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Academic Department of Biochemistry, Royal Marsden Hospital, London SW3 6JJ, UK
¹ The Breast Unit, Royal Marsden Hospital, London SW3 6JJ, UK
² Breast Center and Department of Pathology and Medicine, Baylor College of Medicine, Houston, TX, USA

(Requests for offprints should be addressed to M Dowsett; Email: mitch.dowsett{at}icr.ac.uk)

This paper was presented at the 1st Tenovus/AstraZeneca Workshop, Cardiff (2005). AstraZeneca has supported the publication of these proceedings.

De novo resistance to endocrine therapy is a near-universal feature of oestrogen receptor (ER)- negative breast cancer. Although many ER-positive breast cancers also show no response to tamoxifen or aromatase inhibitors on objective clinical grounds the large majority show reduced proliferation indicating that some oestrogen dependence is present in almost all ER-positive breast cancer. In neoadjuvant studies HER2 positivity is associated with poor response rates to tamoxifen but not aromatase inhibitors, consistent with preclinical models. Acquired resistance to tamoxifen is associated with decreases in ER positivity but most recurrent lesions remain ER-positive. A small proportion of these show increased HER2 expression and in these patients increased phospho-p38 may contribute to the tamoxifen-resistant phenotype. There is an unfortunate paucity of clinical and biological data on acquired resistance to aromatase inhibitors.

This article has been cited by other articles:

				J M W Gee, A Howell, W J Gullick, C C Benz, R L Sutherland, R J Santen, L-A Martin, F Ciardiello, W R Miller, M Dowsett, et al. Consensus Statement Endocr. Relat. Cancer, July 1, 2005; 12(Supplement_1): S1 - S7. [Abstract] [Full Text] [PDF]