Overexpression of HER-2 as a resistance mechanism to hormonal therapy for breast cancer.

in Endocrine-Related Cancer
Author:
M Dowsett Department of Biochemistry, Royal Marsden Hospital, London SW3 6JJ, UK. mitch@icr.ac.uk

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Volume/Issue:
Volume 8: Issue 3
Article Type:
Abstract
Page Range:
191–195
Online Publication Date:
Sep 2001
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Hormonal therapy leads to improved survival in oestrogen receptor (ER) positive early breast cancer and long-term responses in advanced disease. However, resistance to such therapy is a serious clinical problem. This article considers the data for and against there being a significant role for the oncogene HER-2 in such resistance. Transfection of HER-2 into MCF-7 cells leads to resistance to tamoxifen but data differ in relation to the oestrogen dependence of such cells. A number of retrospective studies have been conducted of HER-2 status in adjuvant trials of tamoxifen. Most of these also suggest a negative role but individually the studies do not have the statistical power to be conclusive. Recent studies in the neoadjuvant context have shown a significant antiproliferative effect of endocrine therapy in HER-2 positive/ER positive tumours but this is much less than in HER-2 negative/ER positive tumours. It is concluded that incomplete hormonal resistance results from co-expression of HER-2 and ER and that this may differ between different hormonal agents.

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Print ISSN:
1351-0088
Online ISSN:
1479-6821
Page(s):
5
Print Publication Date:
01 Jan 2001
Online Publication Date:
Sep 2001