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dc.contributor.authorDooley, Alison L.
dc.contributor.authorWinslow, Monte Meier
dc.contributor.authorChiang, Derek Y.
dc.contributor.authorBanerji, Shantanu
dc.contributor.authorStransky, Nicolas
dc.contributor.authorDayton, Talya Lucia
dc.contributor.authorSnyder, Eric
dc.contributor.authorSenna, Stephanie
dc.contributor.authorWhittaker, Charles A.
dc.contributor.authorBronson, Roderick T.
dc.contributor.authorCrowley, Denise G.
dc.contributor.authorBarretina, Jordi
dc.contributor.authorGarraway, Levi A.
dc.contributor.authorMeyerson, Matthew L.
dc.contributor.authorJacks, Tyler E.
dc.date.accessioned2011-10-20T14:24:07Z
dc.date.available2011-10-20T14:24:07Z
dc.date.issued2011-10
dc.date.submitted2011-03
dc.identifier.issn0890-9369
dc.identifier.issn1549-5477
dc.identifier.urihttp://hdl.handle.net/1721.1/66512
dc.description.abstractSmall cell lung cancer (SCLC) is an aggressive cancer often diagnosed after it has metastasized. Despite the need to better understand this disease, SCLC remains poorly characterized at the molecular and genomic levels. Using a genetically engineered mouse model of SCLC driven by conditional deletion of Trp53 and Rb1 in the lung, we identified several frequent, high-magnitude focal DNA copy number alterations in SCLC. We uncovered amplification of a novel, oncogenic transcription factor, Nuclear factor I/B (Nfib), in the mouse SCLC model and in human SCLC. Functional studies indicate that NFIB regulates cell viability and proliferation during transformation.en_US
dc.description.sponsorshipNational Cancer Institute (U.S.) (grant P30-CA14051)en_US
dc.description.sponsorshipDavid H. Koch Institute for Integrative Cancer Research at MIT (Ludwig Center for Molecular Oncology)en_US
dc.description.sponsorshipHoward Hughes Medical Instituteen_US
dc.description.sponsorshipAlfred P. Sloan Foundation (Research Fellowship)en_US
dc.description.sponsorshipInternational Association for the Study of Lung Canceren_US
dc.language.isoen_US
dc.publisherCold Spring Harbor Laboratory Press in association with The Genetics Societyen_US
dc.relation.isversionofhttp://dx.doi.org/10.1101/gad.2046711en_US
dc.rightsCreative Commons Attribution-Noncommercial-Share Alike 3.0en_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/3.0/en_US
dc.sourceJacksen_US
dc.titleNuclear Factor I/B is an Oncogene in Small Cell Lung Canceren_US
dc.typeArticleen_US
dc.identifier.citationDooley, A. L. et al. “Nuclear factor I/B is an oncogene in small cell lung cancer.” Genes & Development 25 (2011): 1470-1475.en_US
dc.contributor.departmentBroad Institute of MIT and Harvarden_US
dc.contributor.departmentDavid H. Koch Institute for Integrative Cancer Research at MITen_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biologyen_US
dc.contributor.approverJacks, Tyler E.
dc.contributor.mitauthorDooley, Alison L.
dc.contributor.mitauthorWinslow, Monte Meier
dc.contributor.mitauthorChiang, Derek Y.
dc.contributor.mitauthorBanerji, Shantanu
dc.contributor.mitauthorStransky, Nicolas
dc.contributor.mitauthorDayton, Talya Lucia
dc.contributor.mitauthorSnyder, Eric
dc.contributor.mitauthorSenna, Stephanie
dc.contributor.mitauthorWhittaker, Charles A.
dc.contributor.mitauthorCrowley, Denise G.
dc.contributor.mitauthorBarretina, Jordi
dc.contributor.mitauthorGarraway, Levi A.
dc.contributor.mitauthorMeyerson, Matthew L.
dc.contributor.mitauthorJacks, Tyler E.
dc.relation.journalGenes and Developmenten_US
dc.eprint.versionAuthor's final manuscripten_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsDooley, A. L.; Winslow, M. M.; Chiang, D. Y.; Banerji, S.; Stransky, N.; Dayton, T. L.; Snyder, E. L.; Senna, S.; Whittaker, C. A.; Bronson, R. T.; Crowley, D.; Barretina, J.; Garraway, L.; Meyerson, M.; Jacks, T.en
dc.identifier.orcidhttps://orcid.org/0000-0001-5785-8911
dc.identifier.orcidhttps://orcid.org/0000-0002-1846-604X
dc.identifier.orcidhttps://orcid.org/0000-0002-7994-7963
mit.licenseOPEN_ACCESS_POLICYen_US


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