Jian Ning

TL;DR: Using cell lines and patient-derived xenograft models, it is shown that high-level FGFR2 amplification initiates a distinct oncogene addiction phenotype, characterized byFGFR2-mediated transactivation of alternative receptor kinases, bringing PI3K/mTOR signaling under FGFR control.

TL;DR: BETi merit clinical evaluation as inhibitors of AR splicing and function, with trials demonstrating their blockade in proof-of-mechanism pharmacodynamic studies.

TL;DR: Rasool et al. as discussed by the authors proposed a small-molecule inhibitor of the p300/CBP conserved bromodomain to inhibit cell proliferation in prostate cancer cell lines and decrease AR- and C-MYC-regulated gene expression.

TL;DR: This data indicates that ATM loss in PC is not always detected by targeted NGS, associates with genomic instability, and is most sensitive to combined ATR and PARP inhibition.

TL;DR: These AR-modulatory miRs and targets correlated with AR activity in patient biopsies, and were elevated in response to long-term enzalutamide treatment of patient-derived CRPC xenografts.