Prostatic adenocarcinoma is the most common noncutaneous malignancy in men and the second leading cause of cancer death in Western populations. Despite its prevalence, an understanding of the molecular alterations affecting the development, progression, and treatment of the disease was largely lacking until recently. Rapid advances in molecular techniques in the past decade have seen a dramatic increase in our understanding of the role molecular alterations play in prostate cancer. Though still early, these developments have provided insight into distinct subsets of prostate cancer that promise to change how the disease is both diagnosed and managed. The molecular alterations discovered have shown that prostate cancer development involves multiple genetic abnormalities and that detection or targeting of a single genetic event is unlikely to impact all cases of prostate cancer. Of the ones that have shown the most promise to changing diagnostic and treatment paradigms are the gene fusion of TMPRSS2 and members of the ETS family of transcription factors, primarily ERG, as well as the inactivation of the tumor suppressor PTEN. A greater understanding of the molecular alterations present in prostate cancer will lead to further improvements in diagnosis, prediction of prognosis, stratification for specific therapies, and ultimately better outcomes for patients.
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