| Autor: |
Parnham, Michael J., Bruinvels, J., Furr, Barrington J. A., Miller, William R. |
| Zdroj: |
Aromatase Inhibitors (978-3-7643-8692-4); 2008, p1-21, 21p |
| Abstrakt: |
The natural history of breast cancer suggests that many tumours are dependent upon oestrogen for their development and continued growth [1]. As a consequence it might be expected that oestrogen deprivation will both prevent the appearance of these cancers and cause regression of established tumours [2]. This provides the rationale behind hormone prevention of breast cancer and endocrine management of the disease. Over the last 25 years hormone therapy has progressed from the irreversible destruction of endocrine glands, as achieved by either surgery or radiation (with high co-morbidity), to the use of drugs that reversibly suppress oestrogen synthesis or action (with minimal side effects). In terms of inhibiting oestrogen biosynthesis, it is relevant that primary sites of oestrogen production differ according to menopausal status. Thus in premenopausal women the ovaries are the major source of oestrogen whereas peripheral tissues such as fat, muscle and the tumour itself are more important in postmenopausal patients [3]. In using drugs to block biosynthesis, it is most attractive to employ agents which specifically affect oestrogen production irrespective of site. Mechanistically, this is most readily achieved by inhibiting the final step in the pathway of oestrogen biosynthesis, the reaction which transforms androgens into oestrogens by creating an aromatic ring in the steroid molecule (hence the trivial name of aromatase for the enzyme catalysing this reaction). [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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