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 |
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| creator | 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 |
| description | 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. |
| doi_str_mv | 10.1038/ng.371 |
| format | Article |
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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.</description><identifier>ISSN: 1061-4036</identifier><identifier>EISSN: 1546-1718</identifier><identifier>DOI: 10.1038/ng.371</identifier><identifier>PMID: 19396167</identifier><identifier>CODEN: NGENEC</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>Agriculture ; Animal Genetics and Genomics ; Animals ; Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; brief-communication ; Cancer ; Cancer Research ; Cell physiology ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Fundamental and applied biological sciences. Psychology ; Fusion ; Gene Function ; Genetic aspects ; Genetic engineering ; Genetics of eukaryotes. Biological and molecular evolution ; Health aspects ; Human Genetics ; Humans ; Kinases ; Male ; Mass spectrometry ; Medical research ; Mice ; Mice, Transgenic ; Molecular and cellular biology ; Oncogene Proteins, Fusion - genetics ; Oncogene Proteins, Fusion - metabolism ; Phosphatidylinositol 3-Kinases - metabolism ; Prostate - metabolism ; Prostate - pathology ; Prostate cancer ; Prostatic Intraepithelial Neoplasia - metabolism ; Prostatic Intraepithelial Neoplasia - pathology ; Prostatic Neoplasms - metabolism ; Protein kinases ; Proteins ; Risk factors ; Rodents ; Signal Transduction</subject><ispartof>Nature genetics, 2009-05, Vol.41 (5), p.524-526</ispartof><rights>Springer Nature America, Inc. 2009</rights><rights>2009 INIST-CNRS</rights><rights>COPYRIGHT 2009 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group May 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c747t-a7763047aa491f56283d386780a8d90cde13a6308d2993aaf49c588d811924713</citedby><cites>FETCH-LOGICAL-c747t-a7763047aa491f56283d386780a8d90cde13a6308d2993aaf49c588d811924713</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,781,785,886,2728,27929,27930</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21431467$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19396167$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sawyers, Charles L</creatorcontrib><creatorcontrib>King, Jennifer C</creatorcontrib><creatorcontrib>Xu, Jin</creatorcontrib><creatorcontrib>Wongvipat, John</creatorcontrib><creatorcontrib>Hieronymus, Haley</creatorcontrib><creatorcontrib>Carver, Brett S</creatorcontrib><creatorcontrib>Leung, David H</creatorcontrib><creatorcontrib>Taylor, Barry S</creatorcontrib><creatorcontrib>Sander, Chris</creatorcontrib><creatorcontrib>Cardiff, Robert D</creatorcontrib><creatorcontrib>Couto, Suzana S</creatorcontrib><creatorcontrib>Gerald, William L</creatorcontrib><title>Cooperativity of TMPRSS2-ERG with PI3-kinase pathway activation in prostate oncogenesis</title><title>Nature genetics</title><addtitle>Nat Genet</addtitle><addtitle>Nat Genet</addtitle><description>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.</description><subject>Agriculture</subject><subject>Animal Genetics and Genomics</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>brief-communication</subject><subject>Cancer</subject><subject>Cancer Research</subject><subject>Cell physiology</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fusion</subject><subject>Gene Function</subject><subject>Genetic aspects</subject><subject>Genetic engineering</subject><subject>Genetics of eukaryotes. Biological and molecular evolution</subject><subject>Health aspects</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Kinases</subject><subject>Male</subject><subject>Mass spectrometry</subject><subject>Medical research</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Molecular and cellular biology</subject><subject>Oncogene Proteins, Fusion - genetics</subject><subject>Oncogene Proteins, Fusion - metabolism</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Prostate - metabolism</subject><subject>Prostate - pathology</subject><subject>Prostate cancer</subject><subject>Prostatic Intraepithelial Neoplasia - metabolism</subject><subject>Prostatic Intraepithelial Neoplasia - pathology</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Protein kinases</subject><subject>Proteins</subject><subject>Risk factors</subject><subject>Rodents</subject><subject>Signal Transduction</subject><issn>1061-4036</issn><issn>1546-1718</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNk1tv0zAUgCMEYqPAL0AoAgHiIcWXxJcXpKoao9LQpnbAo2UcJ_VI7RI7G_33uGvUtYC0yg-xfL7znTjnJEmeQzCEALMPth5iCh8kx7DISQYpZA_jHhCY5QCTo-SJ91cAwDwH7HFyBDnmBBJ6nHwfO7fUrQzm2oRV6qr08svFdDZD2cn0NL0xYZ5eTHD201jpdbqUYX4jV6lUkY85zqbGpsvW-SCDTp1VrtZWe-OfJo8q2Xj9rH8Okq-fTi7Hn7Oz89PJeHSWKZrTkElKCQY5lTLnsCoIYrjEjFAGJCs5UKWGWEaClYhzLGWVc1UwVjIIOcopxIPk48a77H4sdKm0Da1sxLI1C9muhJNG7EesmYvaXQvEOCsAjoK3vaB1vzrtg1gYr3TTSKtd5wWhkGLO2b0gAgVhEK3BV3-BV65rbfwKAiFEMEPxzoPk9QaqZaOFsZWLb6fWRjGC8aqcAk4jNfwPFVepF0Y5qysTz0cEo4IVEOFDE3YrvN9LiEzQv0MtO-_FZDbdl9_HHuo9_3a4d83uevsuqDh0vtXVttUQiPWfIGwt8O1gvNwdjDusH_0IvOkB6ZVsqlZaZfyWQzDHML_l3m04H0O21u1dO_8p-WJDWhm6Vm9VffgPzhIggg</recordid><startdate>20090501</startdate><enddate>20090501</enddate><creator>Sawyers, Charles L</creator><creator>King, Jennifer C</creator><creator>Xu, Jin</creator><creator>Wongvipat, John</creator><creator>Hieronymus, Haley</creator><creator>Carver, Brett S</creator><creator>Leung, David H</creator><creator>Taylor, Barry S</creator><creator>Sander, Chris</creator><creator>Cardiff, Robert D</creator><creator>Couto, Suzana S</creator><creator>Gerald, William L</creator><general>Nature Publishing Group US</general><general>Nature Publishing Group</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SS</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7N</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7TO</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20090501</creationdate><title>Cooperativity of TMPRSS2-ERG with PI3-kinase pathway activation in prostate oncogenesis</title><author>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</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c747t-a7763047aa491f56283d386780a8d90cde13a6308d2993aaf49c588d811924713</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Agriculture</topic><topic>Animal Genetics and Genomics</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>brief-communication</topic><topic>Cancer</topic><topic>Cancer Research</topic><topic>Cell physiology</topic><topic>Cell transformation and carcinogenesis. 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Nature genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sawyers, Charles L</au><au>King, Jennifer C</au><au>Xu, Jin</au><au>Wongvipat, John</au><au>Hieronymus, Haley</au><au>Carver, Brett S</au><au>Leung, David H</au><au>Taylor, Barry S</au><au>Sander, Chris</au><au>Cardiff, Robert D</au><au>Couto, Suzana S</au><au>Gerald, William L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cooperativity of TMPRSS2-ERG with PI3-kinase pathway activation in prostate oncogenesis</atitle><jtitle>Nature genetics</jtitle><stitle>Nat Genet</stitle><addtitle>Nat Genet</addtitle><date>2009-05-01</date><risdate>2009</risdate><volume>41</volume><issue>5</issue><spage>524</spage><epage>526</epage><pages>524-526</pages><issn>1061-4036</issn><eissn>1546-1718</eissn><coden>NGENEC</coden><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.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>19396167</pmid><doi>10.1038/ng.371</doi><tpages>3</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Agriculture Animal Genetics and Genomics Animals Biological and medical sciences Biomedical and Life Sciences Biomedicine brief-communication Cancer Cancer Research Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Fundamental and applied biological sciences. Psychology Fusion Gene Function Genetic aspects Genetic engineering Genetics of eukaryotes. Biological and molecular evolution Health aspects Human Genetics Humans Kinases Male Mass spectrometry Medical research Mice Mice, Transgenic Molecular and cellular biology Oncogene Proteins, Fusion - genetics Oncogene Proteins, Fusion - metabolism Phosphatidylinositol 3-Kinases - metabolism Prostate - metabolism Prostate - pathology Prostate cancer Prostatic Intraepithelial Neoplasia - metabolism Prostatic Intraepithelial Neoplasia - pathology Prostatic Neoplasms - metabolism Protein kinases Proteins Risk factors Rodents Signal Transduction |
| title | Cooperativity of TMPRSS2-ERG with PI3-kinase pathway activation in prostate oncogenesis |
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