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CRPC transformation mechanisms are complex and multifaceted, involving sustained AR pathway activation (5, 6) [through AR mutations, amplification, or variants like AR-V7 that confer ADT insensitivity (7)], bypass signaling pathway activation (e.g., PI3K/AKT, Wnt/-catenin), DNA repair defects, and tumor microenvironment (TME) alterations (8)

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