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• W3030794881 abstract "<h2>Summary</h2> Prostate cancers (PCs) with loss of the potent tumor suppressors <i>TP53</i> and <i>RB1</i> exhibit poor outcomes. <i>TP53</i> and <i>RB1</i> also influence cell plasticity and are frequently lost in PCs with neuroendocrine (NE) differentiation. Therapeutic strategies that address these aggressive variant PCs are urgently needed. Using deep genomic profiling of 410 metastatic biopsies, we determine the relationships between combined <i>TP53</i> and <i>RB1</i> loss and PC phenotypes. Notably, 40% of <i>TP53/RB1</i>-deficient tumors are classified as AR-active adenocarcinomas, indicating that NE differentiation is not an obligate consequence of <i>TP53/RB1</i> inactivation. A gene expression signature reflecting <i>TP53/RB1</i> loss is associated with diminished responses to AR antagonists and reduced survival. These tumors exhibit high proliferation rates and evidence of elevated DNA repair processes. While tumor cells lacking <i>TP53/RB1</i> are highly resistant to all single-agent therapeutics tested, the combination of PARP and ATR inhibition is found to produce significant responses, reflecting a clinically exploitable vulnerability resulting from replication stress." @default.
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• W3030794881 date "2020-05-01" @default.
• W3030794881 modified "2023-10-18" @default.
• W3030794881 title "Combined TP53 and RB1 Loss Promotes Prostate Cancer Resistance to a Spectrum of Therapeutics and Confers Vulnerability to Replication Stress" @default.
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• W3030794881 doi "https://doi.org/10.1016/j.celrep.2020.107669" @default.
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