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dc.contributor.authorGuertin, David A.
dc.contributor.authorStevens, Deanna M.
dc.contributor.authorSaitoh, Maki
dc.contributor.authorKinkel, Stephanie
dc.contributor.authorCrosby, Katherine
dc.contributor.authorSheen, Joon-Ho
dc.contributor.authorMullholland, David J.
dc.contributor.authorMagnuson, Mark A.
dc.contributor.authorWu, Hong
dc.contributor.authorSabatini, David
dc.contributor.authorStevens, Deanna M.
dc.date.accessioned2015-04-24T18:55:24Z
dc.date.available2015-04-24T18:55:24Z
dc.date.issued2009-02
dc.date.submitted2008-10
dc.identifier.issn15356108
dc.identifier.urihttp://hdl.handle.net/1721.1/96802
dc.description.abstractmTOR complex 2 (mTORC2) contains the mammalian target of rapamycin (mTOR) kinase and the Rictor regulatory protein and phosphorylates Akt. Whether this function of mTORC2 is critical for cancer progression is unknown. Here, we show that transformed human prostate epithelial cells lacking PTEN require mTORC2 to form tumors when injected into nude mice. Furthermore, we find that Rictor is a haploinsufficient gene and that deleting one copy protects Pten heterozygous mice from prostate cancer. Finally, we show that the development of prostate cancer caused by Pten deletion specifically in prostate epithelium requires mTORC2, but that for normal prostate epithelial cells, mTORC2 activity is nonessential. The selective requirement for mTORC2 in tumor development suggests that mTORC2 inhibitors may be of substantial clinical utility.en_US
dc.description.sponsorshipW. M. Keck Foundationen_US
dc.description.sponsorshipDamon Runyon Cancer Research Foundation (Research Fellowship)en_US
dc.description.sponsorshipLeukemia & Lymphoma Society of America (Career Development Award)en_US
dc.description.sponsorshipHoward Hughes Medical Institute (Investigator)en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (K99 CA1296613-01A1)en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (R01 CA107166)en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (R01 AI04389)en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (R01 CA103866)en_US
dc.language.isoen_US
dc.publisherElsevier B.V.en_US
dc.relation.isversionofhttp://dx.doi.org/10.1016/j.ccr.2008.12.017en_US
dc.rightsArticle is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use.en_US
dc.sourceElsevieren_US
dc.titlemTOR Complex 2 Is Required for the Development of Prostate Cancer Induced by Pten Loss in Miceen_US
dc.typeArticleen_US
dc.identifier.citationGuertin, David A., Deanna M. Stevens, Maki Saitoh, Stephanie Kinkel, Katherine Crosby, Joon-Ho Sheen, David J. Mullholland, Mark A. Magnuson, Hong Wu, and David M. Sabatini. “mTOR Complex 2 Is Required for the Development of Prostate Cancer Induced by Pten Loss in Mice.” Cancer Cell 15, no. 2 (February 2009): 148–159.© 2009 Elsevier Inc.en_US
dc.contributor.departmentWhitehead Institute for Biomedical Researchen_US
dc.contributor.departmentKoch Institute for Integrative Cancer Research at MITen_US
dc.contributor.mitauthorGuertin, David A.en_US
dc.contributor.mitauthorStevens, Deanna M.en_US
dc.contributor.mitauthorSaitoh, Makien_US
dc.contributor.mitauthorKinkel, Stephanieen_US
dc.contributor.mitauthorSheen, Joon-Hoen_US
dc.contributor.mitauthorSabatini, David M.en_US
dc.relation.journalCancer Cellen_US
dc.eprint.versionFinal published versionen_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsGuertin, David A.; Stevens, Deanna M.; Saitoh, Maki; Kinkel, Stephanie; Crosby, Katherine; Sheen, Joon-Ho; Mullholland, David J.; Magnuson, Mark A.; Wu, Hong; Sabatini, David M.en_US
dc.identifier.orcidhttps://orcid.org/0000-0002-1446-7256
mit.licensePUBLISHER_POLICYen_US
mit.metadata.statusComplete


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