Cooperativity of TMPRSS2-ERG with PI3-kinase pathway activation in prostate oncogenesis

JC King, J Xu, J Wongvipat, H Hieronymus, BS Carver… - Nature …, 2009 - nature.com
JC King, J Xu, J Wongvipat, H Hieronymus, BS Carver, DH Leung, BS Taylor, C Sander
Nature genetics, 2009nature.com
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 …
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.
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