Two common hormone therapies are used to block estrogen and/or progesterone-induced tumor growth. Which pair is correct?

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Multiple Choice

Two common hormone therapies are used to block estrogen and/or progesterone-induced tumor growth. Which pair is correct?

Explanation:
In cancers driven by estrogen signaling, the goal is to shut down the hormone’s ability to fuel tumor growth, either by blocking the receptor itself or by lowering the amount of estrogen produced. Tamoxifen acts as an estrogen receptor blocker, preventing estrogen from binding and stimulating cancer cells. Aromatase inhibitors stop the production of estrogen by inhibiting aromatase, the enzyme that converts androgens to estrogen, which lowers circulating estrogen levels and reduces estrogen-driven growth. These two approaches—receptor blockade and estrogen production reduction—are the classic hormone therapies used in estrogen receptor–positive tumors. The other options involve chemotherapy or non-hormonal targeted therapies that don’t directly interfere with estrogen signaling or synthesis, so they aren’t considered hormone therapies for blocking estrogen- or progesterone-induced tumor growth.

In cancers driven by estrogen signaling, the goal is to shut down the hormone’s ability to fuel tumor growth, either by blocking the receptor itself or by lowering the amount of estrogen produced. Tamoxifen acts as an estrogen receptor blocker, preventing estrogen from binding and stimulating cancer cells. Aromatase inhibitors stop the production of estrogen by inhibiting aromatase, the enzyme that converts androgens to estrogen, which lowers circulating estrogen levels and reduces estrogen-driven growth. These two approaches—receptor blockade and estrogen production reduction—are the classic hormone therapies used in estrogen receptor–positive tumors. The other options involve chemotherapy or non-hormonal targeted therapies that don’t directly interfere with estrogen signaling or synthesis, so they aren’t considered hormone therapies for blocking estrogen- or progesterone-induced tumor growth.

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