Prostate cancer is a heterogeneous disease with co-existence of AR-positive and AR-negative tumour cells in a given patient. Tumour progression is the result of 2 main theories: 

(1) adaptation of AR-positive tumour cells to a low testosterone environment by ligand-dependent and ligand-independent activation of AR signaling

(2) clonal proliferation of AR negative cells which bypass the AR receptor by various mechanisms  (inhibition of apoptosis, stimulation of EMT, cancer stem cells…).

The mode of action of current therapeutic strategies for mCRPC (taxanes, AR targeted agents) will be described.

Content taken from a Sanofi sponsored satellite symposium at ESMO 2013 as part of the official programme.