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Old 02-02-2007, 06:45 PM   #1
BarbH
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Join Date: May 2006
Posts: 2
Question Need some insight on endocrine therapy or not

Hi everyone,

I am 46 years old and I will celebrate 4 years on 14 Feb. At 42, I had a lumpectomy, dense-dose treatments A/C and taxol, radiation, tried tamoxifen (elevated liver enzymes), took Zoladex shots combined with Aromatase Inhibitor until Mar 1, 2005 when I underwent surgical removal of my ovaries. Have not maintained a standard 5 year endocrine adjuvant therapy route, because of so many different problems. A few months ago I started taking an AI inhibitor and had my cholestrol checked and it was 280! I never had high cholestrol and wonder if it is not the lack of estrogen and the drugs. Anyway, I am struggling with the idea of taking an AI since the main source of estrogen is cut-off. I know it is an added precaution, but wonder why they don't monitor estrogen levels in the body while we are on these AI inhibitors. Is this even something to consider? I am finally starting to feel somewhat normal - with the help of Zoloft, Boniva, Synthroid, and Anti-anxiety stuff. Does anyone else deal with this, or have any experience? Oh, and I forgot to mention, I also had a year of preventative herceptin treatments (finished 1 Sep 06) because I am ER+/PR+/HER2NU+, Stage IIIB.

Last edited by BarbH; 02-02-2007 at 06:47 PM.. Reason: I don't know
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Old 02-02-2007, 07:36 PM   #2
Lani
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Join Date: Mar 2006
Posts: 4,782
the breast cancer cells & their extracellular matrix have their own aromatase enzyme

and make their own estradiol--so just knowing the circulating blood level of estradiol in your bloodstream won't tell the whole story--it won't tell the concentration in the cancer cell's local environment which is what stimulates them to grow. Thus, even with low blood levels of estradiol there can still be locally high concentrations of estradiol stimulating the cancer cells to grow.

Aromatase inhibitors seem to inhibit aromatase wherever it is--in fat, in muscle or in the tumor cells. There will probably more targetted antihormonal treatments in the pipeline which might be more directed just to the aromatase that the breast/breast cancer makes, but they seem several years or more away.

her2+ breast cancer cells are less sensitive to AIs than her2- breast cancer cells, but it works in them, just to a lesser degree.

Theoretically, fulvestrant may be better in her2+ breast cancer, but it is only approved for those with metastatic disease who have failed tamoxifen or AIs

This is an area that is actively evolving and the answers are not known yet.

Hope some of this info helped.
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