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Aromasin (Exemestane)
 
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Longer follow-up data from a large international phase III trial of postmenopausal women with breast cancer who switched to the drug exemestane (Aromasin®) after several years on tamoxifen confirm a delay in disease progression and also show a survival advantage, compared to women who stayed on tamoxifen.

Following surgery for breast cancer, women whose tumors grow in response to the hormone estrogen usually take the anti-estrogen drug tamoxifen for five years to reduce their risk that the disease will recur. However, tamoxifen does not prevent all recurrences, and breast cancer cells can become resistant to this drug. In addition, tamoxifen increases a woman's risk for endometrial cancer, blood clots, and stroke.

Tamoxifen and exemestane both block the growth of breast tumors that respond to estrogen, but the two drugs work in different ways. Tamoxifen interferes with the ability of breast cancer cells to use estrogen for growth, whereas exemestane interferes with the body's ability to make estrogen.

Exemestane inactivates the enzyme aromatase, which the body uses to make estrogen. Before menopause, most estrogen is produced in the ovaries, which contain more aromatase than exemestane can block. After menopause, however, the ovaries are no longer a major source of estrogen, and exemestane is able to block estrogen production by other tissues. Therefore, exemestane and other so-called aromatase inhibitors (AIs) are effective only in postmenopausal women.

Early findings from several large international trials have suggested that cancer is less likely to recur in women who take an AI after five years of tamoxifen or switch to an AI after a shorter period on tamoxifen. These studies involved AIs other than exemestane - specifically, anastrozole (Arimidex®) and letrozole (Femara®). Unlike tamoxifen, AIs do not increase the risk of endometrial cancer, blood clots, or stroke.

 

Exemestance

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