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. Author manuscript; available in PMC: 2013 May 1.
Published in final edited form as: Cancer Discov. 2012 Oct 5;2(11):985–994. doi: 10.1158/2159-8290.CD-12-0178

Figure 1. A brief synopsis of recurrent oncogenic lesions in CRPC.

Figure 1

Pathological activation of AR signaling is one of the most clearly understood hallmarks of CRPC, occurring via gene amplification, receptor stabilization, or endocrine production of androgens. The transcriptional repertoire of AR is known to include several genes linked to the patho-biology of CRPC, including the TMPRSS2-ERG fusion protein. In addition, pathological activation of the PI3K signaling axis occurs very commonly in CRPC, principally via inactivation of the tumor suppressor PTEN. The downstream consequences of aberrant PI3K signaling are still being defined, but in some contexts, deregulation of transcriptional programs (e.g. HIF1α, Forkhead family transcription factors) seems to drive the pathology of this event. Finally, the transcription factor MYC is also a well-defined oncogenic driver of prostate cancer, with copy number alterations annotated in approximately 30% of patients.