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Drug and hormone interactions of aromatase inhibitors.

M Dowsett

M Dowsett Academic Department of Biochemistry, The Royal Marsden NHS Trust, London, UK.

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The clinical development of aromatase inhibitors has been largely confined to postmenopausal breast cancer patients and strongly guided by pharmacological data. Comparative oestrogen suppression has been helpful in circumstances in which at least one of the comparitors has caused substantially non-maximal aromatase inhibition. However, the triazole inhibitors, letrozole and anastrozole, and the steroidal inhibitor, exemestane, all cause >95% inhibition. Comparisons between these drugs therefore require more sensitive approaches such as the direct measurement of enzyme activity by isotopic means. None of these three agents has significant effects on other endocrine pathways at its clinically applied doses. Pharmacokinetic analyses of the combination of tamoxifen and letrozole have revealed that these drugs interact, resulting in letrozole concentrations approximately 35-40% lower than when letrozole is used alone.

Article Type:: Abstract

Volume/Issue:: Volume 6: Issue 2

Free access

The biology of neoadjuvant chemotherapy for breast cancer.

S Cleator

S Cleator Academic Department of Biochemistry, Royal Marsden Hospital, Fulham Road, London SW3 6JJ, UK. scleator@icr.ac.uk

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M Parton

M Parton Academic Department of Biochemistry, Royal Marsden Hospital, Fulham Road, London SW3 6JJ, UK. scleator@icr.ac.uk

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M Dowsett

M Dowsett Academic Department of Biochemistry, Royal Marsden Hospital, Fulham Road, London SW3 6JJ, UK. scleator@icr.ac.uk

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Neoadjuvant/pre-surgical medical therapy of breast cancer provides a unique opportunity to derive biological information related to tumour response. Large clinical trials of neoadjuvant chemotherapy have established that pathological complete remission is an independent predictor of improved disease-free survival. Clinical response has been found to parallel substantial reductions in the proliferation of breast cancer cells. Increased apoptosis also occurs, but it is not closely associated with response. Numerous biological markers such as p53, bcl-2, oestrogen receptor (ER) and HER2 have been assessed for their possible role in chemoresistance/response, but the data are not clear at this stage. Continuing work using cDNA microarrays may yield new, more reliable indices of likely response and an improved insight into biological processes related to chemotherapeutic response.