Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/11825
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dc.contributor.authorHarun, Nadiaen
dc.contributor.authorCosta, Patriciaen
dc.contributor.authorChristophi, Christopheren
dc.date.accessioned2015-05-16T01:27:14Z
dc.date.available2015-05-16T01:27:14Z
dc.date.issued2013-07-31en
dc.identifier.citationClinical & Experimental Metastasis 2013; 31(1): 1-14en
dc.identifier.govdoc23900501en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/11825en
dc.description.abstractHepatic resection is the preferred option for curative treatment of colorectal liver metastasis (CLM). However, this is associated with significant recurrence rates in both hepatic and extrahepatic sites. The upregulation of growth factors required for liver regeneration after resection is thought to stimulate the growth of micrometastases. The current study describes temporal changes in the expression of hepatocyte growth factor receptor (c-Met), epidermal growth factor receptor (EGFR) and insulin growth factor I receptor (IGF-IR) in an orthotopic mouse model of liver resection and tumour induction. Mice underwent 70% hepatectomy and induction of liver metastases through intrasplenic injection of colorectal cancer cells. Control groups included sham-operated mice and 70% hepatectomy alone. The expression levels of liver and tumour c-Met, EGFR and IGF-IR were quantified by quantitative RT-PCR at different time points. 70% liver resection stimulates tumour growth; increases the expression of c-Met within established tumours and surrounding liver parenchyma; downregulates EGFR expression and increases IGF-IR expression within the liver parenchyma. In conclusion, we demonstrate in our mouse model that major hepatectomy stimulates engraftment and growth of CLM and that this effect is probably due to the upregulation of c-Met as a result of the liver regeneration process. Liver IGF-IR may also contribute to this phenomenon through a paracrine effect on tumour growth. This study provides support for the role of c-Met in the stimulation of tumour growth after resection possibly through the promotion of tumour cell proliferation.en
dc.language.isoenen
dc.subject.otherAnimalsen
dc.subject.otherCell Proliferationen
dc.subject.otherColorectal Neoplasms.metabolism.pathologyen
dc.subject.otherDisease Models, Animalen
dc.subject.otherHepatectomyen
dc.subject.otherImmunohistochemistryen
dc.subject.otherInsulin-Like Growth Factor I.biosynthesisen
dc.subject.otherLiver Neoplasms.metabolism.secondary.surgeryen
dc.subject.otherLiver Regeneration.physiologyen
dc.subject.otherMaleen
dc.subject.otherMiceen
dc.subject.otherMice, Inbred CBAen
dc.subject.otherProto-Oncogene Proteins c-met.biosynthesisen
dc.subject.otherRNA, Messenger.analysisen
dc.subject.otherReceptor, Epidermal Growth Factor.biosynthesisen
dc.subject.otherReverse Transcriptase Polymerase Chain Reactionen
dc.subject.otherUp-Regulationen
dc.titleTumour growth stimulation following partial hepatectomy in mice is associated with increased upregulation of c-Met.en
dc.typeJournal Articleen
dc.identifier.journaltitleClinical & experimental metastasisen
dc.identifier.affiliationDepartment of Surgery, AH/NH Austin Hospital, University of Melbourne, Heidelberg, VIC, 3084, Australiaen
dc.identifier.doi10.1007/s10585-013-9604-7en
dc.description.pages1-14en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/23900501en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextopen-
item.openairetypeJournal Article-
item.fulltextWith Fulltext-
item.cerifentitytypePublications-
item.languageiso639-1en-
crisitem.author.deptSurgery-
crisitem.author.deptHepatopancreatobiliary Surgery-
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