Author(s): King JC, Xu J, Wongvipat J, Hieronymus H, Carver BS,
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Abstract The TMPRSS2-ERG fusion, present in approximately 50\% of prostate cancers, is less common in prostatic intraepithelial neoplasia (PIN), raising questions about whether TMPRSS2-ERG contributes to disease initiation. We identified the translational start site of a common TMPRSS2-ERG fusion and showed that transgenic TMPRSS2-ERG mice develop PIN, but only in the context of PI3-kinase pathway activation. TMPRSS2-ERG-positive human tumors are also enriched for PTEN loss, suggesting cooperation in prostate tumorigenesis.
This article was published in Nat Genet
and referenced in Journal of Steroids & Hormonal Science