Table 1.

Potentially actionable common genomic aberrations in prostate cancer

	Type	Frequency (ref. 86,92,172)	Potential targeted therapeutic approach
Intracellular transduction pathways
Androgen receptor	Amplification, mutation	40–50%	Novel AR-targeting agents
KRAS	Mutation	1–2%	MEK inhibitor plus PI3K/AKT inhibitor
PI3K/AKT pathway
PTEN	Deletion, mutation	up to 60–65%	PI3K/Akt inhibitor ± AR-targeting agents
PIK3CA	Amplification, mutation
AKT	Mutation
PHLPP	Deletion
INPP4B	Amplification
RAF-MEK-Erk pathway
BRAF	Gene fusion, mutation	1–2%	BRAF or MEK inhibitor
Transcription factors
N-MYC (concurrent with AURKA)	Amplification	5%	Aurora-A inhibitor
		65% NEPC
ETS (ERG, ETV1, ETV4, FLI1)	Gene fusion	50%	PARP inhibitors±AR-targeting agents
Wnt/β-catenin pathway
APC	Deletion, mutation	4–16%	Wnt-targeting drug
B-catenin	Amplification, mutation
Cell cycle control
CDK4, CDK6, CyclinD1	Mutation, amplification	2–10%	CDK4/6 inhibitor
Chromatin remodeling
EZH2	Amplification	2–5%	EZH2 inhibitor
DNA damage repair
ATM, BRCA1 and BRCA2, RAD51	Mutation, deletion	20–25%	PARP inhibitors