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

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 t...

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Veröffentlicht in:Nature genetics 2009-05, Vol.41 (5), p.524-526
Hauptverfasser: Sawyers, Charles L, King, Jennifer C, Xu, Jin, Wongvipat, John, Hieronymus, Haley, Carver, Brett S, Leung, David H, Taylor, Barry S, Sander, Chris, Cardiff, Robert D, Couto, Suzana S, Gerald, William L
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Sprache:eng
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Zusammenfassung: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.
ISSN:1061-4036
1546-1718
DOI:10.1038/ng.371