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M.UmapathyV

2b)and the emerging recognition of BCL-2 as a survival factor driving castration resistance, here we sought to define how AR +/- BCL-2 +/- PCa cell subtypes dynamically evolve in response to castration and during progression to CRPC, understand how AR signaling controls BCL-2 expression in different androgen signaling environments, and, critically, determine whether BCL-2 represents a shared, therapeutically actionable resistance mechanism across distinct CRPC subtypes

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Simultaneously, we will employ meta-analysis techniques to synthesize results from different datasets, thereby enhancing the generalizability of our findings