Prostate Cancer

Disease / Phenomenon

Prostate cancer is one of the most commonly diagnosed cancers in men, arising from the glandular tissue of the prostate. Its defining clinical feature is heterogeneity: many tumors grow so slowly that they never threaten health and are appropriately managed with active surveillance, while a minority behave aggressively and metastasize, most often to bone. Early disease is typically asymptomatic; urinary symptoms such as weak stream, frequency, or nocturia more often reflect benign enlargement. Risk increases with age, family history, and inherited variants in BRCA2 and other DNA repair genes, and incidence and mortality are notably higher among men of African ancestry. Assessment combines PSA testing, imaging, and Gleason grading of biopsy tissue.

Prostate cancer biology is dominated by androgen receptor signaling. Testosterone is converted by 5-alpha-reductase to dihydrotestosterone, which binds the androgen receptor and drives transcription of growth and survival genes. Suppressing this axis is central to treatment, but tumors adapt through receptor amplification, ligand-independent splice variants such as AR-V7, intratumoral androgen synthesis, and bypass signaling through PI3K/AKT following PTEN loss. TMPRSS2-ERG fusions, defects in homologous recombination repair, chronic inflammation, and remodeling of the bone microenvironment via RANKL shape progression. This page separates these processes into their molecular pathways and biomarkers.