Table 1.

Molecular subtypes for prostate cancer (PCa).

Molecular Alteration	Molecular Alteration Subtype	Frequency	Biologic Implication	Proposed Therapy
Androgen Receptor (AR)	Amplification		Resistance to androgen deprivation therapy (ADT)	New antiandrogens (enzalutamide/abiraterone)
	Mutation			Non-NAD-like PARP-1 inhibitors
	Alternative Splicing	4% early stage 20–30% advanced/recurrent disease)		Taxanes
	Changes in the expression of AR Co-regulators			Combine therapies (Antiandrogens + PARPi/Immunotherapy) to modify the immunosuppressive TME
PI3K-AKT	Loss of PTEN AKT/PI3K alteration	49%	Resistance to ADT and PARPi	PTEN, AKT and PI3K INHIBITORS (monotherapy/combinations)
DNA Repair Pathways	Mutation in the DDR system (homologous repair)		PARPi sensitivity	PARPi
Others	Wnt Genetic fusion	23% 18%	Resistance to ADT	Development of new therapeutic targets and combinations

Key: PARPi: PARP inhibitors; TME: tumor microenvironment.