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dc.contributor.authorStankiewicz, E
dc.contributor.authorMao, X
dc.contributor.authorMangham, DC
dc.contributor.authorXu, L
dc.contributor.authorYeste-Velasco, M
dc.contributor.authorFisher, G
dc.contributor.authorNorth, B
dc.contributor.authorChaplin, T
dc.contributor.authorYoung, B
dc.contributor.authorWang, Y
dc.contributor.authorKaur Bansal, J
dc.contributor.authorKudahetti, S
dc.contributor.authorSpencer, L
dc.contributor.authorFoster, CS
dc.contributor.authorMøller, H
dc.contributor.authorScardino, P
dc.contributor.authorOliver, RT
dc.contributor.authorShamash, J
dc.contributor.authorCuzick, J
dc.contributor.authorCooper, CS
dc.contributor.authorBerney, DM
dc.contributor.authorLu, Y-J
dc.date.accessioned2017-06-02T10:25:44Z
dc.date.issued2017-07-11
dc.date.issued2017-07-11
dc.date.submitted2017-05-25T12:10:33.694Z
dc.identifier.urihttp://qmro.qmul.ac.uk/xmlui/handle/123456789/23507
dc.description.abstractProstate cancer is the most common cancer among western men, with a significant mortality and morbidity reported for advanced metastatic disease. Current understanding of metastatic disease is limited due to difficulty of sampling as prostate cancer mainly metastasizes to bone. By analysing prostate cancer bone metastases using high density microarrays, we found a common genomic copy number loss at 6q16.1-16.2, containing the FBXL4 gene, which was confirmed in larger series of bone metastases by fluorescence in situ hybridisation (FISH). Loss of FBXL4 was also detected in primary tumours and it was highly associated with prognostic factors including high Gleason score, clinical stage, prostate-specific antigen (PSA) and extent of disease, as well as poor patient survival, suggesting that FBXL4 loss contributes to prostate cancer progression. We also demonstrated that FBXL4 deletion is detectable in circulating tumour cells (CTCs), making it a potential prognostic biomarker by 'liquid biopsy'. In vitro analysis showed that FBXL4 plays a role in regulating the migration and invasion of prostate cancer cells. FBXL4 potentially controls cancer metastasis through regulation of ERLEC1 levels. Therefore, FBXL4 could be a potential novel prostate cancer suppressor gene, which may prevent cancer progression and metastasis through controlling cell invasion.
dc.format.extent5124 - ?
dc.languageeng
dc.language.isoenen_US
dc.relation.ispartofSci Rep
dc.titleIdentification of FBXL4 as a Metastasis Associated Gene in Prostate Cancer.
dc.typeJournal Article
dc.identifier.doi10.1038/s41598-017-05209-z
pubs.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/28698647
pubs.issue1
pubs.organisational-group/Queen Mary University of London
pubs.organisational-group/Queen Mary University of London/Faculty of Medicine & Dentistry
pubs.organisational-group/Queen Mary University of London/Faculty of Medicine & Dentistry/Barts Cancer Institute
pubs.organisational-group/Queen Mary University of London/Faculty of Medicine & Dentistry/Barts Cancer Institute/Molecular Oncology
pubs.organisational-group/Queen Mary University of London/Faculty of Medicine & Dentistry/Wolfson Institute of Preventive Medicine
pubs.organisational-group/Queen Mary University of London/Faculty of Medicine & Dentistry/Wolfson Institute of Preventive Medicine/Centre for Cancer Prevention
pubs.publication-statusPublished online
pubs.volume7


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