Pushing estrogen receptor around in breast cancer

  1. Carlo Palmieri3,*
  1. 1Garvan Institute of Medical Research and St Vincent’s Hospital, University of New South Wales, Sydney, New South Wales, Australia
  2. 2Dame Roma Mitchell Cancer Research Laboratories and Adelaide Prostate Cancer Research Centre, University of Adelaide, Adelaide, South Australia, Australia
  3. 3Institute of Translational Medicine, University of Liverpool, Clatterbridge Cancer Centre, NHS Foundation Trust, and Royal Liverpool University Hospital, Liverpool, Merseyside, UK
  1. Correspondence should be addressed to W D Tilley or C Palmieri; Email: wayne.tilley{at}adelaide.edu.au or c.palmieri{at}liverpool.ac.uk
  1. Figure 1

    Progesterone receptor (PR) reprograms estrogen receptor (ER) binding towards genes associated with good prognosis. In the absence of progesterone or the PR (left), ER binds to estrogen response elements and activates the expression of genes involved in cell proliferation and survival. In the presence of PR and progesterone (right), PR binds to and physically displaces the ER by binding to progesterone response elements at genes associated with cell differentiation and death. Therefore, progesterone is able to exert influence on the ER genomic binding landscape and expected to promote favourable outcomes in a subset of patients with ER- and PR-positive breast cancer.

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