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dc.contributor.authorHirschey, Matthew D.
dc.contributor.authorDeBerardinis, Ralph J.
dc.contributor.authorDiehl, Anna Mae E.
dc.contributor.authorDrew, Janice E.
dc.contributor.authorFrezza, Christian
dc.contributor.authorGreen, Michelle F.
dc.contributor.authorJones, Lee W.
dc.contributor.authorKo, Young H.
dc.contributor.authorLe, Anne
dc.contributor.authorLea, Michael A.
dc.contributor.authorLocasale, Jason W.
dc.contributor.authorLongo, Valter D.
dc.contributor.authorLyssiotis, Costas A.
dc.contributor.authorMcDonnell, Eoin
dc.contributor.authorMehrmohamadi, Mahya
dc.contributor.authorMichelotti, Gregory
dc.contributor.authorMuralidhar, Vinayak
dc.contributor.authorMurphy, Michael P.
dc.contributor.authorPedersen, Peter L.
dc.contributor.authorPoore, Brad
dc.contributor.authorRaffaghello, Lizzia
dc.contributor.authorRathmell, Jeffrey C.
dc.contributor.authorSivanand, Sharanya
dc.contributor.authorVander Heiden, Matthew G.
dc.contributor.authorWellen, Kathryn E.
dc.date.accessioned2016-12-15T17:09:45Z
dc.date.available2016-12-15T17:09:45Z
dc.date.issued2015-10
dc.date.submitted2015-09
dc.identifier.issn1044579X
dc.identifier.urihttp://hdl.handle.net/1721.1/105828
dc.description.abstractCancer is a disease characterized by unrestrained cellular proliferation. In order to sustain growth, cancer cells undergo a complex metabolic rearrangement characterized by changes in metabolic pathways involved in energy production and biosynthetic processes. The relevance of the metabolic transformation of cancer cells has been recently included in the updated version of the review “Hallmarks of Cancer”, where dysregulation of cellular metabolism was included as an emerging hallmark. While several lines of evidence suggest that metabolic rewiring is orchestrated by the concerted action of oncogenes and tumor suppressor genes, in some circumstances altered metabolism can play a primary role in oncogenesis. Recently, mutations of cytosolic and mitochondrial enzymes involved in key metabolic pathways have been associated with hereditary and sporadic forms of cancer. Together, these results demonstrate that aberrant metabolism, once seen just as an epiphenomenon of oncogenic reprogramming, plays a key role in oncogenesis with the power to control both genetic and epigenetic events in cells. In this review, we discuss the relationship between metabolism and cancer, as part of a larger effort to identify a broad-spectrum of therapeutic approaches. We focus on major alterations in nutrient metabolism and the emerging link between metabolism and epigenetics. Finally, we discuss potential strategies to manipulate metabolism in cancer and tradeoffs that should be considered. More research on the suite of metabolic alterations in cancer holds the potential to discover novel approaches to treat it.en_US
dc.language.isoen_US
dc.publisherElsevieren_US
dc.relation.isversionofhttp://dx.doi.org/10.1016/j.semcancer.2015.10.002en_US
dc.rightsCreative Commons Attribution-NonCommercial-NoDerivs Licenseen_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/en_US
dc.sourceElsevieren_US
dc.titleDysregulated metabolism contributes to oncogenesisen_US
dc.typeArticleen_US
dc.identifier.citationHirschey, Matthew D. et al. “Dysregulated Metabolism Contributes to Oncogenesis.” Seminars in Cancer Biology 35 (2015): S129–S150. © 2015 Elsevier Ltden_US
dc.contributor.departmentHarvard University--MIT Division of Health Sciences and Technologyen_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biologyen_US
dc.contributor.departmentKoch Institute for Integrative Cancer Research at MITen_US
dc.contributor.mitauthorVander Heiden, Matthew G.
dc.contributor.mitauthorMuralidhar, Vinayak
dc.relation.journalSeminars in Cancer Biologyen_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.orderedauthorsHirschey, Matthew D.; DeBerardinis, Ralph J.; Diehl, Anna Mae E.; Drew, Janice E.; Frezza, Christian; Green, Michelle F.; Jones, Lee W.; Ko, Young H.; Le, Anne; Lea, Michael A.; Locasale, Jason W.; Longo, Valter D.; Lyssiotis, Costas A.; McDonnell, Eoin; Mehrmohamadi, Mahya; Michelotti, Gregory; Muralidhar, Vinayak; Murphy, Michael P.; Pedersen, Peter L.; Poore, Brad; Raffaghello, Lizzia; Rathmell, Jeffrey C.; Sivanand, Sharanya; Vander Heiden, Matthew G.; Wellen, Kathryn E.en_US
dspace.embargo.termsNen_US
dc.identifier.orcidhttps://orcid.org/0000-0002-6702-4192
dc.identifier.orcidhttps://orcid.org/0000-0002-6493-9012
mit.licensePUBLISHER_CCen_US


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