Analyses of genetically engineered mouse models reveal the androgen receptor-independent properties of a luminal stem/progenitor cell in the prostate epithelium, and its ability to serve as a cell of origin for castration-resistant prostate cancer.

SPOP mutations underlie a novel, genomically unstable subclass of prostate cancer by altering DNA repair.

PRUNE2/PCA3 axis dysregulation is an early, rather than late, event in prostate cancer tumorigenesis.

A positive feedback loop between the androgen receptor and a key pentose phosphate pathway enzyme, 6PGD, in prostate cancer promotes tumour cell proliferation, survival and intracellular redox control.

Mutual suppression of ETV1 by Capicua (CIC) and ETS2 repressor factor (ERF) limits prostate cancer progression.

DECR1, a rate-limiting enzyme for polyunsaturated fatty acid (PUFA) β-oxidation, is an androgen-repressed gene in prostate cancer cells that limits oxidative stress to promote cancer cell survival.

The transcription factor RUNX1 marks a distinct lineage of luminal castration-resistant prostate cells established early during development and enriched in the periurethral region of adult mouse prostate.

Coregulators mediate selective interactions between DNA-bound androgen receptor and other transcription factors, which control distinct prostate cancer biology, suggesting disruption of critical interactions in these complexes as a novel therapeutic strategy.

A large-scale single-cell RNA sequencing experiment explores single-cell dynamics in epithelial and immune populations within murine prostates upon cancer initiation and progression and validates key findings across orthogonal models and patient specimens.

Epigenetic regulation of the glucocorticoid receptor in castration-resistant prostate cancer can be targeted via the use of BET bromodomain inhibitors.