Table 1.

Clinically Relevant Genomic Alterations in Prostate Cancer

Gene	Alteration Type	Frequency (%)	Potential Treatment Hypotheses
ETS transcription factors	Rearrangement	507	Indirect targeting of ETS gene fusions through PARP or DNAPK inhibitors8
Androgen receptor	Mutation	509,10	Androgen synthesis inhibitors, next-generation androgen receptor antagonists
	Amplification	509,10
PTEN	Loss	509	PI3K pathway inhibitors11
RB1	Loss	25 to 609	Role in disease progression and castrate resistance12 with potential for targeting
PIK3CA	Amplification	1010	PI3K pathway inhibitors11
	Mutation	510
MYC	Amplification	99	Potential for targeting13
		4010	Neuroendocrine prostate cancer
AURKA	Amplification	510	Aurora kinase inhibitors14; co-occurs with MYC in 40% of neuroendocrine prostate cancers
AKT	Mutation	1 to 215	AKT inhibitors
RAF	Rearrangement	1 to 216	RAF inhibitors
	Mutation
KRAS	Mutation	19,18,18	RAF, MEK, or PI3K inhibitors
	Rearrangement

NOTE. Summarizes alterations in prostate cancer that have a treatment hypothesis currently being explored preclinically or in clinical trials. The most common alterations with a treatment hypothesis involve ETS rearrangements, androgen receptor, and PTEN loss. With only a limited number of samples assessed, a majority of these alterations are not necessarily mutually exclusive.

Abbreviation: PI3K, phosphatidylinositide 3-kinase.