identified that the frequent loss of Synaptotagmin Binding Cytoplasmic RNA Interacting Protein (SYNCRIP) as a driver

overactivated APOBEC3B, in SYNCRIP-loss is a mutated genes' source, including FOXA1, EP300 and AR

identified eight crucial drivers for Androgen Receptor (AR)-targeted therapy resistance in PCa that are recurrently mutated by dysregulated APOBEC3B: BRD7, CBX8, EP300, FOXA1, HDAC5, HSF4, STAT3, and AR

reveals that driver mutations in FOXA1 induced by APOBEC3B, evolutionarily outcompete other driver mutations and eventually dominate the resistant tumors

Collectively, these findings uncover a long sought-after, cell-intrinsic mechanism that controls tumor mutational burden and heterogeneity, and mechanistically links both SYNCRIP and overactivated APOBEC3B-driven mutagenesis to some of the most frequently observed driver mutations that confer targeted therapy resistance in PCa.

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