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Histopathological and multiomic analyses of prostate tissues and organoids revealed that Class 1 mutations, in conjunction with\n            <jats:italic toggle=\"yes\">p53<\/jats:italic>\n            inactivation, drive androgen-dependent adenocarcinomas through coactivation of mTORC1\/2 and oncogenic AR signaling stemming from chimeric AR-half enhancers. By contrast, Class 2 mutations induce intraluminal plasticity by reprogramming differentiated luminal cells into a progenitor-like state through activation of KLF5 and AP-1 neo-enhancer circuitries, which enables enhanced survival and proliferation even under castrate androgen levels. 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