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SUMMARY:Quieting the Estrogen Receptor for Therapeutic Benefit in ER+ Brea
 st Cancer - Dr Ciara Metcalfe\; Senior Scientist\, Translational Oncology\
 , Genentech\, San Francisco\, USA 
DTSTART:20210120T170000Z
DTEND:20210120T180000Z
UID:TALK152359@talks.cam.ac.uk
CONTACT:Bobbie Claxton
DESCRIPTION:ER+ breast cancers depend on ER signaling throughout disease p
 rogression\, including after acquired resistance to existing endocrine age
 nts\, providing impetus for further optimization of ER-targeting agents. F
 ulvestrant\, the current best-in-class endocrine agent\, was first discove
 red as a “pure antiestrogen”\, in contrast to earlier generation ER li
 gands that exhibit weak agonistic activity\, such as tamoxifen. After its 
 discovery as a full ER antagonist\, fulvestrant was demonstrated to decrea
 se ER protein levels through proteasome-mediated degradation. These observ
 ations led to the compelling hypothesis that elimination of ER by fulvestr
 ant 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 me
 chanism of action - as we progressed three generations of ER antagonists i
 nto clinical studies.\n\n\nJoin the webinar live using this link:\nhttps:/
 /zoom.us/j/95738930457
LOCATION:Zoom webinar
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