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dc.contributor.authorHirschey, Matthew Den
dc.contributor.authorDeBerardinis, Ralph Jen
dc.contributor.authorDiehl, Anna Mae Een
dc.contributor.authorDrew, Janice Een
dc.contributor.authorFrezza, Christianen
dc.contributor.authorGreen, Michelle Fen
dc.contributor.authorJones, Lee Wen
dc.contributor.authorKo, Young Hen
dc.contributor.authorLe, Anneen
dc.contributor.authorLea, Michael Aen
dc.contributor.authorLocasale, Jason Wen
dc.contributor.authorLongo, Valter Den
dc.contributor.authorLyssiotis, Costas Aen
dc.contributor.authorMacDonnell, Eoinen
dc.contributor.authorMehrmohamadi, Mahyaen
dc.contributor.authorMichelotti, Gregoryen
dc.contributor.authorMuralidhar, Vinayaken
dc.contributor.authorMurphy, Mikeen
dc.contributor.authorPedersen, Peter Len
dc.contributor.authorPoore, Braden
dc.contributor.authorRaffaghello, Lizziaen
dc.contributor.authorRathmell, Jeffrey Cen
dc.contributor.authorSivanand, Sharanyaen
dc.contributor.authorVander, Heiden Matthew Gen
dc.contributor.authorWellen, Kathryn Een
dc.contributor.authorTarget, Validation Teamen
dc.date.accessioned2016-02-16T15:56:46Z
dc.date.available2016-02-16T15:56:46Z
dc.date.issued2015-10-08en
dc.identifier.citationSeminars in Cancer Biology (2016) 35: S129-S150en
dc.identifier.issn1044-579X
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/253794
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.
dc.description.sponsorshipWe would like to thank Leroy Lowe for conceptualization of the Halifax project, the unnamed reviewers of this manuscript for their suggestions, and colleagues in the field who drive the science described in this review. We apologize to those whose work could not be included due to space constraints. Finally, we acknowledge all the co-authors of this review who were part of the Target Validation Team, including (in alphabetical order): Amedeo Amedei, PhD, University of Florence, Italy; Amr Amin, PhD, UAE University, United Arab Emirates; S. Salman Ashraf, PhD, UAE University, United Arab Emirates; Asfar S. Azmi, PhD, Wayne State University, Karmanos Cancer Institute, United States; Dipita Bhakta, M.Sc., PhD, VIT University (Vellore Institute of Technology), India; Alan Bisland, University of Glasgow, Glasgow, UK; Chandra S. Boosani, PhD, Creighton University, United States; Sophie Chen, PhD, Ovarian and Prostate Cancer Research Trust Laboratory, United Kingdom; Hiromasa Fujii, MD, PhD, Nara Medical University, Japan; Alexandros Georgakilas, PhD, National Technical University of Athens, Greece; Gunjan Guha, M.Sc., PhD, Assistant Professor, SASTRA University, India; Dorota Halicka, MD, PhD, New York Medical College, United States; Bill Helferich, PhD, University of Illinois at Urbana Champaign, United States; Kanya Honoki, MD, PhD, Nara Medical University, Japan; W.N. Keith, University of Glasgow, Glasgow, UK; Sulma Mohammed, DVM, PhD, Purdue University Cancer for Cancer Research, United States; Elena Niccolai, University of Florence, Italy; Somaira Nowsheen, Mayo Graduate School, Mayo Clinic College of Medicine, Rochester, Minnesota, United States; Xujuan Yang, University of Illinois at Urbana Champaign, United States.
dc.publisherElsevier
dc.rightsAttribution-NonCommercial-NoDerivs 2.0 UK: England & Wales*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/2.0/uk/*
dc.subjectcancer metabolismen
dc.subjectmitochondriaen
dc.subjectWarburgen
dc.subjecthost metabolismen
dc.subjectcancer therapyen
dc.titleDysregulated Metabolism Contributes to Oncogenesisen
dc.typeArticle
dc.provenanceOA-7041
dc.description.versionThis is the final version of the article. It first appeared from Elsevier via http://dx.doi.org/10.1016/j.semcancer.2015.10.002.en
prism.endingPageS150
prism.publicationDate2015en
prism.publicationNameSeminars in Cancer Biologyen
prism.startingPageS129
prism.volume35en
dcterms.dateAccepted2015-10-05en
rioxxterms.versionofrecord10.1016/j.semcancer.2015.10.002en
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserveden
rioxxterms.licenseref.startdate2015-10-08en
dc.contributor.orcidFrezza, Christian [0000-0002-3293-7397]
dc.contributor.orcidMurphy, Mike [0000-0003-1115-9618]
dc.identifier.eissn1096-3650
rioxxterms.typeJournal Article/Reviewen
pubs.funder-project-idMRC (MC_UU_12022/6)
pubs.funder-project-idMRC (MC_U105663142)


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