| Literature DB >> 19396167 |
Jennifer C King1, Jin Xu, John Wongvipat, Haley Hieronymus, Brett S Carver, David H Leung, Barry S Taylor, Chris Sander, Robert D Cardiff, Suzana S Couto, William L Gerald, Charles L Sawyers.
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.Entities:
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Year: 2009 PMID: 19396167 PMCID: PMC2898503 DOI: 10.1038/ng.371
Source DB: PubMed Journal: Nat Genet ISSN: 1061-4036 Impact factor: 38.330