Publications

Abstract

Endocrine therapies targetting estrogen action (antiestrogens 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 emphasise the importance of deregulation of proliferation and survival signalling in endocrine resistance. However, to date they have offered limited insights into the specific genetic lesions and molecular processes that determine clinical endocrine resistance. The development of large-scale computational and genetic approaches offers the promise of identifying mediators of endocrine resistance that may be exploited as potential therapeutic targets and biomarkers of response in the clinic.