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

doi:10.1038/ng.371

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

School of Veterinary Medicine

Research output: Contribution to journal › Article › peer-review

345 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 language	English (US)
Pages (from-to)	524-526
Number of pages	3
Journal	Nature Genetics
Volume	41
Issue number	5
DOIs	https://doi.org/10.1038/ng.371
State	Published - May 1 2009

ASJC Scopus subject areas

Genetics

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Cooperativity of TMPRSS2-ERG with PI3-kinase pathway activation in prostate oncogenesis. / King, Jennifer C.; Xu, Jin; Wongvipat, John; Hieronymus, Haley; Carver, Brett S.; Leung, David H.; Taylor, Barry S.; Sander, Chris; Cardiff, Robert; Couto, Suzana S.; Gerald, William L.; Sawyers, Charles L.

In: Nature Genetics, Vol. 41, No. 5, 01.05.2009, p. 524-526.

Research output: Contribution to journal › Article › peer-review

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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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