Abstract

Endocrine therapies targeting oestrogen action (anti-oestrogens, such as tamoxifen, and aromatase inhibitors) decrease mortality from breast cancer, but their efficacy is limited by intrinsic and acquired therapeutic resistance. Candidate molecular biomarkers and gene expression signatures of tamoxifen response emphasize the importance of deregulation of proliferation and survival signalling in endocrine resistance. However, definition of the specific genetic lesions and molecular processes that determine clinical endocrine resistance is incomplete. The development of large-scale computational and genetic approaches offers the promise of identifying the mediators of endocrine resistance that may be exploited as potential therapeutic targets and biomarkers of response in the clinic.

Author affiliations

1. Cancer Research Program, Garvan Institute of Medical Research, Sydney, New South Wales 2010, Australia.
2. St Vincent's Clinical School, Faculty of Medicine, University of New South Wales, New South Wales 2052, Australia.
   Email: e.musgrove@garvan.org.au; Email: r.sutherland@garvan.org.au

MORE ARTICLES LIKE THIS

These links to content published by NPG are automatically generated.