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dc.contributor.authorJeong, Joseph H.
dc.contributor.authorWang, Zhenxiong
dc.contributor.authorOuyang, Xuesong
dc.contributor.authorJiang, Shan
dc.contributor.authorGuney, Isil
dc.contributor.authorKang, Gyeong Hoon
dc.contributor.authorAbate-Shen, Cory
dc.contributor.authorGuimaraes, Alexander Savio Ramos
dc.contributor.authorFigueiredo, Jose L.
dc.contributor.authorDing, Zhihu
dc.contributor.authorShin, Eyoung
dc.contributor.authorHahn, William C.
dc.contributor.authorLoda, Massimo
dc.contributor.authorWeissleder, Ralph
dc.contributor.authorChin, Lynda
dc.date.accessioned2011-10-25T14:36:23Z
dc.date.issued2008
dc.identifier.citationJeong, Joseph H., Zhenxiong Wang, Alexander S. Guimaraes, Xuesong Ouyang, Jose L. Figueiredo, Zhihu Ding, Shan Jiang, et al. 2008. BRAF Activation Initiates but Does Not Maintain Invasive Prostate Adenocarcinoma. PLoS ONE 3(12): e3949.en_US
dc.identifier.issn1932-6203en_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:5311766
dc.description.abstractProstate cancer is the second leading cause of cancer-related deaths in men. Activation of MAP kinase signaling pathway has been implicated in advanced and androgen-independent prostate cancers, although formal genetic proof has been lacking. In the course of modeling malignant melanoma in a tyrosinase promoter transgenic system, we developed a genetically-engineered mouse (GEM) model of invasive prostate cancers, whereby an activating mutation of BRAFV600E–a mutation found in ∼10% of human prostate tumors–was targeted to the epithelial compartment of the prostate gland on the background of Ink4a/Arf deficiency. These GEM mice developed prostate gland hyperplasia with progression to rapidly growing invasive adenocarcinoma without evidence of AKT activation, providing genetic proof that activation of MAP kinase signaling is sufficient to drive prostate tumorigenesis. Importantly, genetic extinction of BRAFV600E in established prostate tumors did not lead to tumor regression, indicating that while sufficient to initiate development of invasive prostate adenocarcinoma, BRAFV600E is not required for its maintenance.en_US
dc.language.isoen_USen_US
dc.publisherPublic Library of Scienceen_US
dc.relation.isversionofdoi:10.1371/journal.pone.0003949en_US
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC2597248/pdf/en_US
dash.licenseLAA
dc.subjectmolecular biologyen_US
dc.subjectoncologyen_US
dc.subjectprostate canceren_US
dc.subjecturologyen_US
dc.titleBRAF Activation Initiates but Does Not Maintain Invasive Prostate Adenocarcinomaen_US
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden_US
dc.relation.journalPLoS ONEen_US
dash.depositing.authorGuimaraes, Alexander Savio Ramos
dc.date.available2011-10-25T14:36:23Z
dash.affiliation.otherHMS^Microbiology and Molecular Geneticsen_US
dash.affiliation.otherHMS^Medicine-Brigham and Women's Hospitalen_US
dash.affiliation.otherHMS^Pathologyen_US
dash.affiliation.otherHMS^Radiology-Massachusetts General Hospitalen_US
dash.affiliation.otherHMS^Systems Biologyen_US
dash.affiliation.otherHMS^Dermatology-Brigham and Women's Hospitalen_US
dc.identifier.doi10.1371/journal.pone.0003949*
dash.authorsorderedfalse
dash.contributor.affiliatedFigueiredo, Jose L.
dash.contributor.affiliatedDing, Zhihu
dash.contributor.affiliatedGuimaraes, Alexander Savio Ramos
dash.contributor.affiliatedChin, Lynda
dash.contributor.affiliatedLoda, Massimo
dash.contributor.affiliatedHahn, William
dash.contributor.affiliatedWeissleder, Ralph


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