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.
Publication types
-
Comment
-
Research Support, N.I.H., Extramural
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Humans
-
Male
-
Mice
-
Mice, Transgenic
-
Oncogene Proteins, Fusion / genetics
-
Oncogene Proteins, Fusion / metabolism*
-
Phosphatidylinositol 3-Kinases / metabolism*
-
Prostate / metabolism*
-
Prostate / pathology
-
Prostatic Intraepithelial Neoplasia / metabolism
-
Prostatic Intraepithelial Neoplasia / pathology
-
Prostatic Neoplasms / metabolism*
-
Signal Transduction*
Substances
-
Oncogene Proteins, Fusion
-
TMPRSS2-ERG fusion protein, human
-
Phosphatidylinositol 3-Kinases