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Anti-AR drug resistance caused by phenotype plasticity. Because of ADT, AR-V7 is produced by mRNA abnormal alternative splicing, leading to a protein that lacks ligand binding domain, but conserves DNA binding and transactivation domains. Androgen-independent AR-V7 activates the transcription of a new set of genes producing epithelial plasticity, were TGF-β is a critical factor inducing the production of neuroendocrine, mesenchymal and stem cells showing resistance to anti-AR therapy
