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

Jennifer C. King, Jin Xu, John Wongvipat, Haley Hieronymus, Brett S. Carver, David H. Leung, Barry S. Taylor, Chris Sander, Robert Cardiff, Suzana S. Couto, William L. Gerald, Charles L. Sawyers

Research output: Contribution to journalArticle

340 Scopus citations

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 languageEnglish (US)
Pages (from-to)524-526
Number of pages3
JournalNature Genetics
Volume41
Issue number5
DOIs
StatePublished - May 1 2009

ASJC Scopus subject areas

  • Genetics

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    King, J. C., Xu, J., Wongvipat, J., Hieronymus, H., Carver, B. S., Leung, D. H., Taylor, B. S., Sander, C., Cardiff, R., Couto, S. S., Gerald, W. L., & Sawyers, C. L. (2009). Cooperativity of TMPRSS2-ERG with PI3-kinase pathway activation in prostate oncogenesis. Nature Genetics, 41(5), 524-526. https://doi.org/10.1038/ng.371