Androgen receptor (AR) is the main target for prostate cancer therapy. Clinical approaches for AR inactivation include chemical castration, inhibition of androgen synthesis and AR antagonists (anti-androgens).
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However, treatment resistance occurs for which an important number of therapy escape mechanisms have been identified. Herein, we summarise the current knowledge of molecular mechanisms underlying therapy resistance in prostate cancer. Moreover, the tumour escape mechanisms are arranged into the concepts of target modification, bypass signalling, histologic transformation, cancer stem cells and miscellaneous mechanisms. This may help researchers to compare and understand same or similar concepts of therapy resistance in prostate cancer and other cancer types.
Seminars in cancer biology 2015 Aug 21 [Epub ahead of print]
Frédéric R Santer, Holger H H Erb, Rhiannon V McNeill
Medical University of Innsbruck, Division of Experimental Urology, Department of Urology, Anichstrasse 35, A-6020 Innsbruck, Austria , Yorkshire Cancer Research Unit, University of York, York YO10 5DD, United Kingdom , Jack Birch Unit for Molecular Carcinogenesis, University of York, York YO10 5DD, United Kingdom