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AlaskaAngel · 10-09-2009, 09:03 PM

Hi Dianne,

Tamoxifen works differently than aromatase inhibitors in preventing recurrence.

http://www.healthcentral.com/breast-...aromatase-faqs

"Aromatase is an enzyme that turns the hormone androgen into estrogen. No aromatase = no estrogen. No estrogen = breast cancer cells can't grow (in women with hormone-receptive cancer). An aromatase inhibitor does exactly what it says: it inhibits the enzyme from doing its job. How? By binding itself, either temporarily (Arimidex, Femara) or permanently (Aromasin) to aromatase so that it becomes dysfunctional, and can't turn androgen into estrogen.

Tamoxifen works by preventing estrogen from binding to breast cancer cells and helping them grow. But an AI will actually reduce the amount of estrogen in your body by 90% to 95% - though only in postmenopausal women, which is why AIs are only recommended for women who've stopped having their period. Women whose ovaries are still active, who are still menstruating, produce too much estrogen for AIs to be effective. Thus, the decision for a woman having hormone therapy to start right in on an AI (vs. taking tamoxifen for awhile) may depend on whether her chemotherapy-induced menopause is permanent, or only temporary. If permanent, her doctor might start her on an AI right away. If temporary, and she remains pre-menopausal, she's not a candidate for an AI."

So I think maybe what they are saying in the article is that for those women who are hormone receptor positive and premeno AND for whom tamoxifen is unlikely to work well, instead they would need to bring about menopause with ovarian ablation in some way and then put those women on an AI.

10-09-2009, 09:03 PM	#3
AlaskaAngel Senior Member Join Date: Sep 2005 Location: Alaska Posts: 2,018	Re: CYP2D6 Influence on Tamoxifen Response Hi Dianne, Tamoxifen works differently than aromatase inhibitors in preventing recurrence. http://www.healthcentral.com/breast-...aromatase-faqs "Aromatase is an enzyme that turns the hormone androgen into estrogen. No aromatase = no estrogen. No estrogen = breast cancer cells can't grow (in women with hormone-receptive cancer). An aromatase inhibitor does exactly what it says: it inhibits the enzyme from doing its job. How? By binding itself, either temporarily (Arimidex, Femara) or permanently (Aromasin) to aromatase so that it becomes dysfunctional, and can't turn androgen into estrogen. Tamoxifen works by preventing estrogen from binding to breast cancer cells and helping them grow. But an AI will actually reduce the amount of estrogen in your body by 90% to 95% - though only in postmenopausal women, which is why AIs are only recommended for women who've stopped having their period. Women whose ovaries are still active, who are still menstruating, produce too much estrogen for AIs to be effective. Thus, the decision for a woman having hormone therapy to start right in on an AI (vs. taking tamoxifen for awhile) may depend on whether her chemotherapy-induced menopause is permanent, or only temporary. If permanent, her doctor might start her on an AI right away. If temporary, and she remains pre-menopausal, she's not a candidate for an AI." So I think maybe what they are saying in the article is that for those women who are hormone receptor positive and premeno AND for whom tamoxifen is unlikely to work well, instead they would need to bring about menopause with ovarian ablation in some way and then put those women on an AI.