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dc.contributor.authorMcLaughlin, Men_US
dc.contributor.authorPatin, ECen_US
dc.contributor.authorPedersen, Men_US
dc.contributor.authorWilkins, Aen_US
dc.contributor.authorDillon, MTen_US
dc.contributor.authorMelcher, AAen_US
dc.contributor.authorHarrington, KJen_US
dc.date.accessioned2020-05-22T16:00:57Z
dc.date.issued2020-04en_US
dc.identifier.citationNature reviews. Cancer, 2020, 20 (4), pp. 203 - 217en_US
dc.identifier.issn1474-175Xen_US
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/3630
dc.identifier.eissn1474-1768en_US
dc.identifier.doi10.1038/s41568-020-0246-1en_US
dc.description.abstractThe development of immune checkpoint inhibitors (ICIs) is revolutionizing the way we think about cancer treatment. Even so, for most types of cancer, only a minority of patients currently benefit from ICI therapies. Intrinsic and acquired resistance to ICIs has focused research towards new combination therapy approaches that seek to increase response rates, the depth of remission and the durability of benefit. In this Review, we describe how radiotherapy, through its immunomodulating effects, represents a promising combination partner with ICIs. We describe how recent research on DNA damage response (DDR) inhibitors in combination with radiotherapy may be used to augment this approach. Radiotherapy can kill cancer cells while simultaneously triggering the release of pro-inflammatory mediators and increasing tumour-infiltrating immune cells - phenomena often described colloquially as turning immunologically 'cold' tumours 'hot'. Here, we focus on new developments illustrating the key role of tumour cell-autonomous signalling after radiotherapy. Radiotherapy-induced tumour cell micronuclei activate cytosolic nucleic acid sensor pathways, such as cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING), and propagation of the resulting inflammatory signals remodels the immune contexture of the tumour microenvironment. In parallel, radiation can impact immunosurveillance by modulating neoantigen expression. Finally, we highlight how tumour cell-autonomous mechanisms might be exploited by combining DDR inhibitors, ICIs and radiotherapy.en_US
dc.formatPrint-Electronicen_US
dc.format.extent203 - 217en_US
dc.languageengen_US
dc.language.isoengen_US
dc.rights.urihttp://www.rioxx.net/licenses/under-embargo-all-rights-reserveden_US
dc.subjectAnimalsen_US
dc.subjectHumansen_US
dc.subjectNeoplasmsen_US
dc.subjectDisease Susceptibilityen_US
dc.subjectCaspasesen_US
dc.subjectNucleotidyltransferasesen_US
dc.subjectMembrane Proteinsen_US
dc.subjectRadiotherapyen_US
dc.subjectSignal Transductionen_US
dc.subjectAntigen Presentationen_US
dc.subjectDNA Repairen_US
dc.subjectProtein Processing, Post-Translationalen_US
dc.subjectExosomesen_US
dc.subjectMolecular Targeted Therapyen_US
dc.subjectTumor Microenvironmenten_US
dc.subjectBiomarkers, Tumoren_US
dc.titleInflammatory microenvironment remodelling by tumour cells after radiotherapy.en_US
dc.typeJournal Article
dcterms.dateAccepted2020-02-12en_US
rioxxterms.versionofrecord10.1038/s41568-020-0246-1en_US
rioxxterms.licenseref.startdate2020-04en_US
rioxxterms.typeJournal Article/Reviewen_US
dc.relation.isPartOfNature reviews. Canceren_US
pubs.issue4en_US
pubs.notesNot knownen_US
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology/Targeted Therapy
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Radiotherapy and Imaging
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Radiotherapy and Imaging/Targeted Therapy
pubs.publication-statusPublisheden_US
pubs.volume20en_US
pubs.embargo.termsNot knownen_US
icr.researchteamTargeted Therapyen_US
dc.contributor.icrauthorDillon, Magnusen_US
dc.contributor.icrauthorMcLaughlin, Martinen_US
dc.contributor.icrauthorHarrington, Kevinen_US


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