to the author and hopefully shed some light.
Studies like this one...
What do we know about the mechanisms of aromatase inhibitor resistance?
seem to give people the idea that AI's lose effectiveness but I think that is because some of the statements in the study are being applied out of context are at least partially out of context. Lets look at a coupel lines from the above study....
The article starts off with the following line...
Clinical trials have demonstrated the importance of aromatase inhibitor (AI) therapy in the effective treatment of hormone-dependent breast cancers. Yet, as with all prolonged drug therapy, resistance to aromatase inhibitors does develop.
By itself it would indicate they lose effectiveness, however right after the above quote is this.....
To date, the precise mechanism responsible for resistance to aromatase inhibitors is not completely understood. In this paper, several mechanisms of de novo/intrinsic resistance and acquired resistance to AIs are discussed. These mechanisms are hypothesized based on important findings from a number of laboratories.
It clearly states the mechanism responsible IS NOT understood and the mechanisms are
hypothesized
A bit father down we see the following statement....
Almost all the data on acquired resistance are at present derived from laboratory studies. A major hypothesis is that the adaptation to estrogen withdrawal is involved in the resistance to both tamoxifen and AIs. Due to the ability of breast cancer cells to be adaptive, these endocrine therapies that function to block hormone-dependent signaling cascades required for breast cancer proliferation, may cause novel signaling mechanisms which circumvent the effects of an AI or anti-estrogen. An attractive hypothesis is that the resistance results from estrogen hypersensitivity or estrogen-independent activation of ER.
As well as this one....
There are two types of endocrine resistance. De novo/intrinsic resistance refers to lack of response at initial exposure to endocrine therapy of aromatase-positive and estrogen receptor (ER)-positive breast cancers. Acquired resistance is developed during endocrine therapy of patients who respond to the treatment initially. We and other investigators believe that elucidating the mechanisms of resistance to AIs/antiestrogens, on the molecular level, will be extremely valuable for the effective treatment of hormone-dependent breast cancers and for the development of novel approaches to treat patients who fail endocrine therapy.
Now I have to ask, what is
cancer? Well, as deined by biology online.....
a cell that divides and reproduces abnormally with uncontrolled growth. This cell can break away and travel to other parts of the body and set up another site, referred to as metastasis.
What this study is talking about is the reduced effectiveness of AI's on tumors, cancerous tumors, cancer that divides and reproduces abnormally. If a study says that an E level remains constant for 7 months but its effectiveness falls to 33% after 6 months as I recall seeing in another study you posted, they are specifically referring to the AI's effectiveness against the cancer, not its effectivness at reducing E.