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Androgen receptor (AR) signaling exerts an antiestrogenic, growth-inhibitory influence in normal breast tissue, and this role may be sustained in estrogen receptor α (ERα)-positive luminal breast cancers. Conversely, AR signaling may promote growth of a subset of ERα-negative, AR-positive breast cancers with a molecular apocrine phenotype. Understanding the molecular mechanisms whereby androgens can elicit distinct gene expression programs and opposing proliferative responses in these two breast cancer phenotypes is critical to the development of new therapeutic strategies to target the AR in breast cancer.
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Theresa E. Hickey
The University of Adelaide
Jessica Robinson
University of Auckland
Jason S. Carroll
Brigham Young University
Molecular Endocrinology
University of Cambridge
The University of Adelaide
Cancer Research UK
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Hickey et al. (Fri,) studied this question.
synapsesocial.com/papers/6a1a09831d4d911c80eac354 — DOI: https://doi.org/10.1210/me.2012-1107