University of Cambridge > > Babraham Seminar > Quieting the Estrogen Receptor for Therapeutic Benefit in ER+ Breast Cancer

Quieting the Estrogen Receptor for Therapeutic Benefit in ER+ Breast Cancer

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  • UserDr Ciara Metcalfe; Senior Scientist, Translational Oncology, Genentech, San Francisco, USA
  • ClockWednesday 20 January 2021, 17:00-18:00
  • HouseZoom webinar.

If you have a question about this talk, please contact Bobbie Claxton.

This webinar will be online via zoom. No registration required.

ER+ breast cancers depend on ER signaling throughout disease progression, including after acquired resistance to existing endocrine agents, providing impetus for further optimization of ER-targeting agents. Fulvestrant, the current best-in-class endocrine agent, was first discovered as a “pure antiestrogen”, in contrast to earlier generation ER ligands that exhibit weak agonistic activity, such as tamoxifen. After its discovery as a full ER antagonist, fulvestrant was demonstrated to decrease ER protein levels through proteasome-mediated degradation. These observations led to the compelling hypothesis that elimination of ER by fulvestrant drives full suppression of ER signaling. ER degradation has thus taken center stage in efforts to identify the next generation of ER inhibitors. Here, I’ll describe our learnings, and surprises – related to drug mechanism of action – as we progressed three generations of ER antagonists into clinical studies.

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