By B.J.A. Furr, Angela Brodie, Aman Buzdar, J. Michael Dixon, Per Eystein Lonning, William R. Miller, Robert Paridaens, Evan R. Simpson, Alan E. Wakeling
This publication offers the 1st accomplished assessment at the various aromatase inhibitors. while the 1st aromatase inhibitors for use therapeutically should be proven to supply drug-induced inhibition of the enzyme and healing advantages in sufferers with breast melanoma, they weren't very effective and lacked specificity. besides the fact that, second-generation medications have been built and such a lot lately third-generation inhibitors have advanced which own striking specificity and efficiency.
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Extra resources for Aromatase Inhibitors (Milestones in Drug Therapy)
Example text
As indicated above, formestane is a substrate analogue and mechanism-based inhibitor (suicide inhibitor) that inactivates the enzyme by binding irreversibly [10, 11]. Subsequently, exemestane (aromasin) became available and is also in this class of inhibitors. A number of non-steroidal aromatase inhibitors were later developed and include the highly potent triazole compounds letrozole and anastrozole. Nonsteroidal inhibitors possess a heteroatom such as a nitrogen-containing heterocyclic moiety.
Patients with early breast cancer were treated with anastrozole, tamoxifen, or the combination. Treatment with anastrozole alone proved to be superior to tamoxifen, indicating for the first time that aromatase inhibitors were more effective in treating breast cancer patients than tamoxifen. However, treatment with the combination of anastrozole and tamoxifen was no better than with tamoxifen alone. In recent studies, combining exemestane and tamoxifen showed that the combination was better than either tamoxifen or exemestane alone.
This implies that some transcription via the ER may occur with fulvestrant treatment alone that is not completely blocked by the antioestrogen. The combined treatment resulted in tumour regression, which was maintained throughout the 29-week treatment period [92]. This result indicates that the combination of reducing oestrogen production and downregulating the ER could prevent or delay development of resistance to letrozole. Expression of erbB2 and MAPK were increased, relative to control samples, in tumours treated with letrozole and fulvestrant.