Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/12052
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dc.contributor.authorKoh, Shir Linen
dc.contributor.authorAger, E Ien
dc.contributor.authorCosta, P L Nen
dc.contributor.authorMalcontenti-Wilson, Caterinaen
dc.contributor.authorMuralidharan, Vigayaragavanen
dc.contributor.authorChristophi, Christopheren
dc.date.accessioned2015-05-16T01:41:51Z-
dc.date.available2015-05-16T01:41:51Z-
dc.date.issued2014-01-18en
dc.identifier.citationClinical & Experimental Metastasis 2014; 31(4): 395-405en
dc.identifier.govdoc24442969en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/12052en
dc.description.abstractPartial hepatectomy (PH), the preferred option for selected patients with colorectal cancer liver metastases (CRCLM), is associated with 40-80 % tumor recurrence rates. Renin-angiotensin system (RAS) blockade inhibits tumor growth and has been suggested to improve liver regeneration. We documented the effect of RAS blockade on tumor growth and liver regeneration in a murine model. CRCLM induction followed by 70 % PH was performed on 78 CBA mice. Liver regeneration (days 2, 6) and CRCLM tumor load were measured by liver (and tumor) weights, percentage of CRCLM burden and tumor nodule count (days 16, 21). mRNA expression of the RAS components was characterised. Statistical analysis was performed using 2-independent sample T test or Mann-Whitney test (SPSS). Captopril did not impair liver regeneration. By day 21, Captopril decreased tumor burden (percentage of CRCLM in the liver) (48.7 ± 4.7 % control, 24.4 ± 6.2 Captopril; p = 0.008), tumor volume (1046.2 ± 200.2 mm(3), 388.3 ± 150.4; p = 0.02), tumor nodule count per image field (181.1 ± 28.5, 68 ± 17.6; p = 0.005) and tumor angiogenesis (71.8 ± 6.4 vessels/mm(2), 43.1 ± 7.6; p = 0.015) compared to controls. Captopril enhanced tumor apoptosis (1 ± 0.2 %, 2.5 ± 0.7; p = 0.028). Liver regeneration and tumor development increased liver ACE levels. Blockade of the RAS effectively retarded CRCLM tumor growth at the late stage of tumor development within the regenerating liver without impeding liver regeneration following PH, via anti-angiogenesis and pro-tumor apoptosis. Captopril may be of therapeutic benefit in patients undergoing PH for CRCLM.en
dc.language.isoenen
dc.titleBlockade of the renin-angiotensin system inhibits growth of colorectal cancer liver metastases in the regenerating liveren
dc.typeJournal Articleen
dc.identifier.journaltitleClinical & Experimental Metastasisen
dc.identifier.affiliationDepartment of Surgery, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australiaen
dc.identifier.doi10.1007/s10585-014-9635-8en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/24442969en
dc.type.austinJournal Articleen
local.name.researcherChristophi, Christopher
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextWith Fulltext-
item.grantfulltextopen-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptSurgery-
crisitem.author.deptHepatopancreatobiliary Surgery-
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