摘要
Since the recent identification of recurrent gene fusions in prostate cancer betweenmembers of the ETS family of genes and transmembrane protease, serine 2 （TM PRSS2）, a tremendous amount of interest has developed in the pathways through which these fusions contribute to prostatic carcinogenesis, as well as their diaenostic utilitv.
Since the recent identification of recurrent gene fusions in prostate cancer betweenmembers of the ETS family of genes and transmembrane protease, serine 2 （TM PRSS2）, a tremendous amount of interest has developed in the pathways through which these fusions contribute to prostatic carcinogenesis, as well as their diaenostic utilitv.
