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dc.contributor.authorBradner, James E.
dc.contributor.authorHnisz, Denes
dc.contributor.authorYoung, Richard A.
dc.date.accessioned2018-08-06T18:17:13Z
dc.date.available2018-08-06T18:17:13Z
dc.date.issued2017-02
dc.identifier.issn00928674
dc.identifier.urihttp://hdl.handle.net/1721.1/117285
dc.description.abstractCancer arises from genetic alterations that invariably lead to dysregulated transcriptional programs. These dysregulated programs can cause cancer cells to become highly dependent on certain regulators of gene expression. Here, we discuss how transcriptional control is disrupted by genetic alterations in cancer cells, why transcriptional dependencies can develop as a consequence of dysregulated programs, and how these dependencies provide opportunities for novel therapeutic interventions in cancer.en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (Grant HG002668)en_US
dc.language.isoen_US
dc.publisherElsevieren_US
dc.relation.isversionofhttps://doi.org/10.1016/j.cell.2016.12.013en_US
dc.rightsCreative Commons Attribution-NonCommercial-NoDerivs Licenseen_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/en_US
dc.sourceProf. Youngen_US
dc.titleTranscriptional Addiction in Canceren_US
dc.typeArticleen_US
dc.identifier.citationBradner, James E. et al. “Transcriptional Addiction in Cancer.” Cell 168, 4 (February 2017): 629–643 © 2016 Elsevieren_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biologyen_US
dc.contributor.approverRichard Youngen_US
dc.contributor.mitauthorYoung, Richard A
dc.relation.journalCellen_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.orderedauthorsBradner, James E.; Hnisz, Denes; Young, Richard A.en_US
dspace.embargo.termsNen_US
dc.identifier.orcidhttps://orcid.org/0000-0001-8855-8647
mit.licensePUBLISHER_CCen_US


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