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dc.contributor.authorGilding, LN
dc.contributor.authorSomervaille, Tim CP
dc.date.accessioned2019-03-29T14:22:26Z
dc.date.available2019-03-29T14:22:26Z
dc.date.issued2019en
dc.identifier.citationGilding LN, Somervaille TCP. The diverse consequences of FOXC1 deregulation incCancer. Cancers (Basel). 2019 Feb 5;11(2).en
dc.identifier.pmid30764547en
dc.identifier.doi10.3390/cancers11020184en
dc.identifier.urihttp://hdl.handle.net/10541/621641
dc.description.abstractForkhead box C1 (FOXC1) is a transcription factor with essential roles in mesenchymal lineage specification and organ development during normal embryogenesis. In keeping with these developmental properties, mutations that impair the activity of FOXC1 result in the heritable Axenfeld-Rieger Syndrome and other congenital disorders. Crucially, gain of FOXC1 function is emerging as a recurrent feature of malignancy; FOXC1 overexpression is now documented in more than 16 cancer types, often in association with an unfavorable prognosis. This review explores current evidence for FOXC1 deregulation in cancer and the putative mechanisms by which FOXC1 confers its oncogenic effects.en
dc.language.isoenen
dc.relation.urlhttps://dx.doi.org/10.3390/cancers11020184en
dc.titleThe diverse consequences of FOXC1 deregulation in canceren
dc.typeArticleen
dc.contributor.departmentLeukaemia Biology Laboratory, Cancer Research UK Manchester Institute, The University of Manchester, Manchester M20 4JG, UK.en
dc.identifier.journalCancersen
dc.description.noteen]


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