Steroid hormone receptor binding domain

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Cells of the zona fasciculata and zona reticularis lack aldosterone synthase (CYP11B2) that converts corticosterone to aldosterone, and thus these tissues produce only the weak mineralocorticoid corticosterone. However, both these zones do contain the CYP17A1 missing in zona glomerulosa and thus produce the major glucocorticoid, cortisol. Zona fasciculata and zona reticularis cells also contain CYP17A1, whose 17,20-lyase activity is responsible for producing the androgens, dehydroepiandosterone (DHEA) and androstenedione. Thus, fasciculata and reticularis cells can make corticosteroids and the adrenal androgens, but not aldosterone.





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After a breast cancer is removed, the cells are tested to see if they have receptors for two hormones: estrogen and progesterone. If a breast cancer is hormone-receptor-positive, it means that it has these hormone receptors, which act like ears or antennae. When estrogen in the body attaches to the receptors, the breast cancer cells respond to signals from the estrogen that tell the cells to grow and multiply. By reducing the amount of estrogen in the body or blocking the effects of estrogen, hormonal therapy medicines can slow the growth of or shrink advanced-stage/metastatic estrogen-receptor-positive breast cancers. Lowering the amount of estrogen or blocking its effects also can reduce the risk of an early-stage, estrogen-receptor-positive breast cancer coming back after surgery. Since hormonal therapy affects the action of estrogen but not progesterone in breast cancer cells, the value of hormonal therapy is less clear if your cancer is progesterone-receptor-positive and estrogen-receptor-negative. In this situation, you should discuss the value of hormonal therapy with your doctor.

Steroid hormone receptor binding domain

steroid hormone receptor binding domain

After a breast cancer is removed, the cells are tested to see if they have receptors for two hormones: estrogen and progesterone. If a breast cancer is hormone-receptor-positive, it means that it has these hormone receptors, which act like ears or antennae. When estrogen in the body attaches to the receptors, the breast cancer cells respond to signals from the estrogen that tell the cells to grow and multiply. By reducing the amount of estrogen in the body or blocking the effects of estrogen, hormonal therapy medicines can slow the growth of or shrink advanced-stage/metastatic estrogen-receptor-positive breast cancers. Lowering the amount of estrogen or blocking its effects also can reduce the risk of an early-stage, estrogen-receptor-positive breast cancer coming back after surgery. Since hormonal therapy affects the action of estrogen but not progesterone in breast cancer cells, the value of hormonal therapy is less clear if your cancer is progesterone-receptor-positive and estrogen-receptor-negative. In this situation, you should discuss the value of hormonal therapy with your doctor.

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