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dc.contributor.authorRead, Aen_US
dc.contributor.authorNatrajan, Ren_US
dc.coverage.spatialEnglanden_US
dc.date.accessioned2018-06-15T10:39:02Z
dc.date.accessioned2019-02-25T09:28:15Z
dc.date.issued2018-09en_US
dc.identifierhttps://www.ncbi.nlm.nih.gov/pubmed/29848666en_US
dc.identifierERC-18-0068en_US
dc.identifier.citationEndocr Relat Cancer, 2018, 25 (9), pp. R467 - R478en_US
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/3080
dc.identifier.eissn1479-6821en_US
dc.identifier.doi10.1530/ERC-18-0068en_US
dc.description.abstractBreast cancer is known to be a heterogeneous disease driven by a large repertoire of molecular abnormalities, which contribute to its diverse clinical behaviour. Despite the success of targeted therapy approaches for breast cancer patient management, there is still a lack of the molecular understanding of aggressive forms of the disease and clinical management of these patients remains difficult. The advent of high-throughput sequencing technologies has paved the way for a more complete understanding of the molecular make-up of the breast cancer genome. As such, it is becoming apparent that disruption of canonical splicing within breast cancer governs its clinical progression. In this review, we discuss the role of dysregulation of spliceosomal component genes and associated factors in the progression of breast cancer, their role in therapy resistance and the use of quantitative isoform expression as potential prognostic and predictive biomarkers with a particular focus on oestrogen receptor-positive breast cancer.en_US
dc.format.extentR467 - R478en_US
dc.languageengen_US
dc.language.isoengen_US
dc.relation.replaceshttps://repository.icr.ac.uk/handle/internal/1886
dc.relation.replacesinternal/1886
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en_US
dc.subjectbreasten_US
dc.subjectmolecular geneticsen_US
dc.subjectsplicingen_US
dc.subjectAlternative Splicingen_US
dc.subjectBiomarkersen_US
dc.subjectBreast Neoplasmsen_US
dc.subjectDrug Resistance, Neoplasmen_US
dc.subjectFemaleen_US
dc.subjectHumansen_US
dc.subjectPrognosisen_US
dc.titleSplicing dysregulation as a driver of breast cancer.en_US
dc.typeJournal Article
dcterms.dateAccepted2018-05-30en_US
rioxxterms.versionofrecord10.1530/ERC-18-0068en_US
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0en_US
rioxxterms.licenseref.startdate2018-09en_US
rioxxterms.typeJournal Article/Reviewen_US
dc.relation.isPartOfEndocr Relat Canceren_US
pubs.issue9en_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/Breast Cancer Research
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research/Functional Genomics
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology/Functional Genomics
pubs.publication-statusPublisheden_US
pubs.volume25en_US
pubs.embargo.termsNot knownen_US
icr.researchteamFunctional Genomicsen_US
dc.contributor.icrauthorNatrajan, Rachaelen_US


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