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Evidence of androgen action in endometrial and ovarian cancers.

Abstract
Endometrial cancer (EC) and ovarian cancer are common gynaecological malignancies. The impact of androgen action in these cancers is poorly understood; however, there is emerging evidence to suggest that targeting androgen signalling may be of therapeutic benefit. Epidemiological evidence suggests that there is an increased risk of EC associated with exposure to elevated levels of androgens, and genetic variants in genes related to both androgen biosynthesis and action are associated with an increased risk of both EC and ovarian cancer. Androgen receptors (ARs) may be a potential therapeutic target in EC due to reported anti-proliferative activities of androgens. By contrast, androgens may promote growth of some ovarian cancers and anti-androgen therapy has been proposed. Introduction of new therapies targeting ARs expressed in EC or ovarian cancer will require a much greater understanding of the impacts of cell context-specific AR-dependent signalling and how ARs can crosstalk with other steroid receptors during progression of disease. This review considers the evidence that androgens may be important in the aetiology of EC and ovarian cancer with discussion of evidence for androgen action in normal and malignant endometrial and ovarian tissue.
AuthorsDouglas A Gibson, Ioannis Simitsidellis, Frances Collins, Philippa T K Saunders
JournalEndocrine-related cancer (Endocr Relat Cancer) Vol. 21 Issue 4 Pg. T203-18 (Aug 2014) ISSN: 1479-6821 [Electronic] England
PMID24623742 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
Copyright© 2014 Society for Endocrinology.
Chemical References
  • Androgen Antagonists
  • Androgens
  • Receptors, Androgen
Topics
  • Androgen Antagonists (therapeutic use)
  • Androgens (metabolism, pharmacology)
  • Endometrial Neoplasms (epidemiology, etiology, therapy)
  • Endometrium (drug effects, metabolism)
  • Female
  • Humans
  • Molecular Targeted Therapy
  • Ovarian Neoplasms (epidemiology, etiology, therapy)
  • Ovary (drug effects, metabolism)
  • Receptors, Androgen (genetics, metabolism)

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