Prostatic Neoplasms

The grounding supports a multifactorial etiology involving genetic and somatic alterations, including germline and tumor molecular testing targets. It also indicates that genomic heterogeneity and adaptive responses contribute to disease development and progression, but does not support a single specific cause.

The literature describes prostate cancer as biologically heterogeneous, with tumor-intrinsic and tumor-extrinsic mechanisms operating within the tumor microenvironment. Progression is linked to androgen receptor signaling, gene expression regulation, epigenetic changes such as DNA methylation, signal transduction pathways, and mechanisms of therapeutic resistance, including in castration-resistant disease.

The grounding supports age, sex, family history, lifestyle factors, and genomic information as risk-prediction inputs for prostate cancer. It also supports inherited and tumor genetic variation as relevant to risk stratification, but does not provide additional specific risk factors.

Management is described at the modality and drug-class level as risk stratification, localized-disease treatment, and monitoring or treatment of recurrent and advanced disease. Systemic therapy includes androgen deprivation therapy, secondary hormonal therapy, chemotherapy, and immunotherapy, with treatment intensification in metastatic castration-sensitive disease and sequential addition of hormonal agents in castration-resistant disease.