Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9398
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dc.contributor.authorLiu, Zhanqien
dc.contributor.authorSmyth, Fiona Een
dc.contributor.authorRenner, Christophen
dc.contributor.authorLee, Fook-Theanen
dc.contributor.authorOosterwijk, Egberten
dc.contributor.authorScott, Andrew Men
dc.date.accessioned2015-05-15T22:28:45Z
dc.date.available2015-05-15T22:28:45Z
dc.date.issued2002-03-01en
dc.identifier.citationCancer Immunology, Immunotherapy : Cii 2002; 51(3): 171-7en
dc.identifier.govdoc11941456en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/9398en
dc.description.abstractThe chimeric monoclonal antibody cG250 targets the G250 antigen, a transmembrane protein which is expressed on renal carcinoma cells and is identical to the MN/CAIX antigen. In vitro studies have previously demonstrated that cG250 induces antibody-dependent cellular cytotoxicity (ADCC) of G250-positive targets. In order to investigate the upregulation of ADCC mediated by cG250, ADCC was examined using effector cells cultured in the presence or absence of the cytokines interferon-gamma (IFN-gamma), interferon-alpha isoforms IFN-alpha (2a) and IFN-alpha (2b) and interleukin-2 (IL-2), and the time course of effects over a 7-day period was determined. Renal cell carcinoma lines expressing high (SK-RC-52) and low (SK-RC-09) G250 antigen levels were used as target cells, and freshly isolated peripheral blood mononuclear cells (PBMC) from a healthy donor were used as the effector cells. PBMC were incubated with the respective cytokine at a range of concentrations or with a media alone control for a period of 7 days. The ADCC activity mediated by cG250 or control isotype matched huA33 with the different PBMC treatment groups was assessed in triplicate daily. Corresponding lymphokine activated killing (LAK) activity was measured concurrently for each treatment group. Chimeric G250 specifically recognised G250 antigen on high and low expressing cell lines SK-RC-52 and SK-RC-09, and mediated specific in vitro ADCC of both lines. In the absence of cytokine stimulation, the specific ADCC of cG250 declined rapidly within three days. IL-2 strongly enhanced and maintained cG250-mediated ADCC activity and K562 cytotoxicity when applied to PBMC in culture for seven days. IFN-gamma also enhanced the ADCC of cG250 throughout the study period, but was not as effective as the IL-2 treatment, and the SK-RC-09 line displayed lower specific cytotoxicity than the SK-RC-52 cell line. In contrast, IFN-alpha 2a and 2b increased cG250-mediated ADCC and K562 cytotoxicity for only three days of the study period. The potent and sustained immune effector activity observed with cG250 and cytokines in this in vitro study suggests that the combination immunotherapy of cG250 with cytokines such as IL-2 shows promise in the treatment of renal cell carcinoma (RCC).en
dc.language.isoenen
dc.subject.otherAnimalsen
dc.subject.otherAntibodies, Monoclonal.therapeutic useen
dc.subject.otherAntineoplastic Agents.therapeutic useen
dc.subject.otherCarcinoma, Renal Cell.immunology.therapyen
dc.subject.otherCell Separationen
dc.subject.otherCytokines.metabolismen
dc.subject.otherDose-Response Relationship, Drugen
dc.subject.otherFlow Cytometryen
dc.subject.otherImmunotherapy.methodsen
dc.subject.otherInterferon-gamma.metabolismen
dc.subject.otherInterferons.metabolismen
dc.subject.otherInterleukin-2.metabolismen
dc.subject.otherKidney Neoplasms.immunology.therapyen
dc.subject.otherKiller Cells, Natural.metabolismen
dc.subject.otherMiceen
dc.subject.otherTime Factorsen
dc.subject.otherTumor Cells, Cultureden
dc.titleAnti-renal cell carcinoma chimeric antibody G250: cytokine enhancement of in vitro antibody-dependent cellular cytotoxicity.en
dc.typeJournal Articleen
dc.identifier.journaltitleCancer immunology, immunotherapy : CIIen
dc.identifier.affiliationTumour Targeting Program, Ludwig Institute for Cancer Research, Melbourne Branch, Austin and Repatriation Medical Centre, Heidelberg, Victoria 3084, Australiaen
dc.identifier.doi10.1007/s00262-002-0268-4en
dc.description.pages171-7en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/11941456en
dc.type.austinJournal Articleen
local.name.researcherScott, Andrew M
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextWith Fulltext-
item.grantfulltextopen-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptMolecular Imaging and Therapy-
crisitem.author.deptOlivia Newton-John Cancer Research Institute-
Appears in Collections:Journal articles
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