Regulation of ERBB2 by oestrogen receptor–PAX2 determines response to tamoxifen

Antoni Hurtado, Kelly A. Holmes, Timothy R. Geistlinger, Iain R. Hutcheson, Robert I. Nicholson, Myles Brown, Jie Jiang, William J. Howat, Simak Ali and Jason S. Carroll ()
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Antoni Hurtado: Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK
Kelly A. Holmes: Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK
Timothy R. Geistlinger: Dana-Farber Cancer Institute and Harvard Medical School, 44 Binney Street, Boston, Massachusetts 02115, USA
Iain R. Hutcheson: Tenovus Centre for Cancer Research, Welsh School of Pharmacy, Cardiff University
Robert I. Nicholson: Tenovus Centre for Cancer Research, Welsh School of Pharmacy, Cardiff University
Myles Brown: Dana-Farber Cancer Institute and Harvard Medical School, 44 Binney Street, Boston, Massachusetts 02115, USA
Jie Jiang: Imperial College London, Hammersmith Hospital
William J. Howat: Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK
Simak Ali: Imperial College London, Hammersmith Hospital
Jason S. Carroll: Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK

Nature, 2008, vol. 456, issue 7222, 663-666

Abstract: Tamoxifen resistance mechanism Tamoxifen is commonly used for breast cancer therapy, but a proportion of patients become resistant to the treatment, and their cancer is more likely to return. A study of the relationship between the oestrogen receptor and ERBB2/HER-2 pathways in breast cancer throws light on the mechanism of tamoxifen action and on the basis of tamoxifen-resistance. The new work shows that Pax2 is required for active repression of ErbB2 in breast cancer and that reduction of Pax2 causes ErbB2-driven tamoxifen-resistant cell growth.

Date: 2008
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DOI: 10.1038/nature07483

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