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Nat Genet. 2009 May;41(5):524-6. doi: 10.1038/ng.371. Epub 2009 Apr 26.

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

Author information

1
Memorial Sloan-Kettering Cancer Center, New York, New York, USA.

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.

PMID:
19396167
PMCID:
PMC2898503
DOI:
10.1038/ng.371
[Indexed for MEDLINE]
Free PMC Article

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