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dc.contributor.authorGammage, Payam Aen
dc.contributor.authorFrezza, Christianen
dc.date.accessioned2019-07-31T23:30:33Z
dc.date.available2019-07-31T23:30:33Z
dc.identifier.issn1741-7007
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/295148
dc.description.abstractPerturbed mitochondrial bioenergetics constitute a core pillar of cancer-associated metabolic dysfunction. While mitochondrial dysfunction in cancer may result from myriad biochemical causes, a historically neglected source is that of the mitochondrial genome. Recent large-scale sequencing efforts and clinical studies have highlighted the prevalence of mutations in mitochondrial DNA (mtDNA) in human tumours and their potential roles in cancer progression. In this review we discuss the biology of the mitochondrial genome, sources of mtDNA mutations, and experimental evidence of a role for mtDNA mutations in cancer. We also propose a 'metabolic licensing' model for mtDNA mutation-derived dysfunction in cancer initiation and progression.
dc.description.sponsorshipThis work was supported by the Medical Research Council (MC_UU_00015/4 and MC_UU_12022/6).
dc.languageengen
dc.publisherBioMed Central
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectCanceren
dc.subjectMetabolismen
dc.subjectMitochondriaen
dc.subjectmtDNAen
dc.titleMitochondrial DNA: the overlooked oncogenome?en
dc.typeArticle
prism.number53en
prism.publicationNameBMC Biologyen
prism.volume17en
dc.identifier.doi10.17863/CAM.42217
dcterms.dateAccepted2019-06-08en
rioxxterms.versionofrecord10.1186/s12915-019-0668-yen
rioxxterms.versionVoR
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserveden
rioxxterms.licenseref.startdate2019-06-08en
dc.contributor.orcidFrezza, Christian [0000-0002-3293-7397]
dc.identifier.eissn1741-7007
rioxxterms.typeJournal Article/Reviewen
pubs.funder-project-idMedical Research Council (MC_UU_12022/6)
pubs.funder-project-idMRC (MC_UU_00015/4)
cam.issuedOnline2019-07-08en


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Attribution 4.0 International
Except where otherwise noted, this item's licence is described as Attribution 4.0 International