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dc.contributor.authorWogan, Gerald N.
dc.contributor.authorDedon, Peter C.
dc.contributor.authorTannenbaum, Steven Robert
dc.contributor.authorFox, James G.
dc.date.accessioned2012-11-16T19:22:05Z
dc.date.available2012-11-16T19:22:05Z
dc.date.issued2012-08
dc.date.submitted2012-08
dc.identifier.issn1949-2553
dc.identifier.urihttp://hdl.handle.net/1721.1/74664
dc.description.abstractThe importance of chronic inflammation as a risk factor for major cancers is well documented [1], and the inflammatory state is known to involve contributions of both adaptive and innate immune components. In a recent publication [2] we describe an experimental animal model in which infection, inflammation and cancer are mechanistically linked, and provide evidence that chemical mediators of the innate immune system and bacterial toxins both play key roles in driving colon carcinogenesis. In this model, epithelial injury caused by Helicobacter hepaticus infection enhances access of bacterially-associated products to pattern-recognition receptors located on surfaces of macrophages and dendritic cells. Receptor ligation leads to activation of transcription factors, including NF-kappa B, that regulate production of chemo-attractants for macrophages and neutrophils, recruitment of which is a hallmark of inflammation. These acute inflammatory events are re-enforced by expression of powerful inflammatory mediators such as TNF-α and IL-2, which amplify acute inflammatory gene expression and enhance cell survival. If not properly extinguished, the innate inflammatory response is maintained and further amplified by activation of cell-mediated adaptive immunity.en_US
dc.language.isoen_US
dc.publisherImpact Journalsen_US
dc.relation.isversionofhttp://www.impactjournals.com/oncotarget/index.php?journal=oncotarget&page=article&op=view&path%5B%5D=624&path%5B%5D=934en_US
dc.rightsCreative Commons Attributionen_US
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/en_US
dc.sourcePMCen_US
dc.titleInfection, inflammation and colon carcinogenesisen_US
dc.typeArticleen_US
dc.identifier.citationWogan, G.N. et al. "Infection, inflammation and colon carcinogenesis." Oncotarget 3.8 (2012): 737–738. Web.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biological Engineeringen_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Chemistryen_US
dc.contributor.departmentMassachusetts Institute of Technology. Division of Comparative Medicineen_US
dc.contributor.mitauthorWogan, Gerald N.
dc.contributor.mitauthorDedon, Peter C.
dc.contributor.mitauthorTannenbaum, Steven Robert
dc.contributor.mitauthorFox, James G.
dc.relation.journalOncotargeten_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.orderedauthorsWogan, G.N.; Dedon, P.C.; Tannenbaum, S.R.; Fox, J.G.en_US
dc.identifier.orcidhttps://orcid.org/0000-0003-0011-3067
dc.identifier.orcidhttps://orcid.org/0000-0003-0771-9889
dc.identifier.orcidhttps://orcid.org/0000-0001-9307-6116
mit.licensePUBLISHER_CCen_US


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