Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/11847
Full metadata record
DC FieldValueLanguage
dc.contributor.authorCossigny, Davina A Fen
dc.contributor.authorMouhtouris, Effieen
dc.contributor.authorDushyanthen, Sathanaen
dc.contributor.authorGonzalvo, Augustoen
dc.contributor.authorQuan, Gerald M Yen
dc.date.accessioned2015-05-16T01:28:35Z
dc.date.available2015-05-16T01:28:35Z
dc.date.issued2013-08-18en
dc.identifier.citationJournal of Neuro-oncology 2013; 115(2): 189-96en
dc.identifier.govdoc23955595en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/11847en
dc.description.abstractThe spine is the commonest site of skeletal metastatic disease and uncontrolled growth of cancer in the spine will inevitably cause pain and neurologic compromise. Improved understanding of the pathobiology behind this devastating condition is urgently needed. For this reason, the aim of this study was to establish a clinically relevant, animal model of spinal cancer. A percutaneous orthotopic injection of human breast (MDA-MB-231) or human prostate (PC-3) cancer cells was administered into the upper lumbar spine of nude mice (n = 6). Animals were monitored twice daily for general welfare, gait asymmetry or disturbance, and hindlimb weakness. After sacrifice, plain radiographs, micro-CT imaging and histological analysis of the spines were performed on each mouse. All mice recovered fully from the inoculation procedure and displayed normal gait and behaviour patterns for at least 3 weeks post-inoculation. Subsequently, between 3 and 5 weeks post-inoculation, each mouse developed evolving paralysis in their hindlimbs over 48-72 h. All followed the same pattern of decline following onset of neurological dysfunction; from gait asymmetry and unilateral hindlimb weakness, to complete unilateral hindlimb paralysis and finally to complete bilateral hindlimb paralysis. Plain radiographs, micro-CT scanning and histological analysis confirmed local tumour growth and destruction of the spine in all six mice. An in vivo mouse model of human intraosseous spinal cancer has been established forming cancers that grow within the spine and cause epidural spinal cord compression, resulting in a reproducible, evolving neurological deficit and paralysis that closely resembles the human condition.en
dc.language.isoenen
dc.subject.otherAnimalsen
dc.subject.otherBreast Neoplasms.pathologyen
dc.subject.otherDisease Models, Animalen
dc.subject.otherFemaleen
dc.subject.otherHumansen
dc.subject.otherInjections, Spinalen
dc.subject.otherMaleen
dc.subject.otherMiceen
dc.subject.otherMice, Inbred BALB Cen
dc.subject.otherMice, Nudeen
dc.subject.otherParaplegia.etiology.pathology.radiographyen
dc.subject.otherProstatic Neoplasms.pathologyen
dc.subject.otherSpinal Neoplasms.pathology.radiographyen
dc.subject.otherTumor Cells, Cultureden
dc.titleAn in vivo mouse model of intraosseous spinal cancer causing evolving paraplegia.en
dc.typeJournal Articleen
dc.identifier.journaltitleJournal of neuro-oncologyen
dc.identifier.affiliationSpinal Biology Research Laboratory, Department of Spinal Surgery, University of Melbourne Department of Surgery, Austin Health, 145 Studley Road, PO Box 5555, Heidelberg, VIC, 3084, Australiaen
dc.identifier.doi10.1007/s11060-013-1226-zen
dc.description.pages189-96en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/23955595en
dc.type.austinJournal Articleen
item.grantfulltextopen-
item.languageiso639-1en-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.openairetypeJournal Article-
item.fulltextWith Fulltext-
item.cerifentitytypePublications-
crisitem.author.deptInfectious Diseases-
crisitem.author.deptNeurosurgery-
crisitem.author.deptSurgery (University of Melbourne)-
Appears in Collections:Journal articles
Files in This Item:
File SizeFormat 
23955595.pdf55.56 kBAdobe PDFView/Open
Show simple item record

Page view(s)

4
checked on Feb 5, 2023

Download(s)

32
checked on Feb 5, 2023

Google ScholarTM

Check


Items in AHRO are protected by copyright, with all rights reserved, unless otherwise indicated.