Abstract
Abstract Resistance to the novel androgen receptor (AR)-directed therapies enzalutamide and abiraterone acetate can evolve with an aggressive clinical phenotype and atypical histology, including neuroendocrine features. Genomic studies have also revealed enrichment in TP53 and RB1 alterations in advanced metastatic CRPC when compared with primary disease. In recent work, the Sawyers and Goodrich groups have independently shown that concurrent loss of TP53 and RB1 confers resistance to antiandrogen and lineage plasticity through upregulation of the transcription factor SOX2. These studies implicate key tumor suppressors in lineage switching in resistant prostate cancer, and suggest that antiandrogen resistance may be targeted by epigenetic agents in advanced disease. Citation Format: Wassim Abida. Lineage plasticity in antiandrogen resistance [abstract]. In: Proceedings of the AACR Special Conference: Prostate Cancer: Advances in Basic, Translational, and Clinical Research; 2017 Dec 2-5; Orlando, Florida. Philadelphia (PA): AACR; Cancer Res 2018;78(16 Suppl):Abstract nr IA20.
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