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dc.contributor.authorRead, A
dc.contributor.authorNatrajan, R
dc.date.accessioned2018-06-15T10:39:02Z
dc.date.accessioned2019-02-25T09:28:15Z
dc.date.issued2018-09-01
dc.identifier.citationEndocrine-related cancer, 2018, 25 (9), pp. R467 - R478
dc.identifier.issn1351-0088
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/3080
dc.identifier.eissn1479-6821
dc.identifier.doi10.1530/erc-18-0068
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.
dc.formatPrint-Electronic
dc.format.extentR467 - R478
dc.languageeng
dc.language.isoeng
dc.publisherBIOSCIENTIFICA LTD
dc.relation.replaceshttps://repository.icr.ac.uk/handle/internal/1886
dc.relation.replacesinternal/1886
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.subjectHumans
dc.subjectBreast Neoplasms
dc.subjectPrognosis
dc.subjectAlternative Splicing
dc.subjectDrug Resistance, Neoplasm
dc.subjectFemale
dc.subjectBiomarkers
dc.titleSplicing dysregulation as a driver of breast cancer.
dc.typeJournal Article
dcterms.dateAccepted2018-05-30
rioxxterms.versionofrecord10.1530/erc-18-0068
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0
rioxxterms.licenseref.startdate2018-09
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfEndocrine-related cancer
pubs.issue9
pubs.notesNot known
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.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-statusPublished
pubs.volume25
pubs.embargo.termsNot known
icr.researchteamFunctional Genomics
dc.contributor.icrauthorRead, Abigail
dc.contributor.icrauthorNatrajan, Rachael


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