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.
Original language | English (US) |
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Pages (from-to) | 524-526 |
Number of pages | 3 |
Journal | Nature Genetics |
Volume | 41 |
Issue number | 5 |
DOIs | |
State | Published - May 1 2009 |
ASJC Scopus subject areas
- Genetics